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<title>Angiology</title>
<url>http://ang.sagepub.com:80/icons/banner/title.gif</url>
<link>http://ang.sagepub.com</link>
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<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/529?rss=1">
<title><![CDATA[Hypercoagulability Markers in Patients With Peripheral Arterial Disease: Association to Ankle-brachial Index]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/529?rss=1</link>
<description><![CDATA[<p>Peripheral arterial disease is diagnosed by measuring the ankle-brachial index. Values lower than 0.90 define the disease being usually related to its severity. Patients with peripheral arterial disease may show a hypercoagulability state. The aim of this study was to assess hemostatic variables and to correlate them with the presence of peripheral arterial disease and its severity as assessed by ankle-brachial index values. Plasma levels of D dimer, plasminogen, prothrombin fragment 1+2, plasminogen activator inhibitor and thrombomodulin were measured in 36 patients with peripheral arterial disease (group 1) and 30 without disease (group 2). Significant differences for D dimer, plasminogen, prothrombin fragment 1+2 and plasminogen activator inhibitor type 1 between the 2 groups were found (P&lt;0.05). Significant and inverse correlations were also observed (Pearson correlation, P&lt;0.05) between ankle-brachial index values and levels of both plasminogen and plasminogen activator inhibitor type 1. Although there was no significant correlation between ankle-brachial index and levels of D dimer, higher D dimer values were observed in patients with lower ankle-brachial index values. The results confirm a trend to hypercoagulability and hypofibrinolysis in patients with peripheral arterial disease. Increased levels of plasminogen activator inhibitor type 1 seem to be associated with the severity of the disease, considering the inverse correlation between this inhibitor and ankle-brachial index.</p>]]></description>
<dc:creator><![CDATA[Mota, A. P. L., de Castro Santos, M. E. R., Lima e Silva, F. d. C., de Carvalho Schachnik, N. C., de Oliveira Sousa, M., das Gracas Carvalho, M.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:09 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708325444</dc:identifier>
<dc:title><![CDATA[Hypercoagulability Markers in Patients With Peripheral Arterial Disease: Association to Ankle-brachial Index]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>535</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>529</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/536?rss=1">
<title><![CDATA[Angio-Seal Use in Patients with Peripheral Arterial Disease (ASPIRE)]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/536?rss=1</link>
<description><![CDATA[<p>Purpose: To investigate the incidence of complications after the use of an arterial closure device (Angio-Seal) in patients with peripheral arterial disease. Methods: In 105 consecutive patients after transfemoral catheterization, the puncture site was closed using a closure device (Angio-Seal). Colour-flow-duplexsonography studies were conducted 1 to 4 days before, within 3 days after and 3 month after the intervention. Results: All patients had peripheral arterial disease, 34 had calcification at the puncture site. Detection of calcification did not prevent device deployment. Complications (2 minor bleedings, 1 pseudoaneurysm) were not associated with high risk groups (these were: 69 antegrade punctures, 22 obese and 32 hypertensive patients). Three-month postinterventional diameter and blood velocity changes were &lt;1%. Conclusions: Patients with peripheral arterial disease in the region of the puncture site and patients at higher complication risk can safely and effectively be closed with an Angio-Seal device. At the puncture site, no lumen change can be observed 3 months postinterventional.</p>]]></description>
<dc:creator><![CDATA[Katzenschlager, R., Tischler, R., Kalchhauser, G., Panny, M., Hirschl, M.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708330007</dc:identifier>
<dc:title><![CDATA[Angio-Seal Use in Patients with Peripheral Arterial Disease (ASPIRE)]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>538</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>536</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/539?rss=1">
<title><![CDATA[Increased apoB/apoA-I Ratio Is Predictive of Peripheral Arterial Disease in Initially Healthy 58-Year-old Men During 8.9 Years of Follow-up]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/539?rss=1</link>
<description><![CDATA[<p>The aim of the present study was to investigate, if increased levels of apoB/apoA-I ratios are associated with future peripheral arterial disease as measured by ankle-brachial index. Increased apoB/apoA-I levels are defined as 0.9, which has been suggested for men, and as 0.63, which has observed to be associated with plaques in the femoral artery. The study was performed in a cohort of initially clinically healthy 58-year-old men living in the city of G&ouml;teborg, Sweden.</p><p>The group with an apoB/apoA-I ratio &ge;0.9 had a significantly increased risk of having PAD during 8.9 years of follow-up than the group below that level (OR: 2.15 CI: 1.21 to 3.82, p &lt; 0.01). When applying the lower apoB/apoA-I cut off, results showed that the group with a level &gt;0.63 had more than a three-fold risk of future PAD compared to the group &le;0.63 (OR: 3.28 CI: 1.14 to 9.40, p &lt; 0.05).</p>]]></description>
<dc:creator><![CDATA[Johansson, L., Schmidt, C.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708324925</dc:identifier>
<dc:title><![CDATA[Increased apoB/apoA-I Ratio Is Predictive of Peripheral Arterial Disease in Initially Healthy 58-Year-old Men During 8.9 Years of Follow-up]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>545</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>539</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/546?rss=1">
<title><![CDATA[Relationship Between Peripheral Arterial Disease and Metabolic Syndrome]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/546?rss=1</link>
<description><![CDATA[<p>The aim of the study was to estimate the prevalence of metabolic syndrome among 388 patients with peripheral arterial disease, to determine the relationship between the number of metabolic syndrome components (metabolic syndrome score) and the degree of established and some of the emerging vascular risk factors, and to estimate whether there was any relationship of metabolic syndrome score and other vascular risk factors with the severity of peripheral arterial disease clinical manifestations. Metabolic syndrome was present in 59.8% of the patients with peripheral arterial disease. All metabolic syndrome components were significantly related to metabolic syndrome score. The same was true for the body weight, body mass index, percentage of body fat, total cholesterol/high-density lipoprotein cholesterol ratio, uric acid, and percentage of patients with high-sensitivity C-reactive protein. The metabolic syndrome score was also significantly, but inversely, related to high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and smoking. The degree of peripheral arterial disease clinical manifestations was not related to metabolic syndrome score, but gangrene was significantly positively associated with increased fasting glucose, high-sensitivity C-reactive protein, and lower education.</p>]]></description>
<dc:creator><![CDATA[Maksimovic, M., Vlajinac, H., Radak, D., Marinkovic, J., Jorga, J.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708325445</dc:identifier>
<dc:title><![CDATA[Relationship Between Peripheral Arterial Disease and Metabolic Syndrome]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>553</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>546</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/554?rss=1">
<title><![CDATA[Acute Limb Ischemia Caused by Femoral Arterial Line Induces Remote Liver Injury in a Rabbit Model of Liver Ischemia/Reperfusion Injury]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/554?rss=1</link>
<description><![CDATA[<p>Femoral arterial lines are used for continuous monitoring of arterial blood pressure in experimental studies. However, placement of a catheter in the femoral artery could produce acute limb ischemia with associated systemic effects. The aim of this study was to investigate the effect of femoral arterial line insertion on liver function, in a rabbit liver lobar ischemia-reperfusion (I/R) model. Four groups of animals (n = 6 each) were studied: groups 1 and 2 (sham) underwent laparotomy but no liver ischemia. In groups 3 and 4 (I/R), liver lobar ischemia was induced for 60 minutes followed by 7 hours of reperfusion. In groups 1 and 3, the arterial line was placed in the femoral artery whereas in groups 2 and 4 in the ear artery. Liver function was assessed by serum alanine aminotransferase (ALT) activity, bile flow, plasma lactate levels, and histology. Results are expressed as mean &plusmn; SEM. Alanine aminotransferase activity and lactate levels were significantly higher in the I/R femoral line group compared with the I/R ear line group at 7 hours postreperfusion. Bile production was significantly lower (75 &plusmn; 9.6 vs 112 &plusmn; 10 &micro;L/min per 100 g liver weight). Histopathology showed more extensive hepatocellular necrosis and neutrophil accumulation in the I/R femoral line group compared with I/R ear line group. The sham femoral group showed liver injury, which was more marked than the ear line group (all P &lt; .05). In conclusion, femoral artery cannulation induces remote liver injury. The use of femoral arterial lines should be avoided in experimental studies concerning liver function.</p>]]></description>
<dc:creator><![CDATA[Glantzounis, G. K., Sheth, H., Thompson, C., Hafez, T. S., Kanoria, S., Pamecha, V., Davies, S., Mikhailidis, D. P., Seifalian, A. M., Davidson, B. R.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709338176</dc:identifier>
<dc:title><![CDATA[Acute Limb Ischemia Caused by Femoral Arterial Line Induces Remote Liver Injury in a Rabbit Model of Liver Ischemia/Reperfusion Injury]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>561</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>554</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/562?rss=1">
<title><![CDATA[Evidence for Telomerase Activation in VSMCs Exposed to Hyperglycemic and Hyperhomocysteinemic Conditions]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/562?rss=1</link>
<description><![CDATA[<p>Purpose: While diabetes and homocysteinemia have been demonstrated to be independent risk factors for progression of vascular disease, the activation of telomerase has not been linked to the potent effects of high levels of homocysteine (Hcy) and glucose on vascular smooth muscle cells (VSMC). We examined the proliferative response of VSMCs, resulting from hyperglycemia and hyperhomocysteinemia and their effects on telomerase activity. Methods: Primary cultures of VSMC from human aorta and arteries were used in this experiment from 3rd -5th passages. Hcy or/and glucose were added to the cell culture media in doses equivalent to plasma levels of Hcy in patients with moderate, high homocysteinemia, or physiologically high concentrations of glucose as seen in diabetics. The modified telomeric repeat amplification protocol was used for telomerase activity assay. Cytotoxicity, viability, proliferation, protein phosphorylation, were determined in cultures treated and not treated with Hcy and glucose. Results: The mitogenic effect of Hcy and glucose on VSMC, independently and together, was observed at 48 hours after treatment. The viable cell numbers were significantly increased at doses comparable to plasma levels of Hcy in hyperhomocysteinemia, as compared to untreated cultures (p &lt; 0.01). Cells exposed to high levels of glucose also exhibited an increased proliferation response (p = 0.01). Telomerase activity was detected in all sets of VSMC cultures exposed to high levels of glucose or/and Hcy (p &lt; 0.01). However, a significant difference was not observed in telomerase activity, when high Hcy or high glucose was used alone or in concert. Significant dual phosphorylation of p38 MAPK was observed in treated cultures but it did not correlate with the telomerase activity detected. Conclusion: These data establish a link with telomerase activation and the mitogenic effect of hyperhomocysteinemia and hyperglycemia.</p>]]></description>
<dc:creator><![CDATA[Jacob, T., Hingorani, A., Ascher, E.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709332956</dc:identifier>
<dc:title><![CDATA[Evidence for Telomerase Activation in VSMCs Exposed to Hyperglycemic and Hyperhomocysteinemic Conditions]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>568</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>562</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/569?rss=1">
<title><![CDATA[Gender-specific Effects of Calcitonin Gene-related Peptide and Substance P on Coronary Blood Flow in an Experimental Model]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/569?rss=1</link>
<description><![CDATA[<p>Background: Calcitonin gene-related peptide (CGRP) and substance P (SP) play counter-regulatory roles in coronary flow. This study is to assess whether effects of CGRP and SP are gender-specific. Methods: Langendorff-perfused hearts were used to compare coronary flow rates among 119 wild-type, -CGRP and SP receptor knockout mice under various perfusion pressures (20, 30, 40, 50 mmHg). Results: For mouse heart coronary flow rate, deletion of -CGRP gene resulted in significant reduction for both genders at all pressures; female CGRP knockout showed 15.3% reduction (P &lt; .01); male CGRP knockout showed 13.8% reduction (P &lt; .01); no significant difference between male and female CGRP knockout; female SP receptor knockout showed 13.9% increase (P &lt; .01); female SP receptor knockout had a greater percentage decrease than male (P &lt; .01). Conclusions: CGRP plays similar roles as a vasodilator in males and females. SP seems to act as a vasoconstrictor in females.</p>]]></description>
<dc:creator><![CDATA[Hongbao, M., Yan, Y., Shen, C.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708325450</dc:identifier>
<dc:title><![CDATA[Gender-specific Effects of Calcitonin Gene-related Peptide and Substance P on Coronary Blood Flow in an Experimental Model]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>575</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>569</prism:startingPage>
<prism:section>Articles</prism:section>
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<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/576?rss=1">
<title><![CDATA[The Influence of COX-2 Single Nucleotide Polymorphisms on Abdominal Aortic Aneurysm Development and the Associated Inflammation]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/576?rss=1</link>
<description><![CDATA[<p>Introduction: Cyclooxygenase (COX)-2 influences cardiovascular disease and serum concentration of high-sensitivity C-reactive protein (hsCRP). The study purpose was to determine the influence of single nucleotide polymorphisms (SNPs) of the COX-2 gene on abdominal aortic aneurysm (AAA) development and serum hsCRP concentrations. Patients and Methods: Patients with AAA and disease-free controls were recruited. High-sensitivity C-reactive protein was measured by an enzyme-linked immunosorbent assay (ELISA) test. The distributions of COX-2 SNPs were investigated (rs20417 and rs4648307). The influence of the COX-2 SNPs on the hsCRP serum concentration was assessed.Results: A total of 230 patients with AAA and 279 controls were included. No difference was found in the genotype distribution of the COX-2 SNPs rs20417 (P = .26) and rs4648307 (P = .90). They did not influence the hsCRP concentration (P = .24 and P = .61, respectively). Haplotype analysis of COX-2 SNPs revealed no difference. Conclusion: These COX-2 SNPs do not play any role in AAA development and do not influence serum hsCRP. These results differentiate AAA development from atherosclerotic diseases.</p>]]></description>
