Hemodynamic observations in patients with unstable angina pectoris

Brachial and pulmonary arterial pressures were monitored for 48 hours in 26 patients with unstable angina pectoris and documented occlusive coronary artery disease. The circulatory response during 56 episodes of spontaneous anginal pain permitted the division of responses into three distinctive hemodynamic subsets. Patients in group I had an increased heart rate only with the spontaneous attack of angina; patients in group II had associated increases in brachial arterial pressure and slight increases in heart rate during the episodes of pain; patients in group III demonstrated increases in both brachial and pulmonary arterial diastolic pressures with minimal changes in heart rate. Resting hemodynamic data during pain-free periods were normal in 25 of 26 patients. Patients in all groups who had more than one episode of pain had similar hemodynamic responses to the first and later episodes. Although myocardial hypoxemia appears to be responsible for the spontaneous attack of angina, the hemodynamic responses to the attack varied but were highly specific for any one patient.Our observations suggest that there may be various pathogenic mechanisms for “spontaneous” or resting angina in patients with occlusive coronary artery disease but that the mechanism and associated hemodynamic changes may be specific for individual patients.