Circulation, Vol 68, 124-130, Copyright © 1983 by American Heart Association
H Emanuelsson and S Holmberg
To elucidate the mechanisms of action of nifedipine in angina pectoris, 14
patients were studied before and after sublingual administration of 10 mg
nifedipine. Systemic and coronary hemodynamic and myocardial metabolic
measurements were taken at rest and during pacing. At the pacing rate that
induced pain in the control situation, no patient experienced angina after
nifedipine administration. Lactate production during control turned into
extraction after nifedipine administration (p less than .05), and the
double product was reduced (p less than .001). Systemic and coronary
vascular resistance were reduced by 26% (p less than .001) and 19% (p less
than .005), respectively. Systolic blood pressure fell from 160 +/- 29 to
127 +/- 25 mm Hg (p less than .001) and diastolic from 100 +/- 14 to 79 +/-
11 mm Hg (p less than .001). Pulmonary artery diastolic blood pressure fell
from 14 +/- 4 to 10 +/- 3 mm Hg (p less than .01). When the pacing rate was
further increased after nifedipine administration until pain developed, the
double product and the degree of lactate production were the same as during
pain before nifedipine was administered. The pacing rate was 131 +/- 12
compared with 119 +/- 13 during control (p less than .001). Both the
systolic and diastolic blood pressures were still significantly reduced
compared with control pacing values, 131 +/- 26 mm Hg (p less than .01) and
84 +/- 13 mm Hg (p less than .01), respectively. Our data demonstrate that
the antianginal efficiency can be partly explained by afterload reduction,
which decreases myocardial oxygen consumption. The data also suggest
additional mechanisms, possibly an increase in collateral flow, direct
dilatation of stenotic parts of epicardial arteries, or a decrease in
myocardial back pressure secondary to reduced left ventricular filling
pressure.
ARTICLES
Mechanisms of angina relief after nifedipine: a hemodynamic and myocardial metabolic study
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