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The purpose of the present study was to evaluate the factors which influence the effect of heparin exercise treatment on treadmill capacity, and to examine the long-term efficacy of the treatment in 16 patients with chronic effort angina. Treadmill exercise was performed 20 times for 2 to 3 weeks according to standard Bruce protocol. A single intravenous dose of heparin (5,000 IU) was given 10 min before each exercise period. Exercise with heparin pretreatment increased the total exercise duration from 6.6 +/- 1.6 (SD) to 9.4 +/- 1.9 min (p < 0.05) and the maximal rate-pressure product from 19,200 +/- 4,700 to 24,700 +/- 5,900 mmHg.beats/min (p < 0.05). The rate-pressure product at the onset of angina was also increased by 32% (p < 0.05). The ST segment depression at the same exercise time as in control exercise was ameliorated from 0.16 +/- 0.05 to 0.12 +/- 0.06 mV (p < 0.05). Multivariate analysis of the determinants of the effect of the treatment on treadmill capacity indicated that the treatment is more effective in patients without previous myocardial infarction. All of the above-mentioned variables of treadmill capacity did not change significantly during a follow-up period of 13 +/- 7 months (range; 4-24 months). These findings lend further support to heparin exercise treatment as a possible therapeutic approach in patients with chronic stable effort angina, and particularly in those without previous infarction.

To elucidate whether the presence of significant stenoses in donor coronary arteries compromises collateral flow reserve, coronary arteriography was performed in 22 patients with stable effort angina who had a complete obstruction in one of the major coronary arteries. The patients were divided into two groups according to the absence (group I: n = 11) or presence (group II: n = 11) of significant stenoses (> or = 75% stenosis of the luminal diameter) in donor arteries. After conventional cardiac catheterization, coronary arteriography was repeated before and during rapid atrial pacing. Coronary collateral circulation was evaluated by means of angiographic contrast appearance time (CAT) which was defined as the time (s) until the epicardial segments distal to the site of complete occlusion were opacified after the injection of contrast medium into the donor artery. The pressure gradient across the collateral circulation (mean aortic pressure minus left ventricular end-diastolic pressure) remained unchanged before and during rapid atrial pacing (group I: 95 +/- 14 vs. 99 +/- 15 mmHg; group II: 91 +/- 18 vs. 94 +/- 16 mmHg). Rapid atrial pacing decreased the contrast appearance time in group I from 1.73 +/- 0.34 to 1.47 +/- 0.37 s (P < 0.01), but was not changed in group II from 1.68 +/- 0.36 to 1.73 +/- 0.51 s (P = n.s.). It was concluded that coronary collateral circulation is further augmented in response to an increase in myocardial oxygen demand in patients with non-stenosed donor coronary arteries and significant stenoses in donor arteries compromise an increase in collateral blood flow.

In an attempt to clarify the role of coronary artery spasm in the pathogenesis of unstable angina, acetylcholine (20 and 50 micrograms) was injected directly into the coronary arteries of 19 patients with unstable effort angina (group 1), 30 patients with unstable spontaneous angina (group 2), and 15 patients with stable effort angina due to coronary artery organic stenosis (greater than or equal to 75%) (group 3). Coronary spasm was defined as severe vasoconstriction (greater than or equal to 90% of luminal diameter) with chest pain and/or ischemic ST-segment changes. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in 19 patients (100%) of group 1 and 28 (93%) of group 2 but only 3 (20%) of group 3 (p less than 0.01). When acetylcholine was injected into the left and right coronary arteries separately, multivessel spasm (spasm of both coronary arteries) was induced in 5 of 12 (42%) patients of group 1 and in 9 of 23 (39%) patients of group 2. In contrast, intracoronary acetylcholine did not cause multivessel coronary spasm in any of 15 patients of group 3 (0%). These results suggest that coronary arteries in patients with unstable effort angina as well as spontaneous angina are susceptible to spasm and that coronary artery spasm may be responsible at least in part for the genesis of attacks in these patients.

