Key result
PTCA-induced transient myocardial ischemia linked to ~83% increase in femoral vein ANP secretion.
Why the study?
Does transient myocardial ischemia produced by PTCA increase plasma ANP levels in patients with LAD stenosis?
Observational (n=10)
Does transient myocardial ischemia produced by PTCA increase plasma ANP levels in patients with LAD stenosis?
Transient myocardial ischemia during PTCA leads to immediate ANP secretion even in the absence of significant pressure elevation in the left atrium.
Should not alter PTCA management; leaves open direct ischemia-ANP link independent of atrial pressure.
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 ventricular 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%). Immunoreactive 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) within 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 secretion even in the absence of significant pressure elevation in the left atrium. As a part of the continuous medical education program of the American College of Angiology the second part of the paper reviews the mechanisms that allow the ischemic heart to counteract the ischemic condition and thus to escape from myocardial infarction. A review of this subject is presently not available in the literature.
No takes yet. Share an insight, caveat, or question.
Gasser et al. (1993) conducted an observational in Coronary artery disease and stable angina (n=10). Transient myocardial ischemia produced by PTCA vs. Baseline (before PTCA) was evaluated on Immunoreactive atrial natriuretic polypeptide (ANP) levels in the femoral vein and coronary sinus. Transient myocardial ischemia produced by PTCA increased ANP secretion by 83% in the femoral vein and 11% in the coronary sinus within minutes, returning to baseline after 30 to 60 minutes.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: