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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.

The purpose of this study was to evaluate whether the existence of coronary collateral circulation influences recanalization rates of intracoronary thrombolysis. The study population consisted of 85 consecutive patients undergoing intracoronary thrombolysis within 6 hours after the onset of the first acute myocardial infarction, all of whom had a complete occlusion of the infarct-related coronary artery. Intracoronary thrombolysis with high-dose urokinase (960,000 IU) was attempted at a rate of 24,000 IU/min. Of 18 patients (group A) who had good angiographic collateral circulation to the area perfused by the infarct-related coronary artery, the obstructed artery was recanalized to a residual luminal diameter stenosis of less than or equal to 90% (successful recanalization) in only five (28%). In contrast, of 67 patients (group B) with poor or no collateral circulation, recanalization was successful in 40 (60%) (p less than 0.05). Antegrade flow of infarct-related arteries was observed following thrombolysis in 12 (67%) of 18 group A patients and in 56 (84%) of 67 group B patients (p = NS). It was concluded that (1) the presence of collaterals correlates with the presence of high-grade stenosis; (2) the presence of collaterals correlates with the presence of high-grade stenosis; (2) the presence of collaterals is inversely related to the efficacy of thrombolytic therapy; and (3) the difference in successful recanalization rates observed between the two groups probably reflects the impact of underlying stenosis severity on the effectiveness of lytic therapy.

In order to evaluate the effects of intracoronary acetylcholine on coronary resistance vessels, oxygen saturation in coronary sinus blood was continuously measured to compare its dynamic changes during intracoronary injection of acetylcholine in both patients with variant angina and control subjects. Group 1 consisted of 6 patients without coronary artery disease. Group 2 consisted of 10 patients with variant angina and spasm in the left anterior descending coronary artery. A fiberoptic reflection oximetry system was used for the continuous measurement of coronary sinus venous oxygen saturation. Acetylcholine (20 micrograms) was injected directly into the left coronary artery over 30 s. In the group 1 patients, coronary sinus venous oxygen saturation was increased from 39 +/- 2% (mean +/- SEM) to 54 +/- 3% at 30 s, continuously climbed to 70 +/- 3% at 60 s and then gradually decreased to 53 +/- 5% at 120 s after the initiation of intracoronary injection of acetylcholine. In contrast, in the group 2 patients, coronary sinus venous oxygen saturation was transiently increased from 39 +/- 2% to 56 +/- 4% at 30 s, reversed, decreased to 52 +/- 4% at 60 s and then rapidly decreased to 36 +/- 3% at 120 s with the onset of chest pain associated with electrocardiographic ischemic changes. Coronary arteriography during attacks demonstrated a total or subtotal occlusion of the left anterior descending coronary artery due to severe spasm in all of the 10 patients. The extent of increases in coronary sinus venous oxygen saturation at 30 s after acetylcholine injection was not significantly different between the two groups (group 1: 15 +/- 4%, group 2: 17 +/- 3%). Heart rate, blood pressure and rate-pressure product were essentially unchanged at 30 s after intracoronary injection of acetylcholine in both groups. These data suggest that in control adult humans, coronary blood flow was increased through dilatation of resistance vessels by acetylcholine, while in patients with variant angina, coronary blood flow was transiently increased by dilatation of resistance vessels, after which it was suddenly decreased by spasm of an epicardial artery induced by this agent. Relaxant responses to acetylcholine of coronary resistance vessels appear to be preserved well in patients with variant angina.

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 define the effects of heparin treatment during the acute stage of the first anterior myocardial infarction on coronary collateral development and regional myocardial function, we evaluated angiographically the extent of a collateral visualization (collateral index: 0-3) to the completely obstructed infarct-related coronary artery and regional wall motion in 18 patients during convalescence after infarction. The patients were divided into two groups depending on the presence (group I) or absence (group II) of heparin treatment (170 to 220 IU/kg per day) during the acute phase of infarction. The collateral index was significantly higher in group I (1.5 +/- 0.9) than in group II (0.4 +/- 0.4; p less than 0.05). The left ventricular ejection fraction tended to be greater in group I than in group II (49 +/- 12% vs 38 +/- 16%), and there was a significant difference in regional wall motion of the infarct area that was evaluated by the percentage of segment shortening between the two groups (group I:7.4 +/- 9.2%, group II:-0.8 +/- 4.5%, p less than 0.05). These findings indicate that heparin treatment for patients with acute myocardial infarction is worthwhile in terms of the preservation of left ventricular function as a result collateral development.

The present study evaluated the effects of coronary collateral circulation developing after acute myocardial infarction on global and regional left ventricular function during the chronic stage. The study group consisted of 16 patients with initial myocardial infarction having total occlusion of the proximal left anterior descending coronary artery. To eliminate the effects of collateral circulation existing at the onset of infarction, patients with pre-infarction angina were excluded from this study. The patients were categorized in two groups depending on the extent of their collateral circulation (collateral index: CI 0-3): group A--patients with significant collateral circulation (CI = 2 or 3) to the infarct-related coronary artery; group B--patients without significant collateral circulation (CI = 0 or 1). Their heart rate, left ventricular peak systolic and end-diastolic pressures and cardiac index were similar in the two groups. The left ventricular end-systolic volume index in the group B was significantly greater than that in the group A (60 +/- 21 ml/m2 vs 34 +/- 9 ml/m2, p less than 0.05). Left ventricular ejection fraction in the group A was significantly greater than that of the group B (55 +/- 9% vs 39 +/- 15%, p less than 0.05), and a significant difference was observed in the percentage of segment shortening in the infarct area between the groups A and B (10.8 +/- 9.2% vs -0.2 +/- 5.4%, p less than 0.01). It was concluded that coronary collateral circulation which develops after acute myocardial infarction exerts beneficial effects on global and regional left ventricular function during the chronic stage.

In 31 patients without a history of preinfarction angina, coronary collateral circulation to the completely obstructed coronary artery was evaluated by coronary angiography during a convalescent period of their first myocardial infarction. Collateral visualization (collateral index) was found to be significantly greater in patients with involvement of the right coronary artery (2.1 +/- 1.1, SD) than in those with obstruction of the left anterior descending coronary artery (1.2 +/- 1.0, p less than 0.05). The time interval from the onset of symptoms of acute myocardial infarction to angiographic evaluation did not affect the extent of collateral visualization or the degree of coronary artery disease. These findings indicate that the collateral vessels develop after acute myocardial infarction regardless of the extent of coronary artery disease and accomplish the proliferative process within one month. It is also suggested that the collateral visualization is dependent on the size of perfusion territory of the infarct-related coronary artery.