Vascular and cardiac contractile reserve in the dog heart with chronic multiple coronary occlusions.

Nineteen mongrel dogs survived chronic occlusion of the left circumflex and of the right coronary artery without infarction due to the timely development of a collateral circulation. Only 38 per cent of the conductance of the arteries before occlusion was restored by collateral vessels. In these animals and in 15 control dogs with normal coronary arteries myocardial contractility, contractility reserve, and myocardial blood flow were studied. The same was done in dogs with chronic coronary artery occlusion after aortocoronary bypass. Myocardial blood flow was determined woth the tracer microsphere technique. Contractility reserve was tested and defined as isovolumetric left ventricular pressure and dp/dt max with norepinephrine infusion and cross-clamping of the aorta. Contractile reserve was not significantly different between normal dogs and dogs with chronic coronary artery occlusion before and after aortocoronary bypass. Myocardial blood flow during control conditions was homogenously distributed in all three groups studied. The ratio of blood flow to the endocardium and the epicardium was not significantly different from inity. Coronary reserve was determined at peak reactive hyperemia following a 20 second period of coronary artery occlusion, with ongoing norepinephrine infusion. Under these conditions subendocardial fow in normal dogs rose by a factor of 7.9 while subepicardial flow increased 7.4 times. In dogs with chronic occlusion of two coronary arteries the increase of myocardial flow was nonnomogenous; subendocardial flow to areas supplied by a normal coronary artery rose by a factor of 7.0 while subepicardial flow increased 5.7 times control. Subendocardial collateral flow rose by a factor of 2.4 and subepicardial collateral flow increased 3.5 times control. In normal dogs norepinephrine alone did not result in maximal coronary flow but only 57 per cent thereof. Dogs with chronic coronary occlusion, however, required the entire coronary reserve in areas that were supplied by a normal coronary artery, whereas areas supplied by collaterals became ischemic. Opening of an aortocoronary bypass restored normal flow to previously ischemic areas, and reduced the flow to areas supplied by a normal artery. With the bypass open no differences existed between normal dogs and those with two occluded coronary arteries. We conclude that the norepinephrine-stimulated contractile reserve of hearts with chronic coronary occlusion was comparable to that of normal hearts; however, norepinephrine forced these hearts to spend the entire flow reserve of the remaining normal artery while producing ischemia in collateral-dependent areas. The same dose of norepinephrine did not require the entire flow reserve of normal dogs.     

Multiple experimental coronary occlusion without infarction. Effects of heart rate and vasodilation

Chronic occlusion of the left circumflex artery and of the right coronary artery was produced in 21 dogs with the Ameroid technique. Thirteen animals survived and myocardial infarction was avoided in 12 due to the development of a network of collateral vessels. The functional state of the collaterals was tested by physiologic and pharmacologic stimuli using Tracer Microspheres and 133-Xe as indicators of coronary flow and of collateral flow. Increases in heart rate up to 160 beats per minute caused mild coronary vasodilation and homogeneous distribution of left ventricular myocardial flow.Carbochromene caused moderate-to-marked increase in coronary blood flow. Collateral flow rose also but less than coronary flow. Carbochromene plus tachycardia caused a marked increase in coronary flow but collateral flow to the subendocardial layers actually decreased below control values. An explanation of these findings is offered on the basis of relations between the collateral and coronary resistances.     

Relationship between coronary collateral growth in the dog and ischemic bed size

Summary Two models of gradual coronary occlusion (Ameroid method) were compared in this study: 3 months circumflex and 3 months right coronary occlusion. Following coronary occlusion, the collaterals developed in intact, normally active dogs. The collateral flows were assessed in an isolated heart preparation. The results indicated a pattern for collateral development. Collateral flow was directed primarily toward the left heart with circumflex occlusion, and toward the right heart with right occlusion. Although dominant collateralization was via epicardial collaterals, intramyocardial septal collaterals strongly participated in growth development of both models. Collateral growth to the circumflex with circumflex occlusion was 6.54 fold greater than collateral growth to the right coronary artery with right occlusion. The data suggest a relationship between collateral growth and ischemic bed size.This work was supported by the American Heart Association, and by USPHS grant HL-24323.     

