Coronary Vasoconstriction in Patients with Coronary Artery Disease

The hemodynamic and myocardial metabolic responses to the cold pressor test were studied in 15 patients with coronary artery disease and stable exertional angina. Every patient had abnormal coronary vasoconstriction during a control cold pressor test, even though 14 were receiving propranolol and 12 were receiving long-acting nitrates. Mean coronary vascular resistance for the group increased 18 ± 6% (SD) (from 0.80 ± 0.12 to 0.94 ± 0.20 mm Hg/ml/min, p < 0.05); coronary sinus blood flow was unchanged, and the arterial-coronary sinus oxygen difference widened significantly (from 11.5 i 1.2 to 12.3 ± 1.2 ml/100 ml, p < 0.05), Four patients developed angina, accompanied in each instance by a negative arterial-coronary sinus lactate difference. After the administration of nifedipine (10 mg buccally) in 10 patients, the coronary vascular responses to a repeat cold pressor test were normal in each patient. Mean coronary sinus blood flow increased 27 ± 12% (from 122 ± 32 to 153 ± 35 ml/min, p < 0.05), coronary vascular resistance decreased 10 ± 6% (from 0.85 ± 0.16 to 0.76 ± 0.16 mm Hg/m1/min, p < 0.05), and the arterial-coronary sinus oxygen difference was unchanged. No patient experienced angina. The hemodynamic and coronary vascular responses to a repeat cold pressor test in five patients given placebo were unaltered from control responses. The protective effects of nifedipine were unaccompanied by any change in mean arterial pressure, left ventricular filling pressure or myocardial oxygen consumption either at test or in response to the cold pressor test. Nifedipine appears to exert a selective antivasoconstrictor effect on the coronary vasculature.