<dc:creator><![CDATA[Badger, S. A., Soong, C. V., Young, I. S., McGinty, A., Mercer, C., Hughes, A. E.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709335027</dc:identifier>
<dc:title><![CDATA[The Influence of COX-2 Single Nucleotide Polymorphisms on Abdominal Aortic Aneurysm Development and the Associated Inflammation]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>581</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>576</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/582?rss=1">
<title><![CDATA[Mortality After First Myocardial Infarction in Greek Patients: A 4-Year Follow-Up Study]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/582?rss=1</link>
<description><![CDATA[<p>Background: Death associated with coronary heart disease (CHD) depends in part on the time since the myocardial infarction (MI) and modification of risk factors. Methods: This observational, retrospective 4-year follow-up study consisted of 804 patients (628 men). The participants completed a questionnaire reporting diet, demographic factors, personal behavior (smoking, physical activity), anthropometry, prior medical conditions (hypertension, diabetes mellitus), and recent medication. Results: During 48 months of follow-up, 12% of men and 15% of women died. Older age, longer duration of smoking, and frequency of exercise were significantly different between survivors and the deceased (P = .014, P = .014, P = .001, respectively). Multivariate analysis revealed associations with years of smoking (odds ratio, OR: 1.10, P = .025), treatment with nitrates (OR: 4.81, P = .024), and increased frequency of exercise (OR: 0.42, P = .013), adjusting for age and gender. Conclusions: We should emphasize cessation of smoking and increased physical activity in MI survivors. Antismoking programs should start at an early age.</p>]]></description>
<dc:creator><![CDATA[Kolovou, G. D., Mihas, C., Kotanidou, A., Dimoula, Y., Karkouli, G., Kadda, O., Anagnostopoulou, K., Mikhailidis, D. P., Marvaki, C.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709343285</dc:identifier>
<dc:title><![CDATA[Mortality After First Myocardial Infarction in Greek Patients: A 4-Year Follow-Up Study]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>587</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>582</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/588?rss=1">
<title><![CDATA[Is Polymorphism Within eNOS Gene Associated With the Late Onset of Myocardial Infarction? A Pilot Study]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/588?rss=1</link>
<description><![CDATA[<p>Introduction: Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) is a potent vasodilator. Several polymorphisms in the eNOS gene have been described, some of them being linked with the increased risk of cardiovascular disease, coronary heart disease (CHD), and coronary spasm. Methods and Results: We studied 3 polymorphisms within the gene of eNOS (-786T/C, G10T, and 894 G/T) in patients with their first myocardial infarction (MI) younger than 45 years and in healthy volunteers. We found the relation between the occurrence of eNOS 894G allele and the Gensini score, which describes the severity of CHD (P = .020). Conclusions: The fact that first clinical manifestation of MI occurred in G carriers when the atherosclerotic plaque was much more advanced than in T carriers may suggest that wild-type genotype provided a better compensatory mechanisms due to NO synthesis and/or release. The polymorphisms within eNOS gene G10T, 894G/T, and -786T/C were not associated with the increased risk of MI.</p>]]></description>
<dc:creator><![CDATA[Gluba, A., Banach, M., Rysz, J., Piotrowski, G., Fendler, W., Pietrucha, T.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709335031</dc:identifier>
<dc:title><![CDATA[Is Polymorphism Within eNOS Gene Associated With the Late Onset of Myocardial Infarction? A Pilot Study]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>595</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>588</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/596?rss=1">
<title><![CDATA[Association Between Carotid and Coronary Artery Disease in Patients With Aortic Valve Stenosis: An Angiographic Study]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/596?rss=1</link>
<description><![CDATA[<p>Background: Patients with aortic stenosis have a high prevalence of coronary artery disease, but there is little information about the association of coronary artery disease and carotid artery disease.</p><p>Methods: The study includes 317 consecutive patients with aortic stenosis, who underwent carotid and coronary angiography during the same catheterization before aortic valve replacement.</p><p>Results: At univariate analysis, the prevalence of coronary artery disease was associated with (1) presence of carotid artery disease (P &lt; .001); (2) angina pectoris as presentation symptom (P &lt; .001); (3) age more than 65 years (P &lt; .05); and (4) hypertension (P &lt; .05). At multivariate analysis, only carotid artery disease, angina, and age emerged as independent predictors of coronary artery disease. The combination of 2 variables (carotid artery disease, angina) allowed the identification of 4 groups, with decreasing prevalence of coronary artery disease: (1) angina+/carotid artery disease+: 85%; (2) angina-/ carotid artery disease+: 50%; (3) angina+/carotid artery disease-: 41%; (4) angina-/carotid artery disease-: 21% (P &lt; .001). Conclusion: In patients with symptomatic aortic stenosis, the presence of significant carotid artery disease is a strong marker of significant coronary artery disease.</p>]]></description>
<dc:creator><![CDATA[Antonini-Canterin, F., Leiballi, E., Capanna, M., Burelli, C., Cassin, M., Macor, F., Grandis, U., Nicolosi, G. L.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708327646</dc:identifier>
<dc:title><![CDATA[Association Between Carotid and Coronary Artery Disease in Patients With Aortic Valve Stenosis: An Angiographic Study]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>600</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>596</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/601?rss=1">
<title><![CDATA[Low-dose Fixed Combination of Bisoprolol/Hydrochlorothiazide as First Line for Hypertension: A Review of the Rationale and Clinical Evidence]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/601?rss=1</link>
<description><![CDATA[<p>Essential hypertension is a heterogeneous multifactorial disease. Data from the National Health and Nutritional Examination Survey and from the World Health Organization have clearly demonstrated that, worldwide, less than 30% of hypertensive patients are adequately controlled by our currently accepted blood pressure goals. Although monotherapy is often unable to achieve blood pressure goals, the use of fixed low-dose combination drugs as alternative treatment seems to be related to a better antihypertensive efficacy and higher response rates in the low range of doses as the result of complementary mechanisms of antihypertensive effects. Indeed clinical trials have shown that initial low-dose combination therapy is superior as compared with treatment by the stepped-care and the sequential monotherapy approach, while recently, low-dose combination therapy for initial antihypertensive therapy instead of the stepped-care approach or of sequential monotherapy has been recommended. This review summarizes the beneficial effect of low-dose bisoprolol/ hydrochlorothiazide combination in the treatment of patients with stage I and II hypertension.</p>]]></description>
<dc:creator><![CDATA[Papadopoulos, D. P., Papademetriou, V.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708324926</dc:identifier>
<dc:title><![CDATA[Low-dose Fixed Combination of Bisoprolol/Hydrochlorothiazide as First Line for Hypertension: A Review of the Rationale and Clinical Evidence]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>607</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>601</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/608?rss=1">
<title><![CDATA[Metoprolol Succinate Combination in the Treatment of Hypertension]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/608?rss=1</link>
<description><![CDATA[<p>Metoprolol is a selective &beta;(1)-adrenergic antagonist extensively used since 1975. Metoprolol has proven its efficacy in reducing cardiovascular events and mortality in patients with hypertension and coronary heart disease. A recently developed controlled release/ extended-release formulation of metoprolol succinate was designed to provide relatively constant metoprolol plasma concentrations and &beta;(1)-blockade while retaining the convenience of once daily administration. A 100-mg metoprolol controlled/extended-release tablet contains 95 mg of metoprolol succinate and is considered to have equivalent activity of 100 mg metoprolol tartrate. After ingestion, the tablet disintegrates into individual pellets and each pellet acts as a diffusion cell releasing the drug at a relatively constant rate over a period of approximately 20 hours. The aim of this review was to determine the pharmacokinetic and pharmacodynamic properties of metoprolol succinate and to apply those properties in combination with other drugs mainly diuretics in the treatment of hypertension.</p>]]></description>
<dc:creator><![CDATA[Papadopoulos, D. P., Papademetriou, V.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708326450</dc:identifier>
<dc:title><![CDATA[Metoprolol Succinate Combination in the Treatment of Hypertension]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>613</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>608</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/614?rss=1">
<title><![CDATA[Responses of Blood Lipids to Aerobic, Resistance, and Combined Aerobic With Resistance Exercise Training: A Systematic Review of Current Evidence]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/614?rss=1</link>
<description><![CDATA[<p>This review considers the effectiveness of aerobic exercise training with different intensities (moderate and high) as well as the type of exercise (aerobic, resistance, and combined aerobic with resistance) in altering the blood lipids. We reviewed various trials via a systematic search of PubMed, published reviews, and references from original articles. We selected studies that involved aerobic and/or resistance and/or combined exercise training in healthy adults over a limit of 12 weeks and had examined the response of training to one or more of the following: triglycerides, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. We selected a total of 84 studies, 58 were randomized controlled trials. Comparisons between intensities of aerobic exercise programs resulted in favorable effects only for high intensity. The most frequently observed alteration was an increase in the high-density lipoprotein cholesterol, whereas reductions in triglycerides, total cholesterol, and low-density lipoprotein cholesterol appeared less often. Moreover, the evidence of the positive effect of resistance exercise marks out a trend mainly for the low-density lipoprotein cholesterol levels, whereas for combined exercise, results extracted from a short list of published studies show improvements in values of both the high-density lipoprotein cholesterol and the low-density lipoprotein cholesterol. High-intensity aerobic training results in improvement in high-density lipoprotein cholesterol. For resistance and combined exercise, the results are inconsistent. The heterogeneity between the types of exercise did not allow reliable comparisons.</p>]]></description>
<dc:creator><![CDATA[Tambalis, K., Panagiotakos, D. B., Kavouras, S. A., Sidossis, L. S.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708324927</dc:identifier>
<dc:title><![CDATA[Responses of Blood Lipids to Aerobic, Resistance, and Combined Aerobic With Resistance Exercise Training: A Systematic Review of Current Evidence]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>632</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>614</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/633?rss=1">
<title><![CDATA[Selective Screening for Asymptomatic Carotid Artery Disease Prior to Isolated Heart Valve Surgery]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/633?rss=1</link>
<description><![CDATA[<p>Objective: To assess the yield of screening for asymptomatic carotid artery disease prior to isolated heart valve surgery (IHVS).</p><p>Methods: Retrospective analysis of the preoperative carotid duplex scans performed in neurologically asymptomatic patients who underwent IHVS between 2003 and 2006 was performed. Internal carotid artery (ICA) stenosis of 70% was considered significant. Patients with concomitant coronary artery disease were excluded.</p><p>Results: A total of 177 patients underwent IHVS (one valve in 165 and 2 valves in 12 patients). No or minor ICA disease detected in 172 patients. Four patients (2.25%) had significant unilateral ICA stenosis and 1 patient (0.56%) had unilateral ICA occlusion. Three patients (1.69%) suffered postoperative stroke, while 2 patients (1.1%) suffered transient ischemic attacks. All neurologically affected patients had normal preoperative carotid duplex. The in-hospital mortality was 4.5%.</p><p>Conclusion: Prevalence of significant ICA disease is low in patients undergoing IHVS. This population does not benefit from preoperative carotid screening.</p>]]></description>
<dc:creator><![CDATA[Zayed, H., Ali, A., Wendler, O., Rashid, H.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708325446</dc:identifier>
<dc:title><![CDATA[Selective Screening for Asymptomatic Carotid Artery Disease Prior to Isolated Heart Valve Surgery]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>636</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>633</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/637?rss=1">
<title><![CDATA[The Effect of Age and Other Atherosclerotic Risk Factors on Carotid Artery Blood Velocity in Individuals Ranging From Young Adults to Centenarians]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/637?rss=1</link>
<description><![CDATA[<p>To evaluate the effect of age and other risk factors for atherosclerosis on arterial blood velocity, carotid arteries in 179 healthy individuals ranging from 21 to 102 years old were examined using color Doppler ultrasonography. Velocity in common and internal carotid arteries decreased consecutively from young adults to very elderly people except for peak internal carotid artery velocity. Peak common carotid artery velocity in the elderly (&ge; 65 years old) people was inversely associated with age and diastolic blood pressure and directly associated with pulse pressure. Minimum velocity of common carotid artery was inversely correlated with age and diastolic blood pressure in the elderly people. In elderly group, peak internal carotid artery velocity correlated only with serum high-density lipoprotein cholesterol. Minimum internal carotid artery velocity correlated inversely with systolic blood pressure in adults and diastolic blood pressure in elderly people. Blood velocity in the very elderly population approaches the critical level for thrombogenesis.</p>]]></description>
<dc:creator><![CDATA[Homma, S., Sloop, G. D., Zieske, A. W.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708325447</dc:identifier>
<dc:title><![CDATA[The Effect of Age and Other Atherosclerotic Risk Factors on Carotid Artery Blood Velocity in Individuals Ranging From Young Adults to Centenarians]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>643</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>637</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/5/644?rss=1">
<title><![CDATA[High-density Lipoprotein Cholesterol: Current Perspective for Clinicians]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/5/644?rss=1</link>