Evaluation of noncoronary sources of left ventricular perfusion to intercoronary collateral-dependent myocardium due to chronic major vessel occlusion: absent contribution of luminal and extracardiac channels

Liminal contribution to perfusion of collateral-dependent left ventricular (LV) myocardium was evaluated in six dogs. A portion of LV free wall was rendered collateral-dependent by gradual occlusion of left circumflex artery with Ameroid constrictor. Eight to 10 weeks after implantation of constrictor, measurements of LV myocardial flow were made by left atrial injections of 9-10 micro radioactive microspheres. To measure total collateral flow, microspheres were injected under control conditions, and to measure luminal contribution to collateral flow, microspheres were injected after ligation of right coronary artery during extracorporeal perfusion of left common coronary artery (LCCA) with microsphere-free arterial blood, and during stoppage of flow through LCCA. Under control conditions, myocardial blood flow in collateral-dependent region, 1.01 +/- 0.31 ml/min/gm, was not significantly different from that in normal region, 1.06 +/- 0.32 ml/min/gm. Flow from luminal collateral vessels was negligible (less than 0.005 ml/min/gm) in both collateral-dependent and normal myocardium, and was not affected by stoppage of flow through LCCA. These results indicate that luminal collateral vessels, as well as collateral vessels originating from other noncoronary sources, do not contribute significantly to perfusion of normal or collateral-dependent LV myocardium.     

Coronary collateral development in the rhesus monkey (Macaca mulatta)

Summary The ability of the rhesus monkey to form coronary collaterals was tested in ten animals. Ameroid constrictors were implanted on the left circumflex coronary artery and allowed to remain for 12 weeks. One animal died of an acute myocardial infarction nine days after surgery; the remaining animals survived without clinical signs referable to myocardial ischemia. The hearts were excised at 12 weeks postsurgery for perfusion fixation and coronary vascular injection with barium-gelatin. All hearts exhibited infarction scars in the circumflex-perfused regions, with infarcts varying from a transmural scar to cases with a thin margin of surviving myocardium at the epicardial surface. Coronary collaterals were infrequent and small in size, and particularly evident in the atria. We conclude that the rhesus monkey is unable to develop sufficient coronary collateral blood flow to prevent myocardial infarction after gradual, total coronary occlusion with ameroid constrictors.Florida Agricultural Experiment Station Journal Series No. 4441.     

Morphologic and biochemical studies on the experimental chronic ischemic myocardium with the Ameroid constrictor.

1. Morphologic as well as biochemical alterations in chronic ischemic myocardial tissue without infarction were studied in dogs utilizing the Ameroid constrictor. 2. Serum creatine kinase activity elevated at around three weeks after placing the Ameroid constrictor around the circumflex branch of the left coronary artery suggestive of myocardial tissue injury followed by the initial activation caused by surgery. 3. Subendocardial proliferation of connective tissue was observed in about 60% of the experiments, but the middle and the subepicardial muscles were morphologically intact. 4. The marked increase in glycogen particles was observed in the subendocardial muscle cells in most of the experiments, and mild features of myocardial cellular necrosis were found in approximately 60% of the experiments. 5. ATPase activities of the structural proteins as well as sarcoplasmic reticulum in the ischemic myocardium shoed relatively higher values than those in the non-ischemic myocardium. However, no substructural changes were observed in SDS gel electrophoresis in both the fractions. 6. The alterations in the chronic myocardial ischemia are supposed to be essentially the same as those in myocardial necrosis followed by acute coronary occlusion.     

Coronary collaterals: Role in restoration of blood flow and preservation of cardiac function during exercise

Summary Chronically instrumented dogs were studied at rest and during exercise on two occasions 10–12 weeks apart. The left circumflex coronary artery (LCf) was initially constricted in all dogs. By the time of the second study the LCf was still patent in 9 dogs and had become occluded in 6. In the dogs with chronic coronary occlusion, collaterals restored myocardial flow to normal both at rest and during exercise, and there were no adverse hemodynamic effects when running. Conversely, in dogs with constricted but patent LCfs collateral development was inadequate to return ischemic flows to normal following transient coronary occlusion, and occlusion during exercise produced significant myocardial failure. Thus coronary collaterals can compensate for decreased antegrade coronary flow.This study was supported by National Heart, Lung and Blood Institute Grant HL-17809.     

Effect of beta-adrenergic suppression by propranolol on coronary collateral development in response to chronic coronary ischemia in dogs.

