Effects of propranolol on coronary hemodynamic and metabolic responses to tachycardia stress in patients with and without coronary disease.

Abstract

To clarify the influence of propranolol-and particularly its heart-rate effects-on myocardial ischemia, coronary hemodynamics and metabolism were studied in 15 patients utilizing a protocol to control heart rate. Ten patients had significant coronary narrowing (CAD) and 5 were normal. Systemic pressure, coronary sinus blood flow (CSBF), left ventricular oxygen utilization (LVVO2), ST Segment depression, and myocardial lactate extraction were measured before and after propranolol (10 mg IV), at rest, during pacing-induced tachycardia stress. Propranolol-related reduction in CSBF and LVVO2 at rest was reversed when heart rate was controlled in both patient groups. Propranolol failed to alter heart-rate threshold, tension-time index (TTI), CSBF, or LVVO2 at angina in the CAD patients. Likewise, ischemic-type ST depression, decreases in lactate extraction, and coronary resistance were unchanged compared to values observed during tachycardia stress before propranolol. In normal coronary patients, propranolol also produced no significant change in LVVO2 or coronary resistance when its heart rate effects were controlled. These data imply that a major coronary and metabolic influence of propranolol relates to changes occurring secondary to its influence on heart rate. Furthermore, this agent's anti-ischemic effect is not prominent during tachycardia stress suggesting that this stress test may be clinically useful in patients taking propranolol.