The purpose of this study was to elucidate the mechanism that induces an improvement in exercise capacity by nitrates in patients with stable effort angina pectoris. The study population was composed of 19 patients: group A, 10 patients with chronic stable effort angina who had a well-developed coronary collateral circulation to the potentially ischemic region; group B, 9 patients with chronic stable effort angina who had no collateral circulation to the jeopardized myocardium. Treadmill exercise was performed according to the standard Bruce protocol with and without pretreatment with orally administered 10 mg isosorbide dinitrate. Percent increases (mean +/- SE) in exercise duration were not significantly different between groups A and B (25 +/- 6 vs. 14 +/- 6%). Percent increases in the maximal rate-pressure product tended to be greater in group A than in group B (27 +/- 6 vs. 10 +/- 6%). Percent increases in the rate-pressure product at the onset of angina pectoris were significantly greater in group A than in group B (37 +/- 7 vs. 7 +/- 6%; p less than 0.01). Percent increases in the rate-pressure product at 0.1 mV S-T segment depression were also significantly greater in group A than in group B (26 +/- 6 vs. 1 +/- 5%; p less than 0.01). These results suggest that isosorbide dinitrate dilates epicardial collateral vessels with smooth muscle layers, but fails to dilate the coronary arteries with significant organic stenoses.

To elucidate the possible contribution of coronary artery spasm to the pathogenesis of angina pectoris, coronary arterial responses to intracoronary injection of acetylcholine were examined in patients with various types of angina pectoris. Coronary artery spasm with chest pain and/or electrocardiographic ischemic changes was angiographically demonstrated in 50 (85%) of 59 patients with angina pectoris. The sensitivity for coronary spasm was 92% (24 of 26) in patients with rest angina, 100% (16 of 16) in patients with both rest and effort angina, and 59% (10 of 17) in patients with effort angina, while it was only 6% (1 of 16) in patients without coronary artery disease. When patients with effort angina were subdivided according to the variability of anginal threshold for exertional angina, the sensitivity for coronary spasm was as high as 90% (9 out of 10) in patients with variable-threshold angina. In contrast, coronary spasm was less frequently (p less than 0.05) induced in patients with fixed-threshold angina (1 of 7, 14%). These results suggest that coronary arteries in patients with angina pectoris are quite susceptible to acetylcholine except in those patients with stable exercise tolerance or anginal threshold. Thus coronary artery spasm appears to play a significant role for the pathogenesis of angina pectoris in a large proportion of patients with effort angina as well as in patients with rest angina.

To examine whether intracoronary injections of acetylcholine induce coronary artery spasm in patients with vasospastic angina, incremental doses (20, 30 and 50 micrograms) were injected directly into the coronary arteries in 12 patients with variant angina (Group A: rest angina with electrocardiographic ST-segment elevation during attacks), 19 with vasospastic angina (Group B: rest angina and/or effort angina with variable threshold in the treadmill exercise stress test), 11 with organic coronary artery stenosis but without angina (Group C), and 14 without coronary artery disease (Group D). A temporary cardiac pacemaker was positioned in the right ventricle. Coronary artery spasm was defined as severe vasoconstriction (greater than or equal to 90% of reduction in the luminal diameter) with chest pain and/or ischemic changes in the electrocardiogram. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in all 12 patients (100%) of Group A, in 18 (95%) of Group B, in two (18%) of Group C, and in two (14%) of Group D. Thus, the sensitivity of this method for inducing coronary spasm was 100% in group A, 95% in Group B, and 97% in Group A plus Group B. The specificity for inducing spasm was 86% in Group D, and 84% in Group C and Group D. When acetylcholine was injected separately into the left and right coronary arteries, spasm of both the coronary arteries was observed in two (40%) of Group A, in five (33%) of Group B, and none (0%) of Group C and Group D. Acetylcholine (20 micrograms) induced coronary spasm in 10 (83%) of Group A and only in nine (47%) of Group B.(ABSTRACT TRUNCATED AT 250 WORDS)