冠状动脉侧支循环某些相关因素的临床研究

目的研究冠状动脉侧支循环在冠状动脉完全闭塞与次全闭塞血管病变中的形成情况,观察心肌梗死病史、心肌肥厚及糖尿病对侧支循环形成的影响以及侧支循环对心肌的保护作用。方法回顾分析了我院一年内409例经冠状动脉造影证实的冠状动脉完全或次全闭塞患者,先按有无心肌梗死病史将患者分为两组,对照分析侧支循环形成的良好率,及心功能相关因素方面的差异。再按有无心肌肥厚、有无糖尿病病史分别分为两组,观察其对侧支循环形成的影响。结果冠状动脉完全与次全闭塞对比侧支循环形成的良好率有显著差异。有心肌梗死与无心肌梗死病史两组侧支循环形成的良好率比较无显著差异。两组的左心室舒张末期内径、左心室射血分数、室壁运动异常发生率及室壁瘤形成均有显著差异。而有心肌梗死病史者侧支循环良好组与不良组比较左心室舒张末期内径、左心室射血分数无差异。有无心肌肥厚对侧支循环形成良好率无差异。有糖尿病史者侧支循环血流良好率明显高于无糖尿病史者,且有显著差异。结论冠状动脉侧支循环的开放依赖于冠状动脉血管的完全或次全闭塞。冠状动脉缓慢闭塞下形成的侧支循环对心肌、心功能有保护作用。糖尿病有利于侧支循环的发展。     

Right ventricular hypertrophy is an important determinant of right ventricular infarction complicating acute inferior left ventricular infarction

To explore the role of right ventricular hypertrophy and chronic obstructive pulmonary disease in the pathogenesis of right ventricular infarction, 27 consecutive patients with a first inferior left ventricular infarction were prospectively studied. Right ventricular infarction was diagnosed using established hemodynamic criteria. Right ventricular hypertrophy was defined as right ventricular free wall thickness greater than or equal to 5 mm. Patients were classified into two groups: Group I patients with right ventricular infarction (n = 15), and Group II patients without right ventricular infarction (n = 12). The ratio of forced expiratory volume over forced vital capacity (FEV1/FVC) and forced expiratory flow between 25 and 75% expired volume (FEF) as a percent of predicted values were significantly reduced in Group I versus Group II (90 +/- 5 versus 105 +/- 6% and 63 +/- 13 versus 103 +/- 15%, respectively; p less than 0.05). This was associated with increased right ventricular wall thickness (Group I 5.5 +/- 0.3 mm versus Group II 3.9 +/- 0.2 mm, p less than 0.001). Multiple logistic regression analysis demonstrated that right ventricular wall thickness was the strongest predictor of right ventricular infarction (p less than 0.0005). No significant difference was found in the site of right coronary occlusion, collateral blood supply or extent of coronary artery disease between the two groups. These findings suggest that right ventricular hypertrophy predisposes patients with acute inferior myocardial infarction to right ventricular infarction independent of the site or extent of coronary artery disease.     

Right ventricular myocardial infarction in patients with chronic lung disease: possible role of right ventricular hypertrophy

To determine the relation between right ventricular hypertrophy and right ventricular myocardial infarction in patients with chronic lung disease, the records of 28 patients with chronic lung disease, inferior myocardial infarction and significant coronary artery disease (group I) and 20 patients with right ventricular hypertrophy, chronic lung disease without inferior myocardial infarction or significant coronary artery disease (group II) were reviewed. Chronic lung disease was diagnosed by clinical criteria, chest radiographs and pulmonary function tests. All patients had postmortem examinations. Patients in group I were classified into two subgroups: group Ia (without right ventricular hypertrophy) and group Ib (with right ventricular hypertrophy). Right ventricular wall thickness was 3.3 mm +/- 0.5 in group Ia, 6.0 mm +/- 1.1 in group Ib and 8.8 mm +/- 2.4 in group II (group Ia versus Ib, p less than 0.001; group Ia versus II, p less than 0.001; group Ib versus II, p less than 0.001). Eleven patients (78.6%) in group Ib (chronic lung disease with both right ventricular hypertrophy and inferior myocardial infarction) had right ventricular myocardial infarction compared with only 3 patients (21.9%) in group Ia (chronic lung disease without right ventricular hypertrophy and with inferior myocardial infarction) (p less than 0.008). Isolated right ventricular myocardial infarction occurred in four patients (20%) in group II (chronic lung disease with right ventricular hypertrophy, but without evidence of infarction of the left ventricle or significant coronary artery disease). There was no significant difference in the extent of anatomic coronary disease in groups Ia and Ib.(ABSTRACT TRUNCATED AT 250 WORDS)     

