Coronary artery disease in young patients: arteriographic and clinical review of 40 cases aged 35 and under

Coronary arteriography was performed in 60 patients aged 35 or less with suggested coronary artery disease (CAD). Twenty patients (Group 1) had normal coronary arteries and 40 patients (Group 2) had one or more obstructive lesions. The left anterior descending artery was commonly involved followed by the right coronary and left circumflex arteries. The right coronary artery was most commonly completely obstructed. Single-vessel disease (50 per cent or greater obstruction) was found in 60 per cent of the patients, an incidence that is considerably higher than in studies of older patients. A total of 1.6 diseased vessels per patient was present. A hyperlipoproteinemia (HLP) was found in 68 per cent of Group 2 patients. Patients in Group 2 with an HLP had significantly more CAD than Group 2 patients with normal lipoproteins. The incidence of the following clinical features were not significantly different in Groups 1 and 2: typical angina, atypical angina, positive family history, smoking, hypertension, obesity, abnormal electrocardiogram, positive treadmill test, HLP, and diabetes mellitus. A fourth heart sound and a history of a myocardial infarction were significantly common in Group 2. Since almost all of the previously reported cases of myocardial infarction with normal coronary arteries have occurred in young patients, history of a myocardial infarction does not assure the presence of obstructive coronary artery lesions. It is suggested that coronary arteriography is a justifiable procedure in a young patient who presents with a clinical picture that is either compatible with or cannot be clearly distinguished from CAD.     

The clinical course, early prognosis and coronary anatomy of subendocardial infarction.

The following prospective study was undertaken to observe the clinical course, early prognosis and coronary anatomy of patients with subendocardial infarction. Subendocardial infarction was defined as typical chest apin (greater than 15 minutes), serum enzyme elevation and persistent (greater than 48 hours) new T wave inversion and/or S-T segment depression in the absence of new pathologic Q waves. Fifty consecutive patients were defined, followed in a prospective manner and subjected to early coronary arteriography. A prior history of unstable angina was found in 33 patients (66 per cent); 22 patients (44 per cent) had significant dysrhythmias during the acute hospital phase, and seven patients (14 per cent) had evidence of mild left ventricular failure. Coronary arteriography demonstrated significant lesions (greater than 75 per cent narrowing in at least one vessel) in all 50 patients, with 30 patients (60 per cent) having either double- or triple-vessel disease. Follow-up (mean 10.6 months) revealed that 15 patients (30 per cent) had stable angina, 23 patients (46 per cent) unstable angina and only 12 patients (24 per cent) remained free of angina. Of 28 patients in a medically treated group, acute transmural infarctions developed in six (21 per cent) and one died (3 per cent). We conclude that subendocardial infarction is symptomatically an unstable entity, is associated with severe coronary artery disease and, in a medically treated group, is followed by a significant incidence of early transmural myocardial infarction (21 per cent). Therefore, these patients require in-hospital monitoring, careful follow-up and consideration for early coronary arteriography.     

The predictive value of anginal chest pain as an indicator of coronary disease during exercise testing

To determine the significance of anginal chest pain during exercise testing, a series of 302 patients undergoing coronary arteriography with exercise testing was reviewed. Of the 302 patients, 85 had ischemic ECG changes and chest pain (Group I); 87 patients had ischemic ECG changes but no chest pain (Group II); 25 patients had chest pain but no ischemic ECG changes (Group III); 105 patients had neither chest pain nor ischemic ECG changes (Group IV). Coronary artery disease was present in 95 per cent of Group I, 75 per cent of Group II, 72 per cent of Group III, and 28 per cent of Group IV. Of those patients with coronary disease, multiple vessels were involved in 94 per cent of Group I, 51 per cent of Group II, 67 per cent of Group III, and 21 per cent of Group IV. The predictive value for presence and extent of coronary disease showed Group I > Groups II and III > Group IV (p < 0.025). We conclude that (1) anginal chest pain during exercise testing predicts the presence and extent of coronary disease more accurately than its absence; (2) the presence of chest pain even without an ischemic ECG response during exercise testing appears to be as predictive of coronary disease as an ischemic ECG response alone; and (3) the combination of anginal chest pain during exercise testing and an ischemic ECG response is highly predictive of multivessel coronary artery disease.     

Mechanism of relief of angina after coronary bypass surgery: an angiographic study.

Coronary angiography was performed before and after coronary revascularization in 67 patients. The interval between studies ranged from 1 to 38 months (average 9.9). The patients were separated into four clinical groups on the basis of their symptoms at the time of restudy; Group I, 13 asymptomatic patients; Group II, 19 patients with nonanginal chest pain (18 cases) or dyspnea (1 case); Group III, 12 patients whose angina was relieved but not eliminated; and Group IV, 23 patients whose angina was not alleviated. The graft patency rate was 72 percent in Group I, 78 percent in Group II, 61 percent in Group IIII and 34 percent in Group IV. The sum of diseased, but not bypassed and unsuccessfully bypassed arteries per patient was 1.6 in Groups I and II. 2.9 in Group III and 4.0 in Group IV. The incidence of perioperative myocardial infarction, defined using enzymatic and electrocardiographic criteria, was 8 percent for Group I, 26 percent for Group II, 25 percent for Group III and 52 percent for Group IV. Anginal relief after coronary bypass surgery is achieved by successful and complete revascularization rather than by perioperative myocardial infarction.     

Significance and treatment of nocturnal angina preceding myocardial infarction.

The presence of nocturnal angina and congestive heart failure within the month prior to admission was evaluated in the 174 patients with acute myocardial infarction. Heart size was evaluated radiographically at the time of admission. Twenty-three patients (13 per cent) experienced nocturnal angina. The incidence of nocturnal angina was significantly higher in those with anterior myocardial infarction (p less than 0.005) and subendocardial infarction (p less than 0.02) when compared with patients with inferior MI. Congestive heart failure was more common prior to admission in those with nocturnal angina (9/23) as opposed to those without (3/141) (p less than 0.001). Cardiomegaly was seen in 9/23 patients with nocturnal angina and 22/141 without (p less than 0.02). We conclude that the presence of nocturnal angina in those who develop MI increases the likelihood that the infarction will be either anterior or subendocardial rather than inferior. The association of nocturnal angina and congestive heart failure to anterior myocardial infarction is probably due to more severe and probably significant left coronary artery disease.     

Coronary collateral vessels during the early period of acute myocardial infarction: their development]

The aim of this study was to investigate the incidence and development of coronary collateral circulations in patients with acute myocardial infarction (AMI). We categorized 165 patients with persistent 100% occlusion of the infarct-related artery into 6 groups according to the time from the onset of AMI to angiography. Group I consisted of 55 patