FASTING AND POSTPRANDIAL ISCHEMIC THRESHOLD IN PATIENTS WITH UNSTABLEANGINA WITH AND WITHOUT POSTPRANDIAL ANGINA AT REST

Background Postprandial angina develops within minutes after a meal in patients with unstable angina, but the clinical characteristics of th ese patients and why it develops in only some of those with advanced c oronary artery disease remain largely unknown. A severely reduced coro nary reserve associated with postprandial increases in heart rate coul d be a contributory mechanism. Methods The clinical and angiographic c haracteristics of 277 patients with unstable angina with (23) or witho ut (254) postprandial angina were analyzed. The coronary reserve was a lso 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 lik ely 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] beers/min, p < 0.0001). However, 67 of the 79 patients with the lowest fasting thresh olds (less than or equal to 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 is chemic threshold was also lower in those with postprandial angina (p < 0.005) and there were no differences in left ventricular end-diastoli c pressure or volume. Postprandial pacing was positive in 37 patients but postprandial ischemic threshold was comparable to Fasting threshol d (132 [SD 14] vs 132 [SD 16] beats/min). Moreover, in the 10 patients who experienced in-hospital postprandial angina, heart rate during po stprandial angina was similar to nonpostprandial angina (93.1 [SD 14.7 ] vs 90.3 [SD 17.6]) and lower than the fasting ischemic threshold (13 2.0 [SD 10.8] beats/min, p < 0.0001). Conclusions Thus postprandial an gina tends to occur among elderly and hypertensive patients with advan ced 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 ot hers than increases in heart rate account for postprandial angina. Fur thermore, 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 ploy a major role in postprandial ischemi a.