Mechanism of isoproterenol-induced angina pectoris in patients with obstructive hypertrophic cardiomyopathy and normal coronary arteries

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Abstract

In 14 patients with obstructive hypertrophic cardiomyopathy and angiographically normal coronary arteries, 8 with angina (group B) and 6 without (group A), the effects of intravenous isoproterenol, 2 to 4 μg/min, followed by intravenous propranolol, 0.2 mg/kg, were studied. An intraventricular systolic gradient <50 mm Hg, high-quality echocardiograms and cineangiograms and high-fidelity pressure tracings were selection criteria. Hemodynamic and metabolic variables were assessed during basal conditions, after 5 minutes of isoproterenol infusion or at angina and ST-segment depression, and 5 and 10 minutes after intravenous propranolol infusion. Isoproterenol increased the intraventricular systolic gradient more significantly in group B than in group A (102.4 ± 8.3 vs 52.2 ± 8.2, p < 0.0001). Group B also had higher left ventricular end-diastolic pressure (32.5 ± 3.9 vs 20.2 ± 5.7), lower mean arterial pressure (69.7 ± 3.5 vs 84.7 ± 4.8) and a smaller increase in coronary sinus flow (176.1 ± 9.2 vs 261.5 ± 33.9, all p < 0.0001), concomitant with lactate release and ST-segment depression. Propranolol promptly reversed hemodynamic and metabolic changes caused by isoproterenol, except for a further coronary sinus flow increase (from 176.1 ± 9.2 to 219 ± 14.2 ml/min, p < 0.001), and heart rate decrease below basal values (57.8 ± 7.5 vs 79.9 ± 9.8 beats/min, p < 0.001) in group B. In conclusion, in patients with angina, higher intraventricular systolic gradients develop during isoproterenol infusion, revealing the primary role of true left ventricular outflow obstruction in the pathophysiology of catecholamine-induced angina, and hyperresponse to β-adrenergic stimulation and β blockade could be suggested in angina patients with obstructive hypertrophic cardiomyopathy and normal coronary arteries.

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