<description><![CDATA[<p>High-density lipoproteins are regarded as &lsquo;&lsquo;good guys&rsquo;&rsquo; but not always. Situations involving high-density lipoproteins are discussed and medication results are considered. Clinicians usually consider high-density lipoprotein cholesterol. Nicotinic acid is the best available medication to elevate high-density lipoprotein cholesterol and this appears beneficial for cardiovascular risk. The major problem with nicotinic acid is that many patients do not tolerate the associated flushing. Laropiprant decreases this flushing and has an approval in Europe but not in the United States. The most potent medications for increasing high-density lipoprotein cholesterol are cholesteryl ester transfer protein inhibitors. The initial drug in this class, torcetrapib, was eliminated by excess cardiovascular problems. Two newer cholesteryl ester transfer protein inhibitors, R1658 and anacetrapib, initially appear promising. High-density lipoprotein cholesterol may play an important role in improving cardiovascular risk in the 60% of patients who do not receive cardiovascular mortality/morbidity benefit from low-density lipoproteins reduction by statins.</p>]]></description>
<dc:creator><![CDATA[Whayne, T. F.]]></dc:creator>
<dc:date>Thu, 22 Oct 2009 01:29:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709331392</dc:identifier>
<dc:title><![CDATA[High-density Lipoprotein Cholesterol: Current Perspective for Clinicians]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>649</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>644</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/reprint/60/4/397?rss=1">
<title><![CDATA[Atherosclerotic Renal Artery Stenosis: Medical Therapy Alone or in Combination With Revascularization?]]></title>
<link>http://ang.sagepub.com/cgi/reprint/60/4/397?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Karagiannis, A., Tziomalos, K., Anagnostis, P., Gossios, T., Athyros, V. G.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709334262</dc:identifier>
<dc:title><![CDATA[Atherosclerotic Renal Artery Stenosis: Medical Therapy Alone or in Combination With Revascularization?]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>402</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>397</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/403?rss=1">
<title><![CDATA[Remote Ischemic Preconditioning Stimulus Does Not Reduce Microvascular Resistance or Improve Myocardial Blood Flow in Patients Undergoing Elective Percutaneous Coronary Intervention]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/403?rss=1</link>
<description><![CDATA[<p>Introduction: Remote ischemic preconditioning (RIPC) may limit myocardial infarction by improving microvascular function and maintaining myocardial blood flow. We hypothesized that a RIPC stimulus would reduce coronary microvascular resistance and improve coronary blood flow during elective percutaneous coronary intervention (PCI).</p><p>Method: We prospectively recruited 54 patients with multi-vessel disease (MVD = 32) or single vessel disease awaiting elective PCI. Patients with MVD had non-target vessel (NTV) index of micro-circulatory resistance (IMR) determined, before and after target vessel (TV) PCI (cardiac RIPC). The effect of arm RIPC on serial microvascular resistance (R<SUB>p</SUB>) was assessed in patients with single vessel disease.</p><p>Results: TV balloon occlusion did not alter the NTV IMR: 16.5 (12.4) baseline vs. 17.6 (11.6) post cardiac RIPC, P = 0.65 or hyperaemic transit time. Arm RIPC did not alter R<SUB> p</SUB> in patients with single vessel disease: Rp, mmHg.cm<sup>-1</sup>.s<sup> -1</sup>: 3.5 (1.9) baseline vs. 4.1 (3.0) post arm RIPC, P = 0.19 and coronary flow velocity remained constant. Conclusion: RIPC stimuli during elective PCI do not affect coronary microvascular resistance or coronary flow in humans.</p>]]></description>
<dc:creator><![CDATA[Hoole, S. P., Heck, P. M., White, P. A., Khan, S. N., O'Sullivan, M., Clarke, S. C., Dutka, D. P.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708328921</dc:identifier>
<dc:title><![CDATA[Remote Ischemic Preconditioning Stimulus Does Not Reduce Microvascular Resistance or Improve Myocardial Blood Flow in Patients Undergoing Elective Percutaneous Coronary Intervention]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>411</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>403</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/412?rss=1">
<title><![CDATA[Delayed Enhancement Morphology on Cardiac Magnetic Resonance Imaging is Correlated With Signal-averaged Electrocardiogram and QT Dispersion in Myocardial Infarction]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/412?rss=1</link>
<description><![CDATA[<p>Background: In patients with myocardial infarction, ventricular tachycardia is related with nonconductive ventricular scar. Cardiac magnetic resonance imaging is an excellent modality to evaluate myocardial scars in myocardial infarction. Furthermore, late potential obtained from signal-averaged electrocardiogram and QT dispersion are both well-known parameters for predicting lethal arrhythmias. Methods and Results: To investigate whether the pattern of necrotic scar tissue visualized by delayed enhancement on cardiac magnetic resonance imaging is associated with late potential and QT dispersion, we measured late potential and QT dispersion in 27 patients (68 &plusmn; 8 years old) with a prior myocardial infarction. Cardiac magnetic resonance imaging was also obtained using a 1.5-tesla cardiac magnetic resonance scanner, and delayed enhancement was analyzed in the short axis of the left ventricle. By conducting this, we tried to determine whether the pattern of necrotic scar tissue predicts lethal ventricular arrhythmias. Semiquantitative patchy scores were identified as the mean patchy score and the maximum patchy score in each patient. There were 9 patients with a positive late potential and 18 patients with a negative late potential. Patients with positive late potentials had significantly larger mean (1.7 &plusmn; 0.3) and maximum (2.2 &plusmn; 0.6) patchy scores than patients with negative late potentials (mean, 1.3 &plusmn; 0.2, P &lt; .05; maximum, 1.7 &plusmn; 0.4, P &lt; .05). QT dispersion was significantly correlated with the number of slices showing delayed enhancement, which reflects the size of necrotic scar tissue (r = .59, P &lt; .05). Conclusions: These findings suggest that the pattern of necrotic scar tissue visualized by delayed enhancement with cardiac magnetic resonance imaging was correlated to the predictive indices of lethal ventricular arrhythmias.</p>]]></description>
<dc:creator><![CDATA[Takase, B., Nagata, M.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708329798</dc:identifier>
<dc:title><![CDATA[Delayed Enhancement Morphology on Cardiac Magnetic Resonance Imaging is Correlated With Signal-averaged Electrocardiogram and QT Dispersion in Myocardial Infarction]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>418</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>412</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/419?rss=1">
<title><![CDATA[Role of Pro-/Anti-Inflammatory Cytokines and Their Correlation With Established Risk Factors in South Indians With Coronary Artery Disease]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/419?rss=1</link>
<description><![CDATA[<p>Cytokines are responsible for the modulation of immunological and inflammatory processes and play a significant role in the pathogenesis of coronary artery disease. We estimated the levels of pro-/anti-inflammatory cytokines in South Indian patients with coronary artery disease. The study population comprised of groups 1-3: 100 patients each with acute myocardial infarction, unstable angina, and stable angina, respectively, and group 4 (100 healthy controls). Cytokine levels (interleukin-6, interleukin-8, interleukin-10, and tumor necrosis factor-) were estimated by enzyme-linked immunosorbent assay (ELISA). Interleukin-6, interleukin-8, and tumor necrosis factor- levels were significantly higher in patients from groups 1 and 2, than in group 3 and controls. Acute myocardial infarction patients exhibited higher serum levels of interleukin-10 compared with other groups and control subjects. Patients with unstable angina had significantly lower interleukin-10 concentrations than those with stable angina. The ratios of pro-/anti-inflammatory cytokines in all the study groups increased significantly when patients with unstable angina were compared to other groups. In patients with acute myocardial infarction, interleukin-10 and tumor necrosis factor- levels showed significant correlation with established risk factors such as body mass index, blood pressure, and lipid levels. Acute myocardial infarction patients show elevation in proinflammatory and anti-inflammatory cytokines, while unstable angina is associated with low levels of serum interleukin-10. Higher levels of anti-inflammatory cytokine interleukin-10 may be needed to provide protection in unstable angina. These cytokines are markers of coronary artery disease and may be used for the identification of high-risk patients with unstable angina/acute myocardial infarction.</p>]]></description>
<dc:creator><![CDATA[Rajappa, M., Sen, S.K., Sharma, A.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708321101</dc:identifier>
<dc:title><![CDATA[Role of Pro-/Anti-Inflammatory Cytokines and Their Correlation With Established Risk Factors in South Indians With Coronary Artery Disease]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>426</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>419</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/427?rss=1">
<title><![CDATA[Serial Changes of Circulating Platelet Activation Markers After Carotid Artery Stenting]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/427?rss=1</link>
<description><![CDATA[<p>We investigated serial changes of circulation platelet activation markers in 40 patients undergoing carotid artery stenting under the protection of dual antiplatelet therapy and filter devices. Monocyte-platelet aggregates and PAC-1 (a marker specific for activated glycoprotein IIb/IIIa) analyzed by flow cytometry were determined in patients with symptomatic stenosis undergoing elective carotid artery stenting. Blood samples were obtained immediately before stent implantation and 0.5 hours, 18 hours, and 6 days after the procedure, respectively. All patients were already on dual antiplatelet therapy of aspirin and clopidogrel before carotid artery stenting, and all were stented with embolic protection devices. Both circulation monocyte-platelet aggregates and PAC-1 did not change significantly at the various time points after the procedure. Serial changes of monocyte-platelet aggregates and PAC-1 analyzed by flow cytometry fail to indicate the occurrence of platelet activation after carotid artery stenting under the treatment with dual antiplatelet therapy before carotid artery stenting and the application of embolic protection devices during the procedure.</p>]]></description>
<dc:creator><![CDATA[Liu, F., Li, J., Wang, D.-M., Liu, J.-C., Huang, Y.-N.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708321103</dc:identifier>
<dc:title><![CDATA[Serial Changes of Circulating Platelet Activation Markers After Carotid Artery Stenting]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>430</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>427</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/431?rss=1">
<title><![CDATA[Impact on Diabetes Mellitus on the Epicardial Coronary Flow Velocity Assessed by the Thrombolysis in Myocardial Infarction Frame Count]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/431?rss=1</link>
<description><![CDATA[<p>The aim of this study is to evaluate the effect of type 2 diabetes mellitus on epicardial coronary flow velocity assessed by the thrombolysis in myocardial infarction frame count. The thrombolysis in myocardial infarction frame count was measured in 272 coronary arteries from 101 patients with type 2 diabetes mellitus and in 271 coronary arteries from 104 age- and gender-matched patients without type 2 diabetes mellitus referred for coronary angiography. The thrombolysis in myocardial infarction frame count was measured only in normal arteries or in arteries without significant lesion. By both univariate and multivariate analysis, the thrombolysis in myocardial infarction frame count was not related with either type 2 diabetes mellitus or the duration and glycated hemoglobin levels in the patients with type 2 diabetes mellitus. The thrombolysis in myocardial infarction frame count was significantly associated with body surface area, heart rate, and proximal coronary artery diameter. Type 2 diabetes mellitus did not affect epicardial coronary flow velocity assessed by the thrombolysis in myocardial infarction frame count.</p>]]></description>
<dc:creator><![CDATA[Soylu, A., Ozdemir, K., Duzenli, M. A., Yazici, M., Tokac, M.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708321187</dc:identifier>
<dc:title><![CDATA[Impact on Diabetes Mellitus on the Epicardial Coronary Flow Velocity Assessed by the Thrombolysis in Myocardial Infarction Frame Count]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>440</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>431</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/441?rss=1">
<title><![CDATA[Wall Shear Stress Measurement Using Phase Contrast Magnetic Resonance Imaging With Phase Contrast Magnetic Resonance Angiography in Arteriovenous Polytetrafluoroethylene Grafts]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/441?rss=1</link>
<description><![CDATA[<p>Purpose: The purpose of the present article was to determine the changes in luminal vessel area, blood flow, and wall shear stress in both the inflow artery and the venous stenosis of arteriovenous polytetrafluoroethylene (PTFE) grafts. Methods and materials: Polytetrafluoroethylene grafts were placed from the carotid artery to the ipsilateral jugular vein in 8 castrated juvenile male pigs. Contrast-enhanced magnetic resonance angiography (MRA) with cine phase-contrast magnetic resonance imaging (MRI) was performed 2 weeks after graft placement. Results: The mean wall shear stress at the venous stenosis was 4 times higher than the control vein, while the inflow artery was only 2-fold higher. By day 14, venous stenosis had formed, which was characterized by narrowed area and elevated blood flow. Conclusion: By day 14, there is venous stenosis formation in porcine arteriovenous PTFE grafts with increased shear stress with decreased area when compared to control vein.</p>]]></description>
<dc:creator><![CDATA[Misra, S., Fu, A. A., Misra, K. D., Glockner, J. F., Mukhopadhyay, D.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709335908</dc:identifier>
<dc:title><![CDATA[Wall Shear Stress Measurement Using Phase Contrast Magnetic Resonance Imaging With Phase Contrast Magnetic Resonance Angiography in Arteriovenous Polytetrafluoroethylene Grafts]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>447</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>441</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/448?rss=1">
<title><![CDATA[Effects of Antioxidants on Endothelial Function in Human Saphenous Vein in an Ex vivo Model]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/448?rss=1</link>
<description><![CDATA[<p>This ex vivo study is aimed at determining the beneficial effects of antioxidant agents on human saphenous vein endothelial function. Vein rings harvested during infrainguinal bypass surgery were assessed in an organ bath for endothelium-dependent relaxation, initially without and then with the addition of 10 &micro;M manganese tetrakis benzoic acid porphyrin (MnTBAP), 0.01% N-acetylcysteine (NAC), 0.02% NAC, 10 &micro;M vitamin C, and 100 &micro;M vitamin C. Fifty-five vein rings from 22 patients were analyzed. MnTBAP improved the endothelium-dependent relaxation when compared with control (57.0% vs 37.8%, <I>P</I> &lt; .01). Addition of 0.01% or 0.02% NAC did not improve the endothelium-dependent vasorelaxation (28.2% vs 18.6%, <I>P</I> = ns and 37.8% vs 29.8%, <I>P</I> = ns, respectively). Although 10-&micro;M vitamin C failed to improve endothelial function (50.6% vs 37.2%, <I>P</I> = ns), 100-&micro;M vitamin C significantly enhanced endothelium-dependent relaxation (66.5% vs 38.3%, <I>P</I> &lt; .001). These results suggest that the addition of MnTBAP and high-dose vitamin C can improve the endothelial function of harvested saphenous vein segments in an ex vivo model.</p>]]></description>
