Evidence for transient limitations in coronary blood flow during unstable angina pectoris: hemodynamic changes with spontaneous pain at rest versus exercise‐induced ischemia following stabilization of angina

Abstract The pathophysiologic basis for the deterioration of patients with stable angina pectoris to unstable angina is unclear. Central to this issue is the question of whether myocardial ischemia occurs at the same or at a lower myocardial oxygen demand during unstable periods as during stable periods. Consequently, we compared myocardial oxygen demand in 12 patients at the onset of spontaneous pain during unstable angina to myocardial oxygen demand during exercise‐induced ischemia after resumption of stable angina, 6–12 weeks later. Myocardial oxygen demand was estimated from values for heart rate (HR), systolic blood pressure (BP), and the rate‐pressure product (RPP). Rate‐pressure product is the heart rate × systolic blood pressure × 10 ‐2 (mmHg/min/10 2 ). There was definite evidence for coronary artery spasm for only one patient. There was no difference in heart rate, blood pressure, or rate‐pressure product during pain‐free intervals in the hospital and just before the start of exercise testing. Mean H R (71.2± 11.1 beats/min; mean ± standard deviation) and RPP (95.8±20.0 mmHg/min/10 2 ) just before spontaneous angina during the unstable period were significantly lower (p<0.001) than at the termination of bicycle ergometry in both the supine (HR, 96.9±10.5 beats/min; RPP, 141.8±25.0 mmHg/min/10 2 ) and upright (HR, 98.1±13.6 beats/min; RPP, 143.0±32.2 mmHg/min/10 2 ) positions. Blood pressure (134.5 ± 17.6 mmHg) just before spontaneous angina was significantly lower than at the conclusion of both supine (145.6±13.3 mmHg) and upright (145.1 ±18.6 mmHg) ergometry. The observation that myocardial oxygen demand was lower at the threshold of ischemia with spontaneous angina than with exercise‐induced ischemia is consistent with the hypothesis that there were transient, reversible limitations in coronary blood flow during the period of unstable angina. There was also a moderate but significant rise in estimated myocardial oxygen demand just before spontaneous angina in these patients, but the nature of the data do not allow us to distinguish whether or not this rise was part of the cause or an effect of ischemia. While the results of this study did not identify the cause for the transient limitations in coronary flow, coronary artery spasm without ST‐segment elevation, intracoronary platelet aggregates, and hemorrhage into atherosclerotic plaques are possibilities that are consistent with these hemodynamic observations.