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<title>Angiology current issue</title>
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<description>Angiology RSS feed -- current issue</description>
<prism:coverDisplayDate>October 2009</prism:coverDisplayDate>
<prism:publicationName>Angiology</prism:publicationName>
<prism:issn>0003-3197</prism:issn>
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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>
</item>

<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>

</rdf:RDF>