<dc:creator><![CDATA[Sharif, M. A., Bayraktutan, U., Arya, N., Badger, S. A., O'Donnell, M. E., Young, I. S., Soong, C. V.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708321186</dc:identifier>
<dc:title><![CDATA[Effects of Antioxidants on Endothelial Function in Human Saphenous Vein in an Ex vivo Model]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>454</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>448</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/455?rss=1">
<title><![CDATA[Lipid Profile, Low-Density Lipoprotein Oxidation and Ceruloplasmin in the Progeny of Families With a Positive History of Cardiovascular Diseases and/or Hyperlipidemia]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/455?rss=1</link>
<description><![CDATA[<p>Fifty-eight healthy progeny (mean age &plusmn; SD 13.9 &plusmn; 7.9 years) of 39 families with a positive history for Cardiovascular Diseases ([CVD] n = 44) or hyperlipidemia (n = 14) were included in the study and were compared with 30 age-matched control participants, with a negative family history, to evaluate lipid profile, ceruloplasmin (Cp), and lipid peroxidation product (malondialdehyde [MDA]) levels, as well as in vitro copper-induced Low-density lipoprotein (LDL) oxidizability. Mean serum levels of total cholesterol, LDL cholesterol (LDL-C), apolipoprotein B-100, and MDA of the participants were significantly higher than those of the controls. Lag time, an LDL resistance oxidation marker, was lower in the study group and negatively correlated with LDL-C (r = -.437, P &lt; .05) and Cp (r = -.272, P &lt; .05) serum levels. In conclusion, progeny with a positive family history for CVD or hyperlipidemia have an atherogenic lipid profile and increased LDL susceptibility to oxidation. High Cp levels seem to be related to lower resistance of LDL to oxidation.</p>]]></description>
<dc:creator><![CDATA[Makedou, K. G., Mikhailidis, D. P., Makedou, A., Iliadis, S., Kourtis, A., Vavatsi-Christaki, N., Papageorgiou, G. E.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709338174</dc:identifier>
<dc:title><![CDATA[Lipid Profile, Low-Density Lipoprotein Oxidation and Ceruloplasmin in the Progeny of Families With a Positive History of Cardiovascular Diseases and/or Hyperlipidemia]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>461</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>455</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/462?rss=1">
<title><![CDATA[Significance of Close Surveillance of Patients With Peripheral Arterial Disease]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/462?rss=1</link>
<description><![CDATA[<p>Background. Peripheral arterial disease (PAD) indicates generalized atherosclerosis but is still underdiagnosed and undertreated. Methods. Data were collected from patients with PAD from the Department of Cardiology and Angiology, University of Heidelberg, Germany. The prevalence of cardiovascular risk factors and medication were documented. Results. Atherogenic risk factors, cardiovascular disease, and cerebrovascular disease were highly prevalent. By continuous care at the university clinic, in addition to family medicine treatment, the use of platelet inhibitors, antihypertensives, and lipid-lowering therapy was increased. Ankle&mdash;brachial index and walking distance improved. Conclusion. Long-term treatment at the university clinic had positive effects on atherogenic risk factors. The regular use of secondary preventive medication was improved. Still, this patient population remained undertreated and showed a high incidence of vascular event rates and a need for vascular interventions. This study implies the importance of both specialists and general practitioners in the care of these individuals.</p>]]></description>
<dc:creator><![CDATA[Barrows, R. J., Krumsdorf, U., Zankl, A., Katus, H., Tiefenbacher, C. P.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708322923</dc:identifier>
<dc:title><![CDATA[Significance of Close Surveillance of Patients With Peripheral Arterial Disease]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>467</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>462</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/468?rss=1">
<title><![CDATA[Comparison of Atherosclerotic Indicators Between Cardio Ankle Vascular Index and Brachial Ankle Pulse Wave Velocity]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/468?rss=1</link>
<description><![CDATA[<p>Background: Aortic pulse wave velocity has been used for evaluating atherosclerosis. Recently, the development of the volume plethysmographic method has made it possible to easily measure the index of the pulse wave velocity. The brachial ankle pulse wave velocity and cardio ankle vascular index are used for estimating the extent of atherosclerosis. The diagnostic usefulness of these indexes in predicting coronary artery disease was examined. Methods: The brachial ankle pulse wave velocity, the cardio ankle vascular index, and the high-sensitivity C-reactive protein were measured in 696 patients who had chest pain and underwent coronary angiography. Measurement values of brachial ankle pulse wave velocity were compared with those of cardio ankle vascular index in terms of the baseline covariates and the number of major coronary vessels involved (vessel disease). Results: The brachial ankle pulse wave velocity was significantly correlated with age, systolic blood pressure, and diastolic blood pressure but not with the high-sensitivity C-reactive protein. The cardio ankle vascular index was correlated only with age and the high-sensitivity C-reactive protein. The average of both brachial ankle pulse wave velocity and cardio ankle vascular index values was greater in 3 vessel disease group than in 0 vessel disease group. The receiver operating characteristic curve showed that the diagnostic accuracy of coronary artery disease was significantly higher in the cardio ankle vascular index than in the brachial ankle pulse wave velocity (area under the curve &plusmn; standard error: 0.691 &plusmn; 0.025 vs. 0.584 &plusmn; 0.026; P &lt; .05). Conclusions: As a means of estimating the extent of atherosclerosis in large arteries, our results show that both brachial ankle pulse wave velocity and cardio ankle vascular index are useful and that cardio ankle vascular index may have some advantages in its application to patients taking blood pressure&mdash;lowering medication because of the minimum effect of blood pressure on its measurement values. The cardio ankle vascular index has increased performance over brachial ankle pulse wave velocity in predicting the coronary artery disease.</p>]]></description>
<dc:creator><![CDATA[Horinaka, S., Yabe, A., Yagi, H., Ishimura, K., Hara, H., Iemua, T., Matsuoka, H.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708325443</dc:identifier>
<dc:title><![CDATA[Comparison of Atherosclerotic Indicators Between Cardio Ankle Vascular Index and Brachial Ankle Pulse Wave Velocity]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>476</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>468</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/477?rss=1">
<title><![CDATA[Benefits of Low-Intensity Pain-Free Treadmill Exercise on Functional Capacity of Individuals Presenting With Intermittent Claudication Due to Peripheral Arterial Disease]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/477?rss=1</link>
<description><![CDATA[<p>Patients with intermittent claudication due to peripheral arterial disease (PAD) experience muscle aching during walking secondary to ischemia. The purpose of this study was to examine the effects of low-intensity pain-free exercise (LIPFE) on functional capacity of individuals with PAD. A total of 12 participants with PAD underwent training on treadmill for 6 weeks, twice a week, for about 45 minutes. Outcome measures included walking distance (WDI), walking duration (WDU), mean walking rate (WR), estimated oxygen consumption (EVO<SUB>2</SUB>), metabolic equivalent (MET), estimated total energy expenditure (ETEE), and estimated rate of energy expenditure (EREE). Mean improvement of WDI, WDU, and MWR were 104% (an addition of 1.0 km), 55% (an addition of 13.3 minutes), and 41% (0.9 km/h faster), respectively. Mean improvement of EVO<SUB>2</SUB>, MET, ETEE, and EREE, were 20%, 20%, 80%, and 20%, respectively. In conclusion, it appears that LIPFE training is an effective intervention for individuals presenting with PAD.</p>]]></description>
<dc:creator><![CDATA[Barak, S., Stopka, C. B., Archer Martinez, C., Carmeli, E.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708322388</dc:identifier>
<dc:title><![CDATA[Benefits of Low-Intensity Pain-Free Treadmill Exercise on Functional Capacity of Individuals Presenting With Intermittent Claudication Due to Peripheral Arterial Disease]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>486</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>477</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/487?rss=1">
<title><![CDATA[Effect of Family History on the Incidence of Varicose Veins: A Population-Based Follow-Up Study in Finland]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/487?rss=1</link>
<description><![CDATA[<p>In the literature, the estimates of high risk of family history for varicose veins are based on prevalence rates from cross-sectional studies. The purpose of this study was to compare such prevalence rates with incidence rates from our longitudinal follow-up study to find out whether there is a difference due to the methodology. A validated questionnaire was used in 3 middle-aged cohorts (n = 6874) in Tampere, Finland. Positive family history was more common both in men (prevalence odds ratio 6.6; 95% confidence interval, 4.7-9.3) and women (4.9; 95% confidence interval, 4.0-6.0) with varicose veins compared to those without. However, positive family history was linked much less with the incidence of varicose veins than the prevalence of varicose veins in women (incidence odds ratio 1.8; 95% confidence interval, 1.1-2.8) and men 1.4 (95% confidence interval, 0.7-2.6). There is likely to be a hereditary component of varicose veins, but it is substantially less than usually proposed in literature.</p>]]></description>
<dc:creator><![CDATA[Ahti, T. M., Makivaara, L. A., Luukkaala, T., Hakama, M., Laurikka, J. O.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709335510</dc:identifier>
<dc:title><![CDATA[Effect of Family History on the Incidence of Varicose Veins: A Population-Based Follow-Up Study in Finland]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>491</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>487</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/492?rss=1">
<title><![CDATA[The Difficult Venous Ulcer: Case Series of 177 Ulcers Referred for Vascular Surgical Opinion Following Failure of Conservative Management]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/492?rss=1</link>
<description><![CDATA[<p>Venous leg ulcers are common, chronic, debilitating, and expensive. Evidence supports use of compression bandaging, with superficial venous surgery in selected cases, but these interventions frequently fail to achieve healing. We describe a series of 152 consecutive referrals from a nurse-led specialist dermatology clinic to a vascular surgical service; a group posing particularly challenging problems. This observational study, with median follow-up of 18 months, describes outcomes in a number of important clinically identifiable subgroups. Its findings may assist service planning and discussion of the surgical role within multidisciplinary ulcer management.</p>]]></description>
<dc:creator><![CDATA[Neequaye, S.K., Douglas, A.D., Hofman, D., Wolz, M., Sharma, R., Cummings, R., Hands, L.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709332901</dc:identifier>
<dc:title><![CDATA[The Difficult Venous Ulcer: Case Series of 177 Ulcers Referred for Vascular Surgical Opinion Following Failure of Conservative Management]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>495</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>492</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/496?rss=1">
<title><![CDATA[In-Stent Restenosis of the Renal Artery in a Single Kidney Patient: The Role of ACEI in the Therapeutic Choice]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/496?rss=1</link>
<description><![CDATA[<p>Renal artery stenosis (RAS) caused by atherosclerotic changes of the renal arteries has become a concern as a cause of end-stage renal failure. Percutaneous balloon angioplasty with or without endovascular stenting is an increasingly accepted procedure at the expense of classical approaches such as aortorenal bypass and other types of surgery. Renal percutaneous transluminal angioplasty and stenting (RPTAS) represent the first therapeutic choice; however, there is doubt regarding the satisfactory long-term outcome for primary RPTAS. Currently, there is no clear evidence whether or not RPTAS prevents further progressive renal function decline because comparisons between interventional randomized studies and medical therapy are still lacking. Despite the fact that the use of angiotensin-converting enzyme inhibitors (ACEIs) may be a potential cause of acute renal failure, clinical data suggest that ACEI therapy is associated with better survival in patient with RAS. In our case, the use of ACEIs has been fundamental for the indirect evaluation of restenosis degree and RPTAS.</p>]]></description>
<dc:creator><![CDATA[Cianci, R., Gigante, A., Polidori, L., Di Donato, D., Martina, P., Barbano, B., Renzulli, R., Zaccaria, A., Fuiano, G.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708322172</dc:identifier>
<dc:title><![CDATA[In-Stent Restenosis of the Renal Artery in a Single Kidney Patient: The Role of ACEI in the Therapeutic Choice]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>503</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>496</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/504?rss=1">
<title><![CDATA[Detection of Cytomegalovirus in Atherosclerotic Plaques and Nonatherosclerotic Arteries]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/504?rss=1</link>
<description><![CDATA[<p>Several studies have reported an association between infectious agents and atherosclerosis. Cytomegalovirus (CMV) is the most commonly implicated viral pathogen. However, the role of CMV in atherosclerosis remains obscure. The present study evaluated the presence of CMV DNA in atherosclerotic plaques and normal vessel walls. A total of 40 arterial specimens from coronary plaques and 27 samples from normal vessels were obtained from 26 patients who underwent aortocoronary bypass surgery. The specimens were analyzed by polymerase chain reaction for the presence of the CMV immediate early genomic region. CMV DNA was detected in 9 out of 26 patients (34.6%). Viral DNA was detected in both nonatherosclerotic tissues and atherosclerotic plaques. No statistically significant differences were observed between normal and diseased vessels. Our findings, in accordance with previous studies, do not support a direct causative role of CMV in the development of atherosclerotic plaques.</p>]]></description>
<dc:creator><![CDATA[Xenaki, E., Hassoulas, J., Apostolakis, S., Sourvinos, G., Spandidos, D. A.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708322390</dc:identifier>
<dc:title><![CDATA[Detection of Cytomegalovirus in Atherosclerotic Plaques and Nonatherosclerotic Arteries]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>508</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>504</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/509?rss=1">
<title><![CDATA[Life-Threatening Pacemaker Dysfunction Associated With Therapeutic Radiation: A Case Report]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/509?rss=1</link>