Right ventricular subendocardial infarction in a patient with pulmonary hypertension,right ventricular hypertrophy,and normal coronary arteries

Right ventricular infarction is usually associated with coronary artery disease and concomitant left ventricular infarction. Isolated right ventricular subendocardial necrosis was discovered at autopsy in a 52-year-old woman with pulmonary hypertension, right ventricular hypertrophy, and normal coronary arteries, who died with septicemia 41 days after mitral valve replacement. This represents the first well-documented report of isolated right ventricular subendocardial infarction associated with normal coronary arteries.     

Right ventricular infarction: role of the moderator band artery in determining infarct size

We studied 19 patients with proximal right coronary artery occlusions associated with acute myocardial infarcts less than 30 days old. Right ventricular infarct size, determined as a percentage of right ventricular surface area, ranged from 0% to 29%. Correlation of 24 variables measuring infarct size, chamber size and coronary artery disease failed to demonstrate a significant correlation with the extent of right ventricular infarction. However, estimates of the degree of obstruction to potential collateral flow into the right coronary arterial system from the left anterior descending coronary artery, especially through the moderator band artery, showed a significant positive correlation with infarct size (p less than 0.02). Among the five patients with massive (greater than 25%) right ventricular infarction, four had significant (greater than 75%) obstruction of the left anterior descending system, resulting in potentially impaired collateral blood flow; the other patient had normal coronary arteries and embolic occlusion of the proximal right coronary artery with contraction band necrosis. The study suggests that collateral flow to the right ventricular myocardium, especially through the moderator band artery, protects against massive infarction in the presence of proximal right coronary artery occlusion.     

Changes in right ventricular relaxation during acute anterior myocardial infarction in pigs

To determine the effect of an anteroseptal myocardial infarction on right ventricular systolic and diastolic function, we studied 12 pigs before and 1 h after left anterior descending coronary artery occlusion. Total arterial occlusion was achieved by the percutaneous, transcatheter placement of a 1 mm Teflon plug into the mid portion of the artery. The resulting infarction involved 28 (SEM 3)% of the left ventricular wall, in the anterior and septal regions. A small rim of the right ventricular free wall adjacent to the septum and the right ventricular apex were also affected. End diastolic pressures in both ventricles rose significantly: left ventricular from 12(1) to 20(2) mm Hg and right ventricular from 8(1) to 10(1) mm Hg. Right ventricular peak systolic pressure increased from 29(2) to 35(2) mm Hg while left ventricular peak systolic pressure did not change. One hour after infarction the half time of isovolumic relaxation of the right ventricle was prolonged from 6.9(0.5) to 8.7(0.4) ms. Ejection fraction in both ventricles was depressed: from 46(1) to 34(2)% in the right ventricle and from 69(3) to 49(3) in the left ventricle. There was no change in either right or left ventricular dP/dt. These data suggest that right ventricular systolic and diastolic dysfunction occurs as the result of an anteroseptal myocardial infarction in pigs.     

Right ventricular infarction: frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit

During a 14 month period autopsies were performed on 107 patients with coronary heart disease and the results were evaluated prospectively with special reference to right ventricular infarction. A total of 214 regional infarcts were found, 107 (50%) of which involved the right ventricle. Right ventricular infarction was found in 90 hearts (84%), but only three isolated right ventricular infarcts were seen. Right ventricular involvement was found with equal frequency in anterior and posterior infarction (64 versus 66%), but posterior right ventricular infarcts were much larger (15% of the right ventricle was infarcted versus 1%). Proximal right coronary artery occlusion caused larger right ventricular infarction than did distal occlusion (15 versus 5 g). Right ventricular infarct size was not influenced by coronary artery disease (evaluated angiographically) in noninfarct-related vessels. Anterior right ventricular infarcts were predominantly located near the apex of the heart (to the left of the sternum), whereas posterior right ventricular infarcts were located near the atrioventricular groove (along the right sternal border). Infarct size was equal in patients who died from a first acute anterior or posterior infarct. However, posterior infarcts had more right ventricular involvement (28% of total infarct size versus 7% in anterior infarcts) leaving more of the left ventricular myocardium intact (79 versus 64%). These differences in infarct topography may explain why right ventricular involvement seldom is diagnosed clinically in patients with anterior infarction, and why left ventricular function and prognosis usually are better after posterior compared with anterior infarcts of enzymatically equal size.     

The necessary conditions of chronic total occlusion of all three coronary vessels--the relationship between portions of coronary occlusion and collateral vessels

This study was performed to define the conditions present in chronic total occlusion of all three coronary vessels. Each left descending coronary artery (LAD), left circumflex branch (LCX) and right coronary artery (RCA) was totally occluded angiographically in 5 patients (mean age 64, male 3, female 2). Four of them had history of myocardial infarction. Anginal type was effort angina in all patients, and two cases showed unstable angina. Good collateral supply was found in the distal portions of occluded vessels from proximally located branches, such as Conus branch, Right ventricular branch, Septal branch and Left atrial circumflex branch. Almost all of the occlusions were located at mid portions (13/15: mid, 2/15: proximal). Ejection fractions (EF%) of the 5 patients were 70%, 69%, 60%, 28% and 22% respectively. EF was correlated with the degree of collateral supply and one of them (22%) ended in sudden death. These findings suggest that the mid portion occlusion, good collateral supply and a long history of angina pectoris are important factors involved in chronic total occlusion of the three coronary vessels.     

In situ localization of transforming growth factor beta 1 in porcine heart: enhanced expression after chronic coronary artery constriction

We investigated the expression of transforming growth factor beta 1 (TGF-beta 1), a polypeptide differentiation factor probably associated with angiogenic properties in chronically hypoperfused heart tissue. A slowly swelling ameroid constrictor was implanted around the coronary circumflex artery (CX) of young domestic pigs. Two to three weeks after, significant CX stenosis of more than 90% and coronary collateralization could be demonstrated angiographically. The CX dependent experimental myocardial tissue (E) was investigated, with the LAD dependent area of the same pig serving as a control (C). We found significantly enhanced TGF-beta 1 mRNA expression by northern blot hybridization in the experimental myocardium (E) of those pigs with demonstrable coronary collaterals in the absence of a major myocardial infarction. The presence of TGF-beta 1 protein could be demonstrated quantitatively in extracts of the experimental and the control area by immunoblot analysis. By in situ techniques, TGF-beta 1 mRNA and protein could be localized predominantly in cardiac myocytes. We conclude that one adaptive mechanism of the pig heart in chronic coronary artery constriction is the enhanced expression of TGF-beta 1. Cardiac myocytes are a major source of TGF-beta 1. The observed coronary collateralization could be mediated-at least in part-by the angiogenic properties of TGF-beta 1.     

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.     

Coronary collateral circulation in coronary artery disease and systemic hypertension

The extent and functional capacity of coronary collateral circulation in patients with systemic hypertension has not been elucidated. In the present study, 313 patients with coronary artery disease were studied to evaluate coronary collateral circulation in relation to the presence of systemic hypertension and left ventricular hypertrophy. Patients had greater than or equal to 95% diameter luminal obstruction of either the left anterior descending or the right coronary artery. Patients were classified into 2 groups: The hypertensive group consisted of 61 patients, mean age 55 +/- 9 years, with systemic hypertension, and the normotensive group consisted of 252 patients, mean age 53 +/- 8 years, without hypertension. The hypertensive group had more severe angina pectoris and less history of healed myocardial infarction than the normotensive group (p less than 0.001). Left ventricular wall thickness was 1.26 +/- 0.1 cm in the hypertensive and 1.03 +/- 0.06 cm in the normotensive group (p less than 0.001). The hypertensive group had more extensive coronary collateral circulation than the normotensive group (p less than 0.01). There was a positive relation between coronary collateral circulation and left ventricular wall thickness (p less than 0.001). These results indicate that patients with systemic hypertension and coronary artery disease have an increase in coronary collateral circulation corresponding to the degree of left ventricular wall thickness.     

ST elevation in the anterior precordial leads during right ventricular infarction: lessons learned during primary coronary angioplasty--a case report.

ST elevation in the anterior leads may be due to isolated right ventricular infarction associated with occlusion of a nondominant or codominant right coronary artery. The authors report a case of isolated right ventricular infarction from a dominant right coronary artery's proximal occlusion in the presence of collateral circulation provided by the left coronary artery. Extensive damage occurred owing to compromise of the collateral circulation during primary coronary angioplasty. This is an unusual angiographic pattern for isolated right ventricular infarction. The potential consequences of percutaneous interventions to collateral vessels is discussed.     

Influence of acute arterial hypertension on myocardial infarct size in dogs without left ventricular hypertrophy

During acute myocardial infarction an increase in arterial pressure is common in patients who were previously normotensive and, therefore, do not have left ventricular hypertrophy. However, the effect of hypertension on infarct size in the absence of hypertrophy is uncertain. Thus, 32 open chest dogs underwent a 2 hour occlusion of the mid-left anterior descending coronary artery followed by 3 hours of reperfusion. Immediately after occlusion, 14 dogs were randomized to a hypertension group (intravenous phenylephrine infusion starting 5 minutes after occlusion and terminating at the time of reperfusion, with heart rate kept constant by atrial pacing) and 18 dogs to a control group (equivalent volumes of saline solution intravenously). Twelve of the 32 dogs were excluded from analysis because they developed ventricular fibrillation during coronary occlusion or reperfusion. In the hypertension group (n = 10), the mean arterial pressure increased significantly within 10 minutes of coronary occlusion (146 +/- 7 versus 109 +/- 11 mm Hg in 10 control dogs, p less than 0.01) and was maintained approximately 40 mm Hg higher than in the control group (p less than 0.01) throughout the ischemic period. Heart rate was similar in the two groups throughout the experiment. After the dogs were sacrificed, the region normally supplied by the occluded artery (anatomic "region at risk") was identified by simultaneous perfusion of the aortic root and the coronary artery distal to the occlusion. The heart was sectioned transversely and stained with triphenyltetrazolium-chloride. The infarcted area and the anatomic risk area were determined by video planimetry.(ABSTRACT TRUNCATED AT 250 WORDS)     

Coronary collaterals in the canine heart: development and functional significance

The development and functional significance of coronary collaterals was studied using the tracer microspheres technique in 18 mongrel dogs with complete chronic occlusion of the left circumflex coronary artery.In a first group of eight dogs resistance of the preexisting collaterals was determined during short acute occlusion of the left circumflex coronary artery (LC). The mean value was 8.49 resistance units (R.U.). Six weeks after the implantation of an Ameroid constrictor on the LC, collateral resistance decreased significantly (p < 0.05) to 0.51 R.U. Only two dogs of this group developed a transmural infarction and one a subendocardial infarction after chronic LC occlusion. Aortocoronary bypass grafting restored regional coronary reserve completely in dogs without infarction and partially in dogs with infarction.In the second group of 10 animals no myocardial infarction was found six weeks after Ameroid constrictor implantation. In this group a stress test was performed by infusion of norepinephrine intravenously.In the areas perfused by normal coronary arteries, there was a significant relation between myocardial blood flow (MBF) and pressure-rate product (PRP). The collateralized subendocardium, however, failed to raise its blood flow with increasing PRP. After bypass to the occluded LC, the normal MPF-PRP relation was restored.These observations indicate that a significant collateral circulation develops after chronic coronary obstruction and protects the myocardium against infarction in most cases. The functional capacity of these collaterals, however, is limited and becomes inadequate under stress conditions.     

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).     

Vulnerability of myocardial collateral perfusion: the impact of episodic hypertension

In patients with coronary artery disease, the presence of left ventricular hypertrophy secondary to hypertension is associated with an increased collateral development. A patient is described who was admitted for myocardial ischemia and severe hypertension. One day after admission, coronary angiography revealed a proximal chronic occlusion of the left anterior descending artery with an extensive collateral vascularization originating from the right and circumflex coronary arteries. In addition, left ventriculography showed antero-apical akinesia that was resolved 5 days later, indicating myocardial stunning. This case illustrates the vulnerability of collateral coronary blood flow to an episode of hypertension, giving rise to myocardial ischemia and even myocardial stunning. This finding advocates aggressive antihypertensive therapy in patients with coronary artery disease and regional myocardial perfusion, which exclusively depends on collateral blood flow.     

Altered minimal coronary resistance to antegrade reflow after chronic coronary artery occlusion in swine

We examined coronary pressure-flow relations after chronic coronary artery occlusion induced by placement of an ameroid occluder on the left circumflex coronary artery in swine. An acute open-chest procedure was performed in nine pigs 27 +/- 2 days (mean +/- SEM) after surgical placement of the ameroid occluder, and in eight nonoperated control pigs. Coronary vascular resistances were measured during maximal coronary vasodilation with adenosine. Minimal coronary resistance was assessed before and after cannulation and extracorporeal perfusion of the left circumflex coronary artery distal to the site of the ameroid occluder in pigs from the ameroid group and in a similar site in control pigs. Minimal coronary resistance to antegrade reflow in the left circumflex region was decreased significantly in ameroid pigs compared with control pigs (0.06 +/- 0.01 vs. 0.26 +/- 0.03 mm Hg.min.100 g/ml, p less than 0.001, respectively). Decreased minimal coronary vascular resistance was present transmurally in the left circumflex region of ameroid pigs. Altered vascular resistance occurred only in myocardium distal to the ameroid occluder since the nonoccluded left anterior descending region in ameroid pigs had minimal coronary resistance similar to that of the same region from control pigs (0.23 +/- 0.03 vs. 0.19 +/- 0.02 mm Hg.min.100 g/ml). Thus altered minimal coronary vascular resistance occurs and probably reflects vascular proliferation and/or vascular alterations which result in an increased total cross-sectional area of the vasculature in the myocardium distal to the occlusion.     

Acute right ventricular infarction secondary to massive pulmonary embolism

Isolated right ventricular infarction has been found in casesof right ventricular hypertrophy, but there are no reports onright ventricular infarction secondary to massive pulmonaryembolism. Six autopsied patients with massive pulmonary embolismand pure right ventricular infarction, suspected to be secondaryto the embolism, were selected from a population of 216 autopsies.Pulmonary embolism was the suspected diagnosis in five casesdue to typical clinical, electrocardiographic and haemodynamicdata. Right ventricular infarction was a post-mortem finding,not previously diagnosed. In every case the thickness of theright ventricular myocardium was normal. The necrosis of theright ventricle was transmural in four cases and subendcardialin two and the entire right ventricular wall (anterolateralas well as posterior) was involved. No mural thrombi were presentand in no case did the necrosis involve the left ventricle.In one case the coronary arteries were normal, in the otherfive significant lesions of the right or the left coronary arterieswere observed. These lesions may have been, in part, responsiblefor the necrosis of the right ventricle when the massive pulmonaryembolism was added. We conclude that right ventricular infarctionmay be secondary to pulmonary hypertension in the setting ofmassive pulmonary embolism, even in the absence of right ventricularhypertrophy and with normal or stenotic coronary arteries.     

The impact of right atrial ischemia on inferior myocardial infarction with extension to right ventricle: transesophageal echocardiographic examination

BACKGROUND: The role of the right atrium in adaptation to the hemodynamic changes produced by extension of myocardial infarction (MI) of the left ventricular inferior wall to the right ventricle is fundamental. HYPOTHESIS: The aim of this study was analyze a group of patients with MI with extension of right chambers, and particularly right atrial alterations, by transesophageal echocardiography and to correlate it with clinical and angiographic variables. METHODS: Thirty patients with right ventricular (RV) MI involving obstruction of the right coronary artery without stenosis of the left coronary artery were included; 18 underwent early reperfusion. Transesophageal echocardiography was performed on all within 5 days of coronary angiography. Follow-up was continued from hospitalization to the present. RESULTS: When patients with right atrial ischemia were compared with those with normal right atrium, the RV wall movement score was significantly greater in the group with right atrial ischemia, severe RV dilatation was more frequent, and association with proximal occlusion of the artery responsible for the MI, as well as absence of right atrial branches and poor collateral circulation, were significant. Hospitalization was more prolonged in this group, and there was a higher incidence of arrhythmias, complete atrioventricular block, and mortality. CONCLUSIONS: Right atrial ischemia associated with RV infarction leads to a higher incidence of complications and higher mortality. Transesophageal echocardiography is a safe, reproducible technique that provides detailed anatomic information about right chambers and aids in the determination of prognosis and therapeutic decisions.     

Coronary collateralization: determinants of adequate distal vessel filling after arterial occlusion

BACKGROUND: The protective effect of collateral vessels in coronary artery disease (CAD) is well established. Little is known, however, about factors that influence collateral formation. METHODS: We studied the coronary angiograms of 200 consecutive patients with single-vessel coronary artery occlusion. Patients were excluded if obstructive stenoses were present in other vessels or if prior revascularization had been undertaken. Collateral circulation to the occluded artery was graded as 'poor' (no or incomplete filling) or 'rich' (complete filling). Patient characteristics, including mode of presentation, medications and CAD risk factors, were assessed. RESULTS: Positive univariate correlates of rich collaterals included increasing age [odds ratio (OR) 1.03, P = 0.016], 'statin' use (OR 2.50, P = 0.005), nitrate use (OR 1.96, P = 0.034), calcium-channel blocker (CCB) use (OR 4.07, P < 0.001), presentation with stable angina (OR 2.34, P = 0.006), longer time since diagnosis of CAD (OR 1.12, P = 0.002) and history of hyperlipidemia (OR 3.55, P < 0.001). Significantly poorer collateralization was observed in the setting of acute myocardial infarction (MI) (OR 0.23, P < 0.001), diabetes mellitus (OR 0.33, P = 0.003), impaired left ventricular function (OR 0.64, P = 0.015) and occlusion of the left anterior descending coronary artery (LAD) (OR 0.28, P < 0.001). On multivariate analysis, rich collateralization was associated with hyperlipidemia (P = 0.003) and CCB use (P = 0.028). Independent predictors of poor collaterals were presence of diabetes (P < 0.001), LAD occlusion (P = 0.001) and presentation with acute MI (P = 0.017). CONCLUSION: Diabetes mellitus, occlusion of the LAD and presentation with acute MI are independently associated with poor distal vessel collateralization, whereas hyperlipidemia and use of CCBs are associated with rich collateralization. Factors determining coronary collateral formation may in turn influence outcomes after coronary artery occlusion.