Acute left circumflex coronary artery (LC) occlusion in conscious dogs caused marked ischemia in the myocardium supplied by the occluded artery, as judged by the radioactive microsphere technique for determining blood flow distribution. With the chest open, LC pressure distal to the occlusion fell to 21 +/- 1.9% of aortic pressure. By 8 weeks after gradual LC occlusion with an ameroid constrictor, collateral development had restored coronary blood flow distribution to near-normal under basal conditions and during pacing, at a heart rate of 200 beats/min. The only evidence for ischemia was in the subepicardium within the distribution of the unoccluded left anterior descending artery, which provided the extra collateral blood flow. Distal LC pressure was 70 +/- 1.7% of aortic pressure. Propranolol 160 mg orally every 6 hours for 8 weeks had no detectable effect on coronary collateral development, as judged by blood flow distribution or distal LC pressure. The only significant difference for the propranolol dogs was a slight transmural shift away from the subendocardium in the left anterior descending region.     

Exercise can promote coronary collateral development without improving perfusion of ischemic myocardium.

We studied the effect of exercise training on the coronary collaterals that developed in response to gradual coronary occlusion in dogs. After their proximal left circumflex coronary artery occlusion, 33 dogs were randomly assigned to exercise or sedentary groups. Coronary collateral function was evaluted 5 weeks or 8 weeks later. The exercised dogs developed better epicardial collateral connections to the occluded left circumflex as judged by higher retrograde blood flow from the distal left circumflex and lower pressure drop across the collaterals. No difference in collaterals was apparent angiographically. Microsphere data indicated that exercise dogs were not better protected against tachycardia provoked subendocardial ischenia in the myocardium supplied by the collaterals.     

Effect of nifedipine on myocardial blood flow during exercise in dogs with chronic coronary artery occlusion

The effect of nifedipine, 0.010 mg/kg intravenously, on myocardial blood flow was studied in 15 dogs 4 weeks after placement of an Ameroid constrictor on either the left circumflex or left anterior descending coronary artery to produce total coronary occlusion. Myocardial blood flow was measured with radionuclide-labeled microspheres at rest and during two levels of treadmill exercise to achieve a heart rate of 190 (light exercise) and 230 (heavy exercise) beats/min. During control conditions, increasing exercise resulted in a progressive increase in myocardial blood flow in normally perfused areas, but was associated with worsening subendocardial hypoperfusion in collateral-dependent areas. Nifedipine administration resulted in a transient reduction of arterial pressure and an increase in heart rate. To determine whether nifedipine exerted significant persistent effects on the coronary collateral circulation, measurements of myocardial blood flow were repeated beginning 30 minutes after nifedipine administration, at a time when heart rate and arterial pressure had returned to control levels. In normally perfused areas, nifedipine did not significantly alter myocardial blood flow at rest, but increased mean myocardial blood flow from 2.06 +/- 0.15 to 2.40 +/- 0.20 ml/min per g during light exercise (p less than 0.01), while blood flow during heavy exercise was not significantly altered. In collateral-dependent myocardial areas, the volume and transmural distribution of myocardial blood flow were not significantly altered after nifedipine administration either at rest or during exercise. These results fail to demonstrate persistent vasodilation of the coronary collateral vessels after the systemic hemodynamic effects of nifedipine have subsided.     

Volatile anesthetics and regional myocardial perfusion in chronically instrumented dogs: Halothane versus isoflurane in a single-vessel disease model with enhanced collateral development

The influence of halothane and isoflurane on regional myocardial blood flow was investigated in chronically instrumented dogs with a well developed coronary collateral circulation. Dogs were implanted with an Ameroid constrictor on the left anterior descending (LAD) coronary artery to produce slowly progressive coronary artery occlusion and collateral development. Contractile function in the collateral-dependent region was ascertained periodically during brief balloon cuff occlusion or during atrial pacing to characterize the degree of ongoing collateral development. Following documentation of enhanced collateral perfusion by the lack of contractile dysfunction during brief balloon cuff occlusion or atrial pacing at 50 days postimplantation, dogs were anesthetized (inhalation induction) with halothane (1.5% or 2.5%; n = 7) or isoflurane (2.0% or 3.0%; n = 8) using equihypotensive inspired concentrations of either agent. Radioactive microspheres were administered to measure regional myocardial perfusion during the conscious state and at stable hemodynamic states during both low and high concentrations of each volatile anesthetic. Myocardial blood flow during anesthesia was also determined following the adjustment of arterial pressure and heart rate to conscious levels by administration of phenylephrine and atrial pacing, respectively. Over the course of collateral development, balloon cuff-induced contractile dysfunction and pacing-induced contractile dysfunction in the collateral-dependent zone were reduced, indicating extensive collateral development. Halothane and isoflurane decreased global and regional indices of contractility and arterial pressure in a dosedependent manner, but only isoflurane reduced coronary vascular resistance. Both anesthetics decreased myocardial perfusion within normal and collateral-dependent regions; however, flow was restored to levels found in the conscious state coincidental with control of arterial pressure and heart rate. Neither anesthetic alone, nor with concomitant control of arterial pressure and heart rate, produced a maldistribution of blood flow transmurally or between normal and collateral-dependent zones. The results suggest that both halothane and isoflurane, although decreasing major determinants of myocardial oxygen demand, do not unfavorably alter the regional distribution of coronary blood flow in a single-vessel disease model with enhanced collateral development.     

Survival with total occlusion of the left main coronary artery. Significance of the collateral circulation.

Four patients with total occlusion of the left main coronary artery are described. Angina pectoris was severe (NYHA class 3--4) and had lasted 20 months to seven years. Three patients had experienced a myocardial infarction. All displayed large collaterals arising from a nearly normal right coronary artery and feeding both the left anterior descending and the left circumflex arteries. The left ventricular ejection fractions ranged from 20% to 65%, and all patients had varying degrees of left ventricular asynergy. Coronary artery bypass surgery resulted in a marked improvement in three patients; one patient who underwent an aneurysmectomy died two months after the operation. The data show that total occlusion of the left main coronary artery is compatible with survival if adequate collateral supply develops from the right coronary artery. In this rare angiographic subset collateral circulation is clearly functionally significant.     

Absence of functioning alpha-adrenergic receptors in mature canine coronary collaterals

To determine if mature coronary collateral vascular smooth muscle contains functioning alpha-adrenergic receptors, we studied 13 dogs, 6-10 months after circumflex ameroid occlusion. Regional myocardial blood flow was measured with radioactive microspheres in a blood-perfused heart preparation at constant aortic pressure (80 mm Hg). Normal zone resistance was calculated as aortic pressure divided by normal zone flow, and transcollateral resistance was calculated as aortic pressure minus circumflex pressure distal to the ameroid constrictor divided by coronary collateral flow. Flow and resistance were measured during adenosine vasodilation before and during graded doses of a constant infusion of the alpha-adrenergic agonist methoxamine (n = 6) or the alpha 2-adrenergic agonist clonidine (n = 7). In the hearts that received methoxamine, normal zone resistance increased from a control of 0.29 +/- 0.06 to 0.39 +/- 0.06 mm Hg X min/ml per 100 g (resistance units) during infusion of 10(-5)M methoxamine (p less than 0.05). In contrast transcollateral resistance averaged 0.24 +/- 0.02 resistance units under control conditions and did not change during methoxamine infusion. In the hearts that received clonidine, normal zone resistance averaged 0.24 +/- 0.03 resistance units and increased to 0.39 +/- 0.07 resistance units (p less than 0.05) with the highest dose of clonidine administered (10(-5) M). Transcollateral resistance averaged 0.17 +/- 0.03 resistance units during control conditions and did not change with clonidine infusion. In separate studies isometric tension development by the left anterior descending and coronary collateral vessels was examined in organ baths. The left anterior descending coronary artery demonstrated dose-dependent constriction to phenylephrine (peak response 22 +/- 5% of the response to 100 mM KCl). Clonidine produced weak constrictor responses in the left anterior descending coronary artery (5 +/- 2.5% maximal KCl response). In contrast, neither phenylephrine nor clonidine produced responses in mature collaterals. We also examined responses of mature collateral vessels to nonadrenergic agonists. In the vascular ring preparation the mature collaterals developed tension in the presence of KCl (2.3 +/- 0.9 g), prostaglandin F2 alpha (16 +/- 18% of the KCl responses), and vasopressin (90 +/- 30% of the KCl response). In adenosine-vasodilated hearts, pharmacologic doses of vasopressin caused a two-fold increase in transcollateral resistance. Thus, these studies performed on intact hearts and isolated vascular rings demonstrate that mature coronary collaterals do not contain functioning alpha-adrenergic receptors.(ABSTRACT TRUNCATED AT 400 WORDS)     

Survival with total occlusion of the left main coronary artery. Significance of the collateral circulation

Four patients with total occlusion of the left main coronary artery are described. Angina pectoris was severe (NYHA class 3-4) and had lasted 20 months to seven years. Three patients had experienced a myocardial infarction. All displayed large collaterals arising from a nearly normal right coronary artery and feeding both the left anterior descending and the left circumflex arteries. The left ventricular ejection fractions ranged from 20% to 65%, and all patients had varying degrees of left ventricular asynergy. Coronary artery bypass surgery resulted in a marked improvement in three patients; one patient who underwent an aneurysmectomy died two months after the operation. The data show that total occlusion of the left main coronary artery is compatible with survival if adequate collateral supply develops from the right coronary artery. In this rare angiographic subset collateral circulation is clearly functionally significant.     

Importance of myocardial ischemia for coronary collateral development in conscious dogs

The purpose of this study was to evaluate the effects of myocardial ischemia on the development of collateral circulation. Thirteen conscious dogs were instrumented for serial measurements of subendocardial segment length in the area perfused by the left circumflex coronary artery, left circumflex coronary artery flow and left ventricular pressure. In 6 dogs (group A), 1 min left circumflex coronary artery occlusions were carried out at 30 min intervals. When the 442nd 1 min left circumflex coronary artery occlusion produced a reduction in segment shortening and a significant reactive hyperemia, the occlusion time was increased to 2 min. In the remaining 7 dogs (group B), 2 min left circumflex coronary artery occlusions were conducted hourly. In group A, following 451 +/- 201 (SD) min of total occlusion time with the mixture of 1 and 2 min left circumflex coronary artery occlusions (43 +/- 18 days) a left circumflex coronary artery occlusion produced no reduction in segment shortening and negligible reactive hyperemia. By contrast, in group B, 218 +/- 99 min of total occlusion time (18 +/- 8 days) was required to develop adequate collateral circulation. The relative contribution of the first and second 1 min of left circumflex coronary artery occlusion to the collateral development was mathematically evaluated. This analysis indicated that the second 1 min of left circumflex coronary artery occlusion is 4.43-fold more effective than the first 1 min of occlusion in terms of the collateral induction. We concluded that severe myocardial ischemia plays an important role in the development of collateral circulation.     

Local dilatory reserve in chronic experimental coronary occlusion without infarction. Quantitation of collateral development

The local dilatory reserve of the canine coronary vasculature was studied with the particle distribution technique. Normal ventricles and hearts with slowly progressive narrowing of both the left circumflex coronary artery and the right coronary artery were studied. In spite of chronic occlusion of 2 coronary arteries myocardial infarction did not occur in the majority of animals because of collateral development. Coronary reserve was determined by producing graded to maximal coronary vasodilation. In normal hearts flow increased homogeneously over the entire left ventricle. In hearts with chronic coronary occlusion coronary vasodilation produced non-homogeneous increases in flow: collateral dependent myocardium received less blood flow than myocardium supplied by normal coronary arteries. Early after coronary occlusion the total coronary reserve was less than normal and the dilatory reserve of collateral dependent vessels was markedly diminished. Late (6 months) after coronary occlusion the total coronary reserve was still below normal but the dilatory reserve of collateral dependent vessels had improved. A new quantitative index of collateral function is defined as the level of coronary flow (delivered through normal coronary arteries) at which collateral flow deviates from homogeneous perfusion. Collateral function, when so defined, increases by a factor of almost 6 times between 4 weeks (early after coronary occlusion) and 6 months (late after occlusion) after the implantation of occluding devices.     

Effect of myocardial contraction on systolic coronary resistance in conscious dogs

We studied the effect of cardiac contraction on systolic coronary resistance under the conditions of maximally dilated coronary resistance vessels in six conscious dogs. Subendocardial segment length in areas supplied by the left circumflex coronary artery, left ventricular pressure and left circumflex coronary artery flow were simultaneously measured. At 5 sec after release of the first 2 min of left circumflex coronary artery occlusion, diastolic coronary blood flow revealed its peak value in association with markedly depressed regional contractile function. With collateral development induced by repeated 2 min left circumflex coronary artery occlusions, segmental dysfunction during occlusion and early reperfusion was progressively attenuated. Before and after collateral development, diastolic coronary resistance at 5 sec of reperfusion remained unchanged, but systolic coronary resistance increased by 41% secondary to restoration of regional myocardial shortening. In each animal, normalized regional shortening correlated well with changes in systolic coronary resistance. The fraction of systolic coronary resistance due to active regional myocardial contraction was 52%. These studies demonstrate that when coronary vasomotor tone is abolished, regional myocardial contraction impedes the coronary systolic flow in proportion to the extent of shortening.     

