Background Postprandial angina develops within minutes after a meal in patients with unstable angina, but the clinical characteristics of these patients and why it develops in only some of those with advanced coronary artery disease remain largely unknown. A severely reduced coronary reserve associated with postprandial increases in heart rate could be a contributory mechanism.

Methods The clinical and angiographic characteristics of 277 patients with unstable angina with (23) or without (254) postprandial angina were analyzed. The coronary reserve was also analyzed by measuring the ischemic threshold by atrial pacing in a fasting state in all patients and 15 minutes after a 900-calorie meal in 54.

Results Patients with postprandial angina were older, more likely to be women, and had a higher incidence of hypertension and three-vessel disease than those without (p < 0.005) and had a lower fasting ischemic threshold (131.8 [SD 13.0] vs 147.5 [SD 23.4] beats/min, p < 0.0001). However, 67 of the 79 patients with the lowest fasting thresholds (≤130 beats/min) (84.8%) had no postprandial angina. Moreover, among patients with and without postprandial angina who were matched for age, sex, and extent of coronary disease, the ischemic threshold was also lower in those with postprandial angina (p < 0.005) and there were no differences in left ventricular end-diastolic pressure or volume. Postprandial pacing was positive in 37 patients but postprandial ischemic threshold was comparable to fasting threshold (132 [SD 14] vs 132 [SD 16] beats/min). Moreover, in the 10 patients who experienced in-hospital postprandial angina, heart rate during postprandial angina was similar to nonpostprandial angina (93.1 [SD 14.7] vs 90.3 [SD 17.6]) and lower than the fasting ischemic threshold (132.0 [SD 10.8] beats/min, p < 0.0001).

Conclusions Thus postprandial angina tends to occur among elderly and hypertensive patients with advanced coronary disease and severely reduced ischemic threshold. The fact that the postprandial ischemic threshold was clearly higher than the heart rate attained during postprandial angina suggest that factors others than increases in heart rate account for postprandial angina. Furthermore, the lack of a decline in the postprandial ischemic threshold suggests that, in the absence of postprandial angina, there is not a consistent postprandial change in coronary tone or that the increases in myocardial oxygen demands due to increased myocardial contractility-wall tension do not seem to play a major role in postprandial ischemia. (Am Heart J 1998;136:252-8.)