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Beneficial enhancement of coronary blood flow by nifedipine

Comparison with nitroglycerin and beta blocking agents
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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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