<description><![CDATA[<p>Reports about pacemaker (PM) dysfunction during irradiation (IR) are very rare, which is because of the extensive protective mechanisms that exist in these devices against electromagnetic interference (EMI). We report a case in which one of the most clinically relevant type of PM malfunctions, a runaway PM, occurred during radiation in a 76-year-old woman who was treated for inoperable esophageal cancer with a course of photon IR. The estimated IR dose of 0.11 Gy was the lowest in vivo dose ever reported. So a direct radiation effect as cause for this malfunction appears to be improbable. It could be concluded that the PM dysfunction was most likely induced by EMI during radiotherapy. The real reason of the device&rsquo;s software failure remains unclear.</p>]]></description>
<dc:creator><![CDATA[Zweng, A., Schuster, R., Hawlicek, R., Weber, H. S.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:25 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708315305</dc:identifier>
<dc:title><![CDATA[Life-Threatening Pacemaker Dysfunction Associated With Therapeutic Radiation: A Case Report]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>512</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>509</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/4/513?rss=1">
<title><![CDATA[Tako-Tsubo-Like Syndrome With Atypical Clinical Presentation: Case Report and Literature Review]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/4/513?rss=1</link>
<description><![CDATA[<p>A 78-year-old woman presented herself at emergency for the appearance of severe dyspnea. An electrocardiogram showed signs of inferior and anterior necrosis, and laboratory tests showed a small increase of myocardial cytonecrosis enzymes. An echocardiogram detected a reduction of global systolic function (ejection fraction [EF] approximately 40%) as well as akinesia of the apex, interventricular septum middle segments, and anterior and anterolateral walls, with basal segments showing compensatory hyperkinesia. The coronarography showed a coronary tree substantially free from significant lesions. The patient was transferred to the cardiology unit of our hospital. Based on the contained increase of the cardiac enzymes, the absence of coronary lesions, and the presence of typical echocardiography alterations, we suspected a Tako-tsubo-like syndrome. On deeper anamnestic investigation, an event of strong emotional stress emerged preceding the hospital admission that confirmed the pathology, even though it is atypical to see clinical presentation a long time after a stressful event.</p>]]></description>
<dc:creator><![CDATA[Ripa, C., Olivieri, F., Antonicelli, R.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:26 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708315307</dc:identifier>
<dc:title><![CDATA[Tako-Tsubo-Like Syndrome With Atypical Clinical Presentation: Case Report and Literature Review]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>517</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>513</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/reprint/60/4/518?rss=1">
<title><![CDATA[Response to Letter to Editor of Csajbok E, Gavaller H, Csanady M, Forster T, and Nemes A]]></title>
<link>http://ang.sagepub.com/cgi/reprint/60/4/518?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Miyaki, A., Maeda, S.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:26 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709335515</dc:identifier>
<dc:title><![CDATA[Response to Letter to Editor of Csajbok E, Gavaller H, Csanady M, Forster T, and Nemes A]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>518</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>518</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/reprint/60/4/519?rss=1">
<title><![CDATA[Response to Facial Massage and Bilateral Carotid and Bilateral Vertebral Artery Dissection]]></title>
<link>http://ang.sagepub.com/cgi/reprint/60/4/519?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[RuDusky, B.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:26 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709333227</dc:identifier>
<dc:title><![CDATA[Response to Facial Massage and Bilateral Carotid and Bilateral Vertebral Artery Dissection]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>519</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>519</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/reprint/60/4/520?rss=1">
<title><![CDATA[Erratum]]></title>
<link>http://ang.sagepub.com/cgi/reprint/60/4/520?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:26 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709343197</dc:identifier>
<dc:title><![CDATA[Erratum]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>520</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>520</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/reprint/60/4/521?rss=1">
<title><![CDATA[Information for Authors]]></title>
<link>http://ang.sagepub.com/cgi/reprint/60/4/521?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 23:57:26 PDT</dc:date>
<dc:identifier>info:doi/10.1177/00033197090600042301</dc:identifier>
<dc:title><![CDATA[Information for Authors]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>522</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>521</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/reprint/60/3/273?rss=1">
<title><![CDATA[Irradiation-Induced Carotid Artery Stenosis: A Preventable Complication of Neck Radiotherapy?]]></title>
<link>http://ang.sagepub.com/cgi/reprint/60/3/273?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Paraskevas, K. I., Giannoukas, A. D., Mikhailidis, D. P.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709336419</dc:identifier>
<dc:title><![CDATA[Irradiation-Induced Carotid Artery Stenosis: A Preventable Complication of Neck Radiotherapy?]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>275</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>273</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/276?rss=1">
<title><![CDATA[Angiographic Characteristics of Radiation-Induced Carotid Arterial Stenosis]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/276?rss=1</link>
<description><![CDATA[<p>Purpose: This study aimed to clarify the angiographic characteristics of radiation-induced carotid stenosis. Methods: We evaluated 11 carotid arteries of patients after radiotherapy (radiotherapy group) and 26 carotid arteries of age- and gender-matched patients without a history of radiotherapy (control group). All patients had carotid stenosis detected by digital subtraction angiography (DSA). We developed an original coordinate system on the DSA to determine the accurate length and location of the carotid lesion. Results: Radiation-induced carotid lesions were significantly longer than carotid lesions caused by atherosclerosis. The maximal stenosis of radiation-induced carotid lesions tended to be at the end of the stenotic area and within a wider range than the nonradiation-induced lesions, including in the proximal common carotid artery (CCA). Conclusions: Radiation-induced stenotic lesions seem to exist in a wide range of carotid artery, including the CCA, along the vessel, and show maximal stenosis near the end of the stenotic area.</p>]]></description>
<dc:creator><![CDATA[Shichita, T., Ogata, T., Yasaka, M., Yasumori, K., Inoue, T., Ibayashi, S., Iida, M., Okada, Y.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709335905</dc:identifier>
<dc:title><![CDATA[Angiographic Characteristics of Radiation-Induced Carotid Arterial Stenosis]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>282</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>276</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/283?rss=1">
<title><![CDATA[Elevated Serum Estradiol/Testosterone Ratio in Men With Primary Varicose Veins Compared With a Healthy Control Group]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/283?rss=1</link>
<description><![CDATA[<p>The role of sex hormones in men with varicose veins remains unclear. Therefore, we set up a prospective pilot-study. In 34 men, venous blood was sampled during morning hours, for the determination of serum estradiol (E2), dehydroepiandrostendion, androstendion, and free testosterone (fT). Serum E2:fT ratio was calculated. The study protocol also included patient history, physical examination, color duplex ultrasound of both limbs, and assignment of CEAP clinical stage (C) classification. About 21 symptomatic varicose men (VM [C &ge; 2] mean age of 40.3/+6.9 years) and 13 healthy men (HM [C &le; 1] mean age of 38.1/+ 7.4 years) were analyzed. The serum E2:fT ratio (VM 2.83/+ 0.79 and HM 2.32/+0.63) was significantly different (P &lt; .05) between the two groups. No major differences were seen on the serum levels of the sex hormones. In summary, our results demonstrate a changed serum E2:fT ratio among men with varicose veins compared to healthy men. By the fact of a small study sample, the interpretabillity of this result is limited.</p>]]></description>
<dc:creator><![CDATA[Kendler, M., Blendinger, Ch., Haas, E.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708323493</dc:identifier>
<dc:title><![CDATA[Elevated Serum Estradiol/Testosterone Ratio in Men With Primary Varicose Veins Compared With a Healthy Control Group]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>289</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>283</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/290?rss=1">
<title><![CDATA[The Effect of Negative Pressure Therapy on the Femoral Vein Blood Flow and Wall Structure]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/290?rss=1</link>
<description><![CDATA[<p>Negative pressure therapy has been recently used for managing lymphatic or infective groin complications. The aim of this study was to investigate any possible association between application of negative pressure therapy in the groin area and deep-vein thrombosis. Acute surgical wounds were created at the inguinal areas in 7 pigs. Different negative pressures ranging from &ndash;50 to &ndash;200 mmHg were applied directly over the femoral vessels, and blood flow alterations were studied using a Doppler ultrasound. Femoral vein specimens were also removed for histological examination after 12 hours of therapy. It has been demonstrated that negative pressure therapy does not significantly alter the baseline lower limb venous return. Histology demonstrated several changes, which are associated with vein thrombogenesis. The hemodynamic and pathological findings still leave a potential for thrombogenic effects of negative pressure therapy and warrant care to protect the femoral veins, with the use of thrombosis prophylaxis measures.</p>]]></description>
<dc:creator><![CDATA[Lioupis, C., Kotsis, T., Barbatis, C., Seretis, E., Nomikos, A., Volondakis-Baltatzis, I., Papalois, A., Andrikopoulos, V., Leaper, D.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708318376</dc:identifier>
<dc:title><![CDATA[The Effect of Negative Pressure Therapy on the Femoral Vein Blood Flow and Wall Structure]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>300</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>290</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/301?rss=1">
<title><![CDATA[Screening for Deep Vein Thrombosis in Asymptomatic High-risk Patients: A Comparison Between Digital Photoplethysmography and Venous Ultrasonography]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/301?rss=1</link>
<description><![CDATA[<p>Objective: To determine the role of digital photoplethysmography in screening asymptomatic patients who are susceptible for developing deep vein thrombosis.</p><p>Methods: Three hundred and thirty-seven limbs in 169 patients who were high risk for development of deep vein thrombosis were assessed by ultrasonography digital photoplethysmography and the results were compared.</p><p>Results: Thirteen limbs were found to have deep vein thrombosis as demonstrated by ultrasonography. All limbs with a venous refilling time greater than 12 seconds had a normal ultrasonography. Compared with</p><p>ultrasonography and using refilling time less than 12 seconds as the cutoff point, digital photoplethysmography achieved a sensitivity, specificity, positive predictive value, and negative predictive value of 100%, 73.8%, 13.3%, and 100% respectively, for detecting deep vein thrombosis in asymptomatic high-risk patients.</p><p>Conclusion: Digital photoplethysmography is a simple, noninvasive, and highly sensitive test for screening of deep vein thrombosis.</p>]]></description>
<dc:creator><![CDATA[Sharif-Kashani, B., Behzadnia, N., Shahabi, P., Sadr, M.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708323494</dc:identifier>
<dc:title><![CDATA[Screening for Deep Vein Thrombosis in Asymptomatic High-risk Patients: A Comparison Between Digital Photoplethysmography and Venous Ultrasonography]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>307</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>301</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/308?rss=1">
<title><![CDATA[Vascular Effects of Estrogen and Progestins and Risk of Coronary Artery Disease: Importance of Timing of Estrogen Treatment]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/308?rss=1</link>
<description><![CDATA[<p>The effects of estrogen and progestins on the vascular wall have drawn major medical attention, and significant controversy over various studies has been developed. Several experimental and observational studies have shown cardioprotective effects; however, prospective randomized trials showed an increase in cardiovascular events in postmenopausal women on estrogen/ medroxyprogesterone acetate treatment. The most significant parameter for cardiovascular benefit of estrogen seems to be the interval since the onset of menopause. In the early postmenopausal years, estrogen has beneficial effects on the vascular wall by inhibition of atherosclerosis progression, whereas in the late postmenopause, adverse effects like upregulation of the plaque inflammatory processes and plaque instability may develop. The effects of progestins on the cardiovascular system are not as clear and may differ according to the choice of progestins that is used. The aim of this review is to summarize the effects of estrogen and progestins on the vascular wall and their clinical implications.</p>]]></description>
<dc:creator><![CDATA[Gungor, F., Kalelioglu, I., Turfanda, A.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708318377</dc:identifier>
<dc:title><![CDATA[Vascular Effects of Estrogen and Progestins and Risk of Coronary Artery Disease: Importance of Timing of Estrogen Treatment]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>317</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>308</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/318?rss=1">
<title><![CDATA[Outcomes in Patients With Abnormal Myocardial Perfusion Imaging and Normal Coronary Angiogram]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/318?rss=1</link>
<description><![CDATA[<p>A subset of subjects undergoing myocardial perfusion imaging has perfusion abnormalities that are subsequently labeled false positive based on coronary angiography. We evaluated the long-term prevalence of cardiovascular events in these patients. We retrospectively identified 48 patients who had reversible perfusion abnormalities with myocardial perfusion imaging and normal coronary angiography. Patients with known coronary artery disease, left ventricular dysfunction, valvular disease, and cardiomyopathy were excluded. Patient follow-up, conducted for at least 3 (mean interval, 7.4) years from the index myocardial perfusion imaging, was accomplished by a review of medical records and telephone interviews. Study endpoints were cardiovascular events defined as sudden cardiac death, myocardial infarction, percutaneous coronary revascularization, coronary artery bypass grafting, and cerebrovascular or peripheral revascularization. Thirty-one percent (15 of 48) of the patients had cardiovascular events. Six of the 48 patients had coronary events. These patients had abnormal myocardial perfusion imaging and normal coronary angiogram. The time between myocardial perfusion imaging and coronary event was 0.5 to 8.67 years. There was a strong correlation between the regions of original perfusion abnormality and the ultimate coronary ischemia or revascularization. Abnormal findings on myocardial perfusion imaging may predict a higher prevalence of coronary and peripheral vascular events than suggested by a normal coronary angiogram.</p>]]></description>