Regional redistribution of myocardial blood flow after coronary occlusion and reperfusion in the conscious dog

Early and late changes in regional myocardial blood flow distribution within the left circumflex coronary arterial bed after occlusion and after occlusion and reperfusion were compared with the extent of myocardial tissue necrosis. Radiolabeled microspheres, 15 μm, were used to study regional myocardial blood flow in conscious dogs at 5 minutes, 2 and 6 hours and 1 month after coronary occlusion. Blood flow was measured in conscious dogs whose hearts were reperfused for 72 hours after 2, 6 and 24 hours of occlusion. Blood flow was measured in four distinct transmural myocardial zones dellneated by dye injections and gross infarct features of the occluded left circumflex coronary bed. After occlusion, myocardial flow was redistributed from deep layers to outer layers, and within 6 hours after occlusion collateral flow was increased to the outer zones in excess of redlstributed flow. After reperfusion, blood flow greatly increased to regions containing predominantly normal tissue, and flow was redlstrlbuted away from the necrotic zones. The indigenous collateral circulation was a major determinant of infarct size in the occluded and reperfused myocardium. The concept of a migrating and narrowing marginal zone is discussed.     

Differential electrocardiographic effects of myocardial ischemia induced by atrial pacing in dogs with various locations of coronary stenosis

The spatial distribution of abnormal repolarization potentials caused by regional myocardial ischemia was determined in 45 dogs. Ameroid constrictors were placed around the left circumflex artery in 10, the left anterior descending artery in 10, and the right coronary artery in 10. Ten dogs without constrictors served as controls. Electrocardiographic events were determined from body surface isopotential distributions, which were computed from potentials sensed by 84 torso electrodes. In control dogs, pacing to heart rates of 230 to 250 beats/min increased the intensity of positive and negative surface extrema during the ST segment without altering their spatial features. Two weeks after placement of the ameroid constrictors, tachycardia induced abnormal negative potentials during the ST segment. Localization of these ischemic forces varied with the placement of the constrictor in a manner consistent with the affected perfusion territories. However, much of the torso surface was involved by all lesions, and only small zones of ST segment depression unique to specific lesions could be identified. In five additional dogs a constrictor was placed on the right coronary artery 3 months after implantation of a device on the circumflex vessel. ST segment patterns during pacing in dogs with two lesions were consistent with the sum of the two individual lesions. Thus, the regional nature of myocardial ischemia is detectable in the body surface isopotential distributions, but the degree of spatial overlap may limit the value of such techniques in extending the usefulness of clinical exercise-stress electrocardiography.     

Coronary collateral circulation

The occurrence and influence of coronary collateral circulation and obstruction of the supplying coronary arteries on left ventricular contractility, prevalence of myocardial infarction, and bicycle exercise ergometer test were studied in a random sample of 286 patients with angiographically documented coronary artery disease. Collaterals appeared increasingly in all three main coronary arteries with grade of obstruction. The highest prevalence of collaterals occurred in stenosis of the right coronary artery (60%), followed by the left descending artery (45%); they occurred least in the left circumflex artery (21%) (p less than 0.001). The frequency of intra-arterial collateral circulation was 42%, 11%, and 12%, respectively (p less than 0.001). With total occlusion of the left anterior descending coronary artery, 22% of the patients had normokinetic anterior and apical left ventricular wall when collaterals were present. More often, the inferior wall showed normal contraction with total occlusion of the right coronary artery and collaterals [52%, p less than 0.001 compared with left anterior descending artery (LAD)]. The prevalence of inferior myocardial infarction was 39%, with collateral circulation to the totally occluded right coronary artery. The respective prevalence of anterior infarction and total occlusion in the left coronary artery was 58% (p less than 0.02). The presence or absence of collaterals had no obvious influence on ST-segment response during bicycle ergometer test. In triple-vessel disease, peak work capacity was better when collaterals to LAD were not jeopardized (427 kpm) than when jeopardized (321 kpm) (p less than 0.02).