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Abstract
In 36 patients with isolated stenoses (70 percent or greater) of the anterior descending
or circumflex branches of the left coronary artery, regional myocardial blood flow
was assessed using xenon133 washout at rest and during pacing-induced ischemia, and during atrial pacing at identical
heart rates, after the following agents had been given sublingually: nifedipine, 20
mg (11 patients); nitroglycerin, 0.8 mg (12 patients); or propranolol, 5 mg (13 patients).
Pacing-induced ischemia was diagnosed by the onset of angina, the appearance on the
electrocardiogram of ST depression of at least 0.1 millivolt, or both.
The following changes in myocardial blood flow in poststenotic and normal areas of
the left ventricle, and in the rate-pressure product, were observed:
Tabled
1
Myocardial Blood Flow (ml/min. '100 g) | |||
Poststenotic Areas | Normal Areas | Rate-Pressure Product (× 10−2) | |
1. Control | 57.1 ± 10.4 | 70.7 ± 12.8 | 96.9 |
2. Pacing-induced ischemia | 77.6 ± 20.7 | 91.2 ± 18.5 | 181.7 |
3. 2 + nifedipine | 82.3 ± 14.8 | 86.8 ± 14.8 | 142.0 |
1. Control | 55.3 ± 8.6 | 66.2 ± 12.5 | 97.4 |
2. Pacing-induced ischemia | 76.9 ± 12.1 | 95.0 ± 14.5 | 180.4 |
3. 2 + nitroglycerin | 68.1 ± 11.6 | 72.4 ± 16.1 | 151.6 |
1. Control | 52.8 ± 10.4 | 63.7 ± 12.5 | 84.9 |
2. Pacing-induced ischemia | 75.3 ± 10.7 | 87.3 ± 15.3 | 153.5 |
3. 2 + propranolol | 63.4 ± 9.6 | 70.2 ± 12.8 | 155.5 |
The coronary-sinus oxygen concentration was recorded continuously and did not decrease
after propranolol.
The antianginal mechanism of nifedipine thus differs markedly from the effects seen
with both nitrates and beta blocking agents. Nifedipine decreases peripheral resistance,
thereby decreasing afterload, and increases myocardial blood flow by reducing coronary
resistance; nitrates reduce pre- and afterload and accordingly decrease myocardial
blood flow by autoregulation (exceptions are variant angina and severe ischemia with
increased compressive resistance attributable to elevated left ventricular diastolic
pressure); beta blocking agents reduce myocardial oxygen consumption by direct cardiac
action and secondarily reduce myocardial blood flow (by autoregulation rather than
vasoconstriction resulting from unopposed alpha-adrenergic tone).
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© 1981 Published by Elsevier Inc.