<dc:creator><![CDATA[Delcour, K. S., Khaja, A., Chockalingam, A., Kuppuswamy, S., Dresser, T.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708319938</dc:identifier>
<dc:title><![CDATA[Outcomes in Patients With Abnormal Myocardial Perfusion Imaging and Normal Coronary Angiogram]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>321</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>318</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/322?rss=1">
<title><![CDATA[Percutaneous Coronary Interventions Affect Concentrations of Interleukin 6 and Its Soluble Receptors in Coronary Sinus Blood in Patients With Stable Angina]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/322?rss=1</link>
<description><![CDATA[<p>Coronary stenting may create local inflammatory reaction. Interleukin 6 effects depend on the presence of soluble receptors (sIL-6R and sgp130) that facilitate or impede interleukin 6 signal transduction. Concentrations of interleukin 6 and its soluble receptors were assessed in aorta and coronary sinus after stenting in optimally treated stable angina patients scheduled for elective stenting. Baseline levels of interleukin 6 and its soluble receptors in patients did not differ from healthy controls. Initial levels of sIL-6R in aorta were significantly higher than in coronary sinus but this difference disappeared after intervention. Stenting caused interleukin 6 concentration increase to a similar extent both in coronary sinus and in aorta. Moreover, there was significantly higher sgp130 concentration in coronary sinus than in aorta. Coronary intervention increases concentration of interleukin 6 in patients with stable angina. It affects the cardiac level of interleukin 6 soluble receptors what may influence the local inflammatory reaction.</p>]]></description>
<dc:creator><![CDATA[Kaminski, K. A., Kozieradzka, A., Bonda, T., Banach, M., Kozuch, M., Wojtkowska, I., Dobrzycki, S., Kralisz, P., Nowak, K., Prokopczuk, P., Mikhailidis, D. P., Musial, W. J.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708330008</dc:identifier>
<dc:title><![CDATA[Percutaneous Coronary Interventions Affect Concentrations of Interleukin 6 and Its Soluble Receptors in Coronary Sinus Blood in Patients With Stable Angina]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>328</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>322</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/329?rss=1">
<title><![CDATA[Ankle-Brachial Index and Extent of Atherosclerosis in Patients From the Middle East (the AGATHA-ME Study): A Cross-Sectional Multicenter Study]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/329?rss=1</link>
<description><![CDATA[<p>To assess the extent of atherothrombosis and the use of the ankle-brachial index (ABI) in populations from the Middle East, we conducted a multicenter study similar to AGATHA (a Global Atherothrombosis Assessment), AGATHA-ME, which included 1341 patients from 18 centers from 5 countries (United Arab Emirates, Kuwait, Qatar, Bahrain, and Oman). Patients were assigned to 2 groups: the with-disease and at-risk groups. Abnormal ABI (&le;0.9) was seen in 31.5% of at-risk patients and 28.2% of with-disease patients. Patients with peripheral arterial disease had the highest frequency of abnormal ABI (77.6%), with 97.8 negative predictive value. The AGATHA-ME study confirms that atherothrombosis disease often occurs at more than 1 site. The ABI is related to the risk factor profile and to the site and extent of atherothrombosis. Gender and diabetes mellitus are associated with the worst parameters.</p>]]></description>
<dc:creator><![CDATA[El-Menyar, A., Amin, H., Rashdan, I., Souliman, K., Deleu, D., Saadat, K., Al Mahmeed, W., Bakir, S., Wasif, A., Ben Brek, A., Bazargani, N., Aziz, A. A., Singh, R., Hatou, I., Mahmoud, H., Al Suwaidi, J.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708321585</dc:identifier>
<dc:title><![CDATA[Ankle-Brachial Index and Extent of Atherosclerosis in Patients From the Middle East (the AGATHA-ME Study): A Cross-Sectional Multicenter Study]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>334</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>329</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/335?rss=1">
<title><![CDATA[The Association of Active and Passive Smoking With Peripheral Arterial Disease: Results From NHANES 1999-2004]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/335?rss=1</link>
<description><![CDATA[<p>We aim to quantify the association between different forms of tobacco use and peripheral arterial disease (PAD) and to characterize the association between secondhand smoke exposure and PAD in a large nationally representative sample of the US population. We observed significant associations between current and former cigarette smoking and PAD. The association between noncigarette forms of tobacco and PAD was not significant even after adjustment for clinical and demographic variables. Secondhand smoke was not significantly associated with PAD. Interestingly, a ``threshold phenomenon'' for tobacco exposure was demonstrated for PAD occurrence. Individuals with serum cotinine &gt;155 ng/ mL were at significantly higher risk of having PAD as compared with a nonexistent or a minimal risk below this threshold value. Lack of association between PAD and secondhand smoke exposure in conjunction with the threshold phenomenon described above leads us to speculate existence of striking differences between the systemic circulation and lower extremity vasculature in terms of pathogenesis of atherosclerosis.</p>]]></description>
<dc:creator><![CDATA[Agarwal, S.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708330526</dc:identifier>
<dc:title><![CDATA[The Association of Active and Passive Smoking With Peripheral Arterial Disease: Results From NHANES 1999-2004]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>345</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>335</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/346?rss=1">
<title><![CDATA[Relationship Between Aortic Atherosclerosis and Dental Loss in an Inner-City Population]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/346?rss=1</link>
<description><![CDATA[<p>Prior studies have suggested an association between atherosclerosis and periodontal disease, both of which are more prevalent in certain minority and economically disadvantaged groups. Few studies have addressed the relationship between cardiovascular disease and dentition among ethnically diverse populations. We studied 131 subjects (60% females, age 59 &plusmn; 15 years) who were referred for clinically indicated transesophageal echocardiography. Dental loss was more severe in patients with hypertension (<I>P</I> &lt; .001), diabetes (<I>P</I> = .05), coronary artery disease (<I>P</I> = .04), and calcium channel blocker use (<I>P</I> = .04). On univariate analysis, maximal aortic intima&mdash;media thickness (MAIMT) was significantly correlated with dental loss (<I>r</I> = .40; <I>P</I> &lt; .001). Age was correlated with MAIMT (<I>R</I> = .41; <I>P</I> &lt; .001) and with dental loss (<I>r</I> = .57; <I>P</I> &lt; .001). On multivariate analysis, dental loss (<I>P</I> = .03) and history of coronary artery disease (<I>P</I> = .04) were independent predictors of MAIMT (<I> R</I><sup>2</sup> = .44). In this inner-city predominantly African American population, atherosclerosis and dental loss are age dependent and are interrelated independent of age.</p>]]></description>
<dc:creator><![CDATA[Castillo, R., Fields, A., Qureshi, G., Salciccioli, L., Kassotis, J., Lazar, J. M.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708319783</dc:identifier>
<dc:title><![CDATA[Relationship Between Aortic Atherosclerosis and Dental Loss in an Inner-City Population]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>350</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>346</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/351?rss=1">
<title><![CDATA[Effect of Weight Reduction With Dietary Intervention on Arterial Distensibility and Endothelial Function in Obese Men]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/351?rss=1</link>
<description><![CDATA[<p>Obesity and reduction in central arterial distensibility, respectively, have been identified as powerful and independent risk factors for cardiovascular disease. However, the effect of weight reduction on central arterial function in obese subjects has not yet been clarified. We investigated whether low-calorie diet-induced weight reduction affects central arterial distensibility and endothelial function in middle-aged obese men. Twelve obese men (age: 45+2 yrs, BMI: 30+1 kg/m<sup> 2</sup>) completed a 12-week dietary intervention. Caloric restriction induced significantly weight loss and decrease in BMI. After the program, carotid arterial compliance significantly increased and b-stiffness index and aortic pulse-wave velocity remarkably decreased. Concentrations of plasma endothelin-1 (ET-1) significantly decreased and plasma nitric oxide (NO) markedly increased after the program. Weight reduction by low-calorie diet in obese men increases central arterial distensibility, which may contribute to the improvement in endothelial function, as noted by a decrease in ET-1 and an increase in NO.</p>]]></description>
<dc:creator><![CDATA[Miyaki, A., Maeda, S., Yoshizawa, M., Misono, M., Saito, Y., Sasai, H., Endo, T., Nakata, Y., Tanaka, K., Ajisaka, R.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708325449</dc:identifier>
<dc:title><![CDATA[Effect of Weight Reduction With Dietary Intervention on Arterial Distensibility and Endothelial Function in Obese Men]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>357</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>351</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/358?rss=1">
<title><![CDATA[Evaluation of Point-of-care Activated Partial Thromboplastin Time Testing by Comparison to Laboratory-based Assay for Control of Intravenous Heparin]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/358?rss=1</link>
<description><![CDATA[<p>Introduction: Patients on intravenous heparin require regular activated partial thromboplastin time monitoring. Laboratory-based activated partial thromboplastin time assays necessitate a delay between blood sampling and dose adjustment. Point-of-care testing could permit immediate dose adjustments, potentially enabling tighter control of anticoagulation. Aim: To assess equivalence of activated partial thromboplastin time measured by conventional laboratory assay and by a novel proprietary point-of-care testing system (Hemochron Response, ITC, Thoratec Corporation, Edison, NJ) among surgical ward patients on intravenous heparin. Methods: A total of 39 blood samples from patients on intravenous heparin were tested with both laboratory and point-of-care assays. Assay equivalence was assessed by Bland-Altman analysis. Results. Point-of-care measurements exceeded laboratory activated partial thromboplastin time by a mean of 15 seconds (standard deviation 19). In 19 cases (49%), the point-of-care measurement would have resulted in different heparin dosing from the laboratory activated partial thromboplastin time. Conclusions: The Hemochron Response system is not sufficiently accurate for routine ward use compared with laboratory activated partial thromboplastin time assays.</p>]]></description>
<dc:creator><![CDATA[Douglas, A. D., Jefferis, J., Sharma, R., Parker, R., Handa, A., Chantler, J.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709332958</dc:identifier>
<dc:title><![CDATA[Evaluation of Point-of-care Activated Partial Thromboplastin Time Testing by Comparison to Laboratory-based Assay for Control of Intravenous Heparin]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>361</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>358</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/362?rss=1">
<title><![CDATA[Platelet Function Following Acute Cerebral Ischemia]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/362?rss=1</link>
<description><![CDATA[<p>Background: Studies have previously identified increased levels of platelet activation following acute ischemic stroke. In order to evaluate new antiplatelet agents and their combinations, there is a need for accurate measures of platelet activation. Methods: Blood was taken from 17 patients within 24 hours of an acute ischemic stroke, and then at 3, 7, 14 and 42 days. For comparison, a group of 18 stable arteriopaths had identical tests performed. Platelet aggregation was measured using a free platelet counting technique, and platelet surface P-selectin and monocyte platelet aggregates (MPAs) were measured using flow cytometry. Soluble P-selectin and D-dimers were measured by an enzyme linked immune assay. Results: The initial level of MPAs was significantly raised in the stroke patients compared with the stable patients (p = 0.04, 14.2% vs. 9.3%); however, this difference was not significantly higher than later study points (14.2%, 10.1%, 9.3%, 11.9%, 11.3%; days 1, 3, 7, 14 and 42 respectively. Day 1 vs. day 7 p = 0.07 ANOVA). No changes in P-selectin or platelet aggregation were identified. D-dimer levels were significantly higher on day 7 than day 42 (p &lt; 0.01), and fibrinogen levels were elevated on both days 3 and 14 compared with day 42. Fibrinogen levels were not elevated compared with stable patients. Conclusions: MPA levels are elevated following an acute ischemic stroke compared to stable patients, but no significant change was seen with other platelet markers. This study suggests MPAs are a more sensitive marker of platelet activation than either P-selectin or aggregation.</p>]]></description>
<dc:creator><![CDATA[Smout, J., Dyker, A., Cleanthis, M., Ford, G., Kesteven, P., Stansby, G.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709332959</dc:identifier>
<dc:title><![CDATA[Platelet Function Following Acute Cerebral Ischemia]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>369</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>362</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/370?rss=1">
<title><![CDATA[Effects of Atorvastatin on Vascular Intimal Hyperplasia: An Experimental Rodent Model]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/370?rss=1</link>
<description><![CDATA[<p><b>Introduction</b> Vascular intimal hyperplasia is associated with increased mortality and morbidity. The authors investigated the effects of atorvastatin on vascular intimal hyperplasia. <b>Materials and methods</b> Rats were divided into 4 groups. Groups 1, 2, and 3 had experimental aortic injury and received intraperitoneal injection of atorvastatin, solvent, or 0.9% NaCl, respectively. Group 4 was a nonintervention (laparotomy only) control group. Animals were sacrificed after 3 weeks. Blood samples and injured aortic segment were analyzed. <b> Results</b> Atorvastatin administration significantly lowered total and low-density lipoprotein cholesterol levels (<I>P</I> = .012 and <I>P</I> = .001, respectively), intima&mdash;media ratio (<I>P</I> = .002), and intimal smooth muscle cell accumulation (<I>P</I> &lt; .05) in group 1. Luminal narrowing in animals in group 1 was significantly lower than that in animals in groups 2 and 3, but was higher than in animals in group 4 (<I>P</I> = .009). <b>Conclusions</b> Atorvastatin suppresses intimal hyerplasia and aids in intimal regeneration by lowering blood lipids and intimal smooth muscle cell accumulation.</p>]]></description>
<dc:creator><![CDATA[Aydin, U., Ugurlucan, M., Gungor, F., Ziyade, S., Inan, B., Banach, M., Kalko, Y., Yasar, T.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708321102</dc:identifier>
<dc:title><![CDATA[Effects of Atorvastatin on Vascular Intimal Hyperplasia: An Experimental Rodent Model]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>377</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>370</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/378?rss=1">
