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Angiology
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Observations on Plasma ANP Levels During Short-Term Transient Myocardial Ischemia Produced by PTCA in Patients with LAD Stenosis

R. Gasser

Department of Medicine, University of Graz and Department of Nuclear Medicine, University of Graz, Graz, Austria

O. Luha

Department of Medicine, University of Graz and Department of Nuclear Medicine, University of Graz, Graz, Austria

J. Dusleag

Department of Medicine, University of Graz

B. Eber

Department of Medicine, University of Graz

R. Rotman

Department of Medicine, University of Graz

W. Klein

Department of Medicine, University of Graz

G.R. Fueger

Department of Medicine, University of Graz

Ten patients with coronary artery disease and stable angina (mean age fifty- seven) were included in the study. Five of the patients had normal left ventricu lar function, 5 had local hypokinesia or akinesia; 8 had one-stem and 2 had two- stem disease, but all had left anterior descending (LAD) lesions ranging from 75% to 100%. Ejection fraction varied between 35% and 75% (mean 59%). Im munoreactive atrial natriuretic polypeptide (ANP) levels in the femoral vein (FV) and the coronary sinus (CS) were measured before, immediately after, and up to twenty-four hours after percutaneous transluminal coronary angioplasty (PTCA) of the LAD. ANP secretion increased by 83% (FV) and 11% (CS) with in minutes after PTCA and reached control levels after thirty to sixty minutes. In patients with hypokinesia of the anterior wall, ANP secretion was significantly lower, 48% (FV) and 11% (CS) respectively. ANP secretion during PTCA was higher in patients with concomitant increase in pulmonary capillary pressure (PCP) but was also observed without an increase of PCP, suggesting ventricular ANP secretion.

In conclusion, transient myocardial ischemia leads to immediate ANP secre tion even in the absence of significant pressure elevation in the left atrium.

As a part of the continuous medical education program of the American Col lege of Angiology the second part of the paper reviews the mechanisms that al low the ischemic heart to counteract the ischemic condition and thus to escape from myocardial infarction. A review on this subject is presently not available in the literature.

Angiology, Vol. 44, No. 4, 278-288 (1993)
DOI: 10.1177/000331979304400403


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