<title><![CDATA[Intermittent Claudication Caused by Frequent Premature Ventricular Complexes: Resolution After Radiofrequency Ablation]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/378?rss=1</link>
<description><![CDATA[<p>A case of a 55-year-old woman with psoriasis and long-lasting history of typical intermittent claudication associated with frequent premature ventricular complexes is reported. Atherosclerotic and nonarterial pathologic conditions were taken into consideration and were excluded. Applying 6-minute walk test and resting and peak-exercise pulsed Doppler ultrasonography, it was possible to prove a decrease in perfusion during exercise-persistent ventricular bigeminy. Rapid improvement in symptoms was observed after a single dose of propafenone; however, it led to a worsening of psoriasis. The patient was referred for radiofrequency ablation. Radiofrequency ablation in the right ventricular outflow tract resulted in complete abolition of premature ventricular complexes and intermittent claudication. The patient remained free of claudication and symptoms related to arrhythmia with an ability to walk more than 5 km, without stopping. Relief of symptoms may be achieved by antiarrhythmic treatment; however, side effects of antiarrhythmic drugs or their ineffectiveness should encourage the use of radiofrequency ablation.</p>]]></description>
<dc:creator><![CDATA[Stec, S., Zaborska, B., Pilus, A., Lewandowski, P., Kulakowski, P.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319707312520</dc:identifier>
<dc:title><![CDATA[Intermittent Claudication Caused by Frequent Premature Ventricular Complexes: Resolution After Radiofrequency Ablation]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>381</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>378</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/3/382?rss=1">
<title><![CDATA[Chronic Effort-Induced Angina as Presentation of a Totally Occluded Left Main Coronary Artery: A Case Report and Review]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/3/382?rss=1</link>
<description><![CDATA[<p>In this report, the case of a 40-year-old patient with chronic total occlusion of the left main coronary artery is discussed. Total occlusion of the left main coronary artery is a rare finding at coronary angiography. When present, patients most often have extensive collateral circulation from the right coronary artery. The mainstay of treatment is surgical with coronary artery bypass grafting.</p>]]></description>
<dc:creator><![CDATA[Koster, N. K., White, M.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708314247</dc:identifier>
<dc:title><![CDATA[Chronic Effort-Induced Angina as Presentation of a Totally Occluded Left Main Coronary Artery: A Case Report and Review]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>384</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>382</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/reprint/60/3/385?rss=1">
<title><![CDATA[Unilateral Isolated Partial Oculomotor Nerve Paralysis After Percutaneous Intervention]]></title>
<link>http://ang.sagepub.com/cgi/reprint/60/3/385?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kocabay, G., Bayram, T.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708327647</dc:identifier>
<dc:title><![CDATA[Unilateral Isolated Partial Oculomotor Nerve Paralysis After Percutaneous Intervention]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>386</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>385</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/reprint/60/3/387?rss=1">
<title><![CDATA[LDL-Cholesterol is the King]]></title>
<link>http://ang.sagepub.com/cgi/reprint/60/3/387?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Goumas, G. S.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709334121</dc:identifier>
<dc:title><![CDATA[LDL-Cholesterol is the King]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>388</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>387</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/reprint/60/3/389?rss=1">
<title><![CDATA[Physical Training-Induced Weight Reduction Is Associated With Improved Aortic Distensibility]]></title>
<link>http://ang.sagepub.com/cgi/reprint/60/3/389?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Csajbok, E., Gavaller, H., Csanady, M., Forster, T., Nemes, A.]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 23:49:59 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319709334263</dc:identifier>
<dc:title><![CDATA[Physical Training-Induced Weight Reduction Is Associated With Improved Aortic Distensibility]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>390</prism:endingPage>
<prism:publicationDate>2009-06-01</prism:publicationDate>
<prism:startingPage>389</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/141?rss=1">
<title><![CDATA[Predictors of Long-Term Major Adverse Cardiac Events and Clinical Restenosis Following Elective Percutaneous Coronary Stenting]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/141?rss=1</link>
<description><![CDATA[<p>Limited data exist regarding the predictors of long-term clinical outcomes following elective percutaneous coronary intervention (PCI) in the current era of stenting. The authors investigated the predictors of major adverse cardiac events (MACE) and clinical restenosis in 740 consecutive patients who underwent successful elective PCI with bare metal stents (BMSs) or drug-eluting stents (DESs). At 30-month follow-up, compared with BMS recipients, DES recipients had a significantly lower rate of MACE, which was mainly driven by a decreased repeat target vessel PCI. The rate of 30-month clinical restenosis was significantly lower in DES recipients. The authors conclude that baseline clinical, angiographic, and procedural characteristics determine long-term MACE and clinical restenosis after elective PCI, with DES being the independent predictor for both.</p>]]></description>
<dc:creator><![CDATA[Qiangjun Cai,  , Skelding, K., Armstrong, A., Desai, D., Wood, G. C., Blankenship, J.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708321587</dc:identifier>
<dc:title><![CDATA[Predictors of Long-Term Major Adverse Cardiac Events and Clinical Restenosis Following Elective Percutaneous Coronary Stenting]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>147</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>141</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/148?rss=1">
<title><![CDATA[Avoiding and Managing Bleeding Complications in Patients With Non-ST-Segment Elevation Acute Coronary Syndromes]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/148?rss=1</link>
<description><![CDATA[<p>Antithrombotic therapy coupled with early use of cardiac catheterization and revascularization have decreased morbidity and mortality rates in patients who have acute ischemic heart disease but who carry a risk for bleeding. Bleeding complications in patients with acute coronary syndromes are associated with worse clinical outcomes, including recurrent ischemic events and death. Determining the appropriate balance between preventing ischemic events and causing bleeding in patients with acute coronary syndromes present a challenging problem for clinicians. Antithrombotics studied in recent clinical trials that have focused on bleeding reduction include bivalirudin and fondaparinux. In this review, the incidence, predictors, and clinical outcomes associated with bleeding are discussed. Furthermore, the association between antithrombotic agents and bleeding and propose strategies to prevent bleeding complications are also discussed.</p>]]></description>
<dc:creator><![CDATA[Potsis, T. Z., Katsouras, C., Goudevenos, J. A.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708317339</dc:identifier>
<dc:title><![CDATA[Avoiding and Managing Bleeding Complications in Patients With Non-ST-Segment Elevation Acute Coronary Syndromes]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>158</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>148</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/159?rss=1">
<title><![CDATA[The Physiological Effects of Short-term Smoking Cessation in Claudicants]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/159?rss=1</link>
<description><![CDATA[<p>Introduction: Smoking contributes to atherosclerosis and causes significant postoperative morbidity. New antismoking law forces short-term pre-operative abstinence. Demonstrable clinical benefit might motivate complete cessation. Our aim was to determine the effects of 24-hr smoking cessation on cardiorespiratory function and claudication distance. Methods: Smoking claudicants were randomized to 24hr smoking or abstinence. Following these separate periods, cardiopulmonary exercise testing was performed. Pre- and post-exercise, serum lactate and ankle brachial pressure index (ABPI) were measured. During exercise, cardiorespiratory function, initial and absolute claudication (IC,AC) distances and visual analogue scores (VAS) of pain were recorded. Results: 16 patients completed both tests. IC, AC and VAS were unchanged with abstinence (P = .43, .66, .96, .83). ABPI drop post-exercise was unchanged with abstinence (P = .08, .09). Cardiorespiratory function was not affected by smoking cessation. Conclusion: Cardiorespiratory function and claudication symptoms are unchanged following 24-hr smoking cessation., No deterioration in respiratory function is important when considering anaesthetic administration. However, lack of symptomatic improvement may discourage patients from abstaining. Further investigation should determine correlation between short-term abstinence and postoperative morbidity.</p>]]></description>
<dc:creator><![CDATA[Dickinson, K.J., Cockbain, A.J., MacDonald, W., Shah, M., Homer-Vanniasinkam, S.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708325448</dc:identifier>
<dc:title><![CDATA[The Physiological Effects of Short-term Smoking Cessation in Claudicants]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>163</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>159</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/164?rss=1">
<title><![CDATA[Coronary Collaterals in Obese Patients: Impact of Metabolic Syndrome]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/164?rss=1</link>
<description><![CDATA[<p>Obesity is a growing pandemic. Among obese patients with significant coronary artery stenosis, development of coronary collaterals was investigated. Consecutive 104 obese patients with stable angina pectoris were enrolled. Coronary collaterals were assessed according to the Cohen and Rentrop grading system and classified into 2 as those with poor collaterals (grade 0-1, Group 1) and those with good collaterals (grade 2-3, Group 2). Group 1 had higher body mass index, shorter duration of angina pectoris than Group 2. Poor collaterals were present in 82.3% and 59.5% of patients with and without (<I>P</I> = .019) metabolic syndrome, respectively. Metabolic syndrome score (sum of each component) was found to be negatively correlated with Rentrop score (<I>r</I> = &mdash;691; <I> P</I> &lt; .001). After controlling for symptom duration and body mass index, metabolic syndrome kept independent association with poor collaterals among obese patients (<I>P</I> = .043, B = 1.8). Metabolic syndrome appears to influence the development of coronary collaterals among obese patients with stable coronary artery disease.</p>]]></description>
<dc:creator><![CDATA[Sasmaz, H., Yilmaz, M. B.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708316007</dc:identifier>
<dc:title><![CDATA[Coronary Collaterals in Obese Patients: Impact of Metabolic Syndrome]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>168</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>164</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/169?rss=1">
<title><![CDATA[Comparison of Quantitative Coronary Angiography With Intracoronary Ultrasound. Can Quantitative Coronary Angiography Accurately Estimate the Severity of a Luminal Stenosis?]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/169?rss=1</link>
<description><![CDATA[<p>In this study we investigated the accuracy of monoplane and biplane quantitative coronary angiography in estimating the luminal dimensions, using intracoronary ultrasound as gold standard. Biplane angiography and intracoronary ultrasound were performed in 24 arterial segments. The end-diastolic intracoronary ultrasound frames were manually selected and segmented. In 2 end-diastolic X ray projections, quantitative coronary angiography was performed and a novel methodology was applied to register the segmented frames onto the processed angiographic images. The luminal areas determined by quantitative coronary angiography in 1 (monoplane) and 2 projections (mean) were compared with those determined by intracoronary ultrasound. The obtained correlation coefficients for the monoplane and mean estimations were 0.69 &plusmn; 0.12 and 0.77 &plusmn; 0.08, respectively. It would appear that by increasing the angle between the biplane projections, the correlation between intracoronary ultrasound and mean estimations improves. Our results provide evidence that orthogonal biplane angiography is more reliable and should be preferred to assess luminal dimensions.</p>]]></description>
<dc:creator><![CDATA[Bourantas, C. V., Tweddel, A. C., Papafaklis, M. I., Karvelis, P. S., Fotiadis, D. I., Katsouras, C. S., Michalis, L. K.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708317338</dc:identifier>
<dc:title><![CDATA[Comparison of Quantitative Coronary Angiography With Intracoronary Ultrasound. Can Quantitative Coronary Angiography Accurately Estimate the Severity of a Luminal Stenosis?]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>179</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>169</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/180?rss=1">
<title><![CDATA[Promoter Polymorphism of Interleukin-18 in Angiographically Proven Coronary Artery Disease]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/180?rss=1</link>
<description><![CDATA[<p>Interleukin 18 (IL-18) is a pro-atherogenic cytokine associated with the occurrence of various cardiac complications. The IL-18 gene has a functional -137 G/C polymorphism (rs187238) in the promoter region. Using the ligase detection reaction-polymerase chain reaction, we genotyped a cohort of patients in Chinese Han population in Xiangfan region. Case patients of coronary artery disease and control patients were identified by coronary angiography. The plasma IL-18 concentrations were measured by ELISA. A significant increase of G allele or GG-genotype was observed in 241 case patients compared to 145 control individuals (frequency of G allele = 0.90 vs 0.83, p=0.004; frequency of GG-genotype = 0.81 vs 0.68, p = 0.005). In case patients, G allele carriers in multi-vessel disease patients had a higher occurrence rate when compared to single-vessel disease patients, but no significant difference was detected (frequency of G allele = 0.92 vs 0.88, p=0.107; frequency of GG-genotype = 0.84 vs 0.75, p = 0.089). IL-18 protein concentration of the -137GG genotype was much higher than concentration of the CG and CC genotype (case patients: 229.1&plusmn;131.5 vs 122.7&plusmn;73.6 pg/ml, P &lt; 0.001; control patients: 65.9&plusmn;31.6 vs 42.4&plusmn;19.5 pg/ml, P &lt; 0.001). To conclude, IL-18 promoter -137G/C polymorphism influences IL-18 levels and the occurrence of coronary artery disease, suggesting that IL-18 is causally involved in the development of atherosclerosis.</p>]]></description>
<dc:creator><![CDATA[Wenwei Liu,  , Qizhu Tang,  , Hua Jiang,  , Xiangwu Ding,  , Yongsheng Liu,  , Rui Zhu,  , Yongqian Tang,  , Bin Li,  , Min Wei,  ]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708319939</dc:identifier>
<dc:title><![CDATA[Promoter Polymorphism of Interleukin-18 in Angiographically Proven Coronary Artery Disease]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>185</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>180</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/186?rss=1">
<title><![CDATA[Serum Selenium and Glutathione Peroxidase Concentrations in Iranian Patients With Angiography-Defined Coronary Artery Disease]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/186?rss=1</link>
<description><![CDATA[<p>This study investigated the relationship between serum selenium (Se) and glutathione peroxidase (GPx) levels and the presence of coronary artery disease (CAD) among Iranian patients. Three groups were compared: patients undergoing angiography with angiographically defined CAD, individuals with a normal angiogram, and apparently healthy controls with no evidence of overt CAD. Anthropometric measurements, blood pressure, fasting blood glucose and lipid profiles, serum Se and GPx measurements, and angiographic assessment were carried out using standard protocols. Mean serum Se concentrations were not significantly different between patients with and without CAD and the control group. The mean value of serum GPx in the control group was significantly higher than in patients with or without CAD. Selenium status did not differentiate between patients with and without CAD, which may be related to the fact that angiography is not a very sensitive index of global atherosclerosis, and it is possible that patients who were CAD negative by angiogram still have significant disease. It may also be that Se is not a good marker of CAD.</p>]]></description>
<dc:creator><![CDATA[Seyyed Mohammad Reza Parizadeh,  , Moohebati, M., Ghafoori, F., Ghayour-Mobarhan, M., Seyyed Mohammad Reza Kazemi-Bajestani,  , Tavallaie, S., Azimi-Nezhad, M., Ferns, G. A.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708319780</dc:identifier>
<dc:title><![CDATA[Serum Selenium and Glutathione Peroxidase Concentrations in Iranian Patients With Angiography-Defined Coronary Artery Disease]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>191</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>186</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/192?rss=1">
<title><![CDATA[Glycoprotein IIb/IIIa Inhibitor (Tirofiban) in Acute ST-Segment Elevation Myocardial Infarction]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/192?rss=1</link>
<description><![CDATA[<p>Studies have shown conflicting results for glycoprotein IIb/IIIa inhibitor (tirofiban) use in ST-segment elevation myocardial infarction (STEMI). The authors aimed to determine if an upstream conventional dose of tirofiban in addition to a standard treatment regimen improved coronary patency and clinical outcomes in patients with STEMI. A retrospective analysis of consecutive patients with STEMI, who underwent emergent percutaneous coronary intervention (PCI) in the authors' hospital from July 2000 to April 2006 was performed. All patients received loading doses of aspirin, clopidogrel or ticlopidine, and unfractionated heparin with or without tirofiban in the emergency department prior to PCI. It was found that adding a conventional dose of tirofiban to the standard treatment regimen prior to PCI did not improve coronary patency in STEMI patients. Tirofiban also failed to show favorable outcomes for 90 days of follow-up, but there was a favorable trend for short-term 30-day survival.</p>]]></description>
<dc:creator><![CDATA[Fang, C.-C., Yeun Tarl Fresner NgJao,  , Yi Chen,  , Yu, C.-L., Wang, S.-P.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708316168</dc:identifier>
<dc:title><![CDATA[Glycoprotein IIb/IIIa Inhibitor (Tirofiban) in Acute ST-Segment Elevation Myocardial Infarction]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>200</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>192</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/201?rss=1">
<title><![CDATA[Fate of Internal Mammary Artery Grafted to Left Anterior Descending Artery Is Influenced by Native Vessel Stenosis and Viable Myocardium]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/201?rss=1</link>
<description><![CDATA[<p>In this study, factors leading to the failure of internal mammary artery grafting was investigated among patients with coronary bypass. In all, 1323 patients were evaluated. It was found that lower grade diameter stenosis in the native vessel during postoperative angiogram and wall motion score index independently affected the fate of internal mammary artery as a graft. Grafting with internal mammary artery to native vessels with lower grade stenosis and to myocardium with poor wall score might not be a rational approach.</p>]]></description>
<dc:creator><![CDATA[Yilmaz, M. B., Guray, Y., Altay, H., Demirkan, B., Caldir, V., Guray, U., Biyikoglu, S. F., Sasmaz, H., Kisacik, H. L., Korkmaz, S.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708316010</dc:identifier>
<dc:title><![CDATA[Fate of Internal Mammary Artery Grafted to Left Anterior Descending Artery Is Influenced by Native Vessel Stenosis and Viable Myocardium]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>206</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>201</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/207?rss=1">
<title><![CDATA[Sport Therapy for Hypertension: Why, How, and How Much?]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/207?rss=1</link>
<description><![CDATA[<p>Exercise may prevent or reduce the effects of metabolic and cardiovascular diseases, including arterial hypertension. Both acute and chronic exercise, alone or combined with lifestyle modifications, decrease blood pressure and avoid or reduce the need for pharmacologic therapy in patients with hypertension. The hypotensive effect of exercise is observed in a large percentage of subjects, with differences due to age, sex, race, health conditions, parental history, and genetic factors. Exercise regulates autonomic nervous system activity, increases shear stress, improves nitric oxide production in endothelial cells and its bioavailability for vascular smooth muscle, up-regulates antioxidant enzymes. Endurance training is primarily effective, and resistance training can be combined with it. Low-to-moderate intensity training in sedentary patients with hypertension is necessary, and tailored programs make exercise safe and effective also in special populations. Supervised or home-based exercise programs allow a nonpharmacological reduction of hypertension and reduce risk factors, with possible beneficial effects on cardiovascular morbidity.</p>]]></description>
<dc:creator><![CDATA[Manfredini, F., Malagoni, A. M., Mandini, S., Boari, B., Felisatti, M., Zamboni, P., Manfredini, R.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708316012</dc:identifier>
<dc:title><![CDATA[Sport Therapy for Hypertension: Why, How, and How Much?]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>216</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>207</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/217?rss=1">
<title><![CDATA[Effect of Antihypertensive Therapy on Serum Lipids in Newly Diagnosed Essential Hypertensive Men]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/217?rss=1</link>
<description><![CDATA[<p>The effect of antihypertensives on serum lipids in newly diagnosed male essential hypertensive patients was studied. The participants (n = 99) were randomly allocated to receive amlodipine, atenolol, enalapril, hydrochlorothiazide, and a combination of amlodipine and atenolol. Lipid parameters were estimated before and after 8 weeks of therapy. The atenolol and thiazide group showed a significant increase in triglycerides (TGs) and very-low-density lipoprotein cholesterol (VLDL-C). High-density lipoprotein cholesterol (HDL-C) and HDL-C to low-density lipoprotein cholesterol (LDL-C) ratio were significantly increased and TC to HDL-C ratio was significantly decreased in the amlodipine and amlodipine&mdash; atenolol combination groups. In the enalapril group, we found a significant reduction in TC, TGs, VLDL-C, nonHDL-C, and TG to HDL-C ratio after treatment. It can be concluded from the present study that some drugs have beneficial effects on the lipid status, whereas others adversely affect the lipid status in hypertension.</p>]]></description>
<dc:creator><![CDATA[Nandeesha, H., Pavithran, P., Madanmohan, T.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708316167</dc:identifier>
<dc:title><![CDATA[Effect of Antihypertensive Therapy on Serum Lipids in Newly Diagnosed Essential Hypertensive Men]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>220</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>217</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/221?rss=1">
<title><![CDATA[Oxidative Stress in Prehypertension: Rationale for Antioxidant Clinical Trials]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/221?rss=1</link>
<description><![CDATA[<p>Prehypertension has been recently described as an independent category of blood pressure. Mounting evidence suggests that blood pressure in the prehypertensive range is associated with an increased risk of developing hypertension and cardiovascular disease. Several reports have assigned a critical role for oxidative stress in these disease processes. This review focuses on the clinical and experimental studies done in prehypertension and hypertension within the context of oxidative stress. This article also provides insights into why diverse therapeutic interventions, which have in common the ability to reduce oxidative stress, can impede or delay the onset of hypertension in prehypertension subjects.</p>]]></description>
<dc:creator><![CDATA[Nambiar, S., Viswanathan, S., Zachariah, B., Hanumanthappa, N., Sridhar Gopalakrishna Magadi,  ]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708319781</dc:identifier>
<dc:title><![CDATA[Oxidative Stress in Prehypertension: Rationale for Antioxidant Clinical Trials]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>234</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>221</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/235?rss=1">
<title><![CDATA[Decreasing Incidence of Critical Limb Ischemia After Intra-aortic Balloon Pump Counterpulsation]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/235?rss=1</link>
<description><![CDATA[<p>The authors investigated the incidence of critical limb ischemia (CLI) in 187 patients with intra-aortic balloon pump (IABP) support during a 6-year study period and determined risk factors and long-term outcome (median 5 years) after discharge from a cardiac intensive care unit. Cardiogenic shock following acute myocardial infarction was the predominant cause of IABP support. CLI occurred in 10% of the patients after IABP implantation. Nevertheless, in light of the overall high mortality in this patient population, CLI seems not a primary concern. Furthermore, its incidence significantly decreased during recent years. Duration of IABP support was a significant predictor for CLI.</p>]]></description>
<dc:creator><![CDATA[Dick, P., Mlekusch, W., Delle-Karth, G., Nikfardjam, M., Schillinger, M., Heinz, G.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708319782</dc:identifier>
<dc:title><![CDATA[Decreasing Incidence of Critical Limb Ischemia After Intra-aortic Balloon Pump Counterpulsation]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>241</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>235</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/242?rss=1">
<title><![CDATA[Cyclooxygenase-2 in Cancer and Angiogenesis]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/242?rss=1</link>
<description><![CDATA[<p>Tumor angiogenesis is a process where new blood vessels are formed from preexisting ones, resulting in several pathologies. Solid tumors induce angiogenesis to obtain the required nutrients and oxygen. Otherwise, tumors do not grow beyond 2 to 3 mm in diameter. Cyclooxygenase-2, an inducible enzyme important in inflammation, catalyzes the production of prostanoids from arachidonic acid. Cyclooxygenase-2 plays an important role in several cancer types, including colorectal, gastric, prostate, breast, lung, and endometrial cancer. Besides, cyclooxygenase-2 has been implicated in the progression and angiogenesis of cancers. Cyclooxygenase-2 inhibitors have been used to block angiogenesis and tumor proliferation. In this review, the recent studies related to the role of cyclooxygenase-2 in several cancer types and tumor-induced angiogenesis were compiled.</p>]]></description>
<dc:creator><![CDATA[Sahin, M., Sahin, E., Gumuslu, S.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708318378</dc:identifier>
<dc:title><![CDATA[Cyclooxygenase-2 in Cancer and Angiogenesis]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>253</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>242</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/254?rss=1">
<title><![CDATA[Ephedrine-Induced Acute Myocardial Infarction in a Young Athlete: A Case of Thrombus Management]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/254?rss=1</link>
<description><![CDATA[<p>A case of acute myocardial infarction in a young athlete provoked by ephedrine abuse has been described in this study. An intracoronary thrombus found in the left anterior descending coronary artery at urgent angiography was successfully removed using the Pronto (Vascular Solutions, Minneapolis, Minnesota) aspiration catheter. The intravascular ultrasound examination performed thereafter showed a nonobstructive atherosclerotic plaque in the culprit artery; there was no evidence whatsoever of possible plaque disruption. The result of percutaneous coronary intervention was satisfactory, and no stent implantation was needed. The patient experienced no adverse events until his outpatient visit 3 months later.</p>]]></description>
<dc:creator><![CDATA[Kranjec, I., Cerne, A., Noc, M.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319707310280</dc:identifier>
<dc:title><![CDATA[Ephedrine-Induced Acute Myocardial Infarction in a Young Athlete: A Case of Thrombus Management]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>258</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>254</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/content/abstract/60/2/259?rss=1">
<title><![CDATA[Angina Pectoris With Pharyngeal Pain Alone: A Case Report]]></title>
<link>http://ang.sagepub.com/cgi/content/abstract/60/2/259?rss=1</link>
<description><![CDATA[<p>Patients with pharyngeal pain are frequently encountered in the department of otorhinolaryngology. The pharyngeal pain is usually caused by an inflammation or a malignant disease. In some cases, anginal pain radiates to the pharynx. However, patients with angina pectoris who suffer from pharyngeal pain without chest pain are believed to be very rare. The patient was a 70-year-old man whose chief complaint was only pharyngeal pain on exertion. The pharyngeal pain was similar to acute pharyngitis with burning pain. Upon cardiac catheterization, no abnormality was found in the right coronary artery or in the circumflex artery, but 99% stenosis was found in the middle portion of the left anterior descending artery. There was no collateral circulation to the left anterior descending artery. Thus, percutaneous coronary intervention was performed, and the pharyngeal pain vanished.</p>]]></description>
<dc:creator><![CDATA[Sone, M., Koizumi, A., Tamiya, E., Inoue, K., Ebihara, I., Koide, H., Okazaki, S., Kato, Y., Suzuki, J., Daida, H.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319707311537</dc:identifier>
<dc:title><![CDATA[Angina Pectoris With Pharyngeal Pain Alone: A Case Report]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>261</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>259</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://ang.sagepub.com/cgi/reprint/60/2/262?rss=1">
<title><![CDATA[Are Statin Effects Mediated Through, or in Spite of, Their Cholesterol-lowering Action?]]></title>
<link>http://ang.sagepub.com/cgi/reprint/60/2/262?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mascitelli, L., Pezzetta, F., Goldstein, M. R.]]></dc:creator>
<dc:date>Thu, 16 Apr 2009 22:05:33 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0003319708330527</dc:identifier>
<dc:title><![CDATA[Are Statin Effects Mediated Through, or in Spite of, Their Cholesterol-lowering Action?]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>60</prism:volume>
<prism:endingPage>263</prism:endingPage>
<prism:publicationDate>2009-04-01</prism:publicationDate>
<prism:startingPage>262</prism:startingPage>
<prism:section>Article</prism:section>
</item>

</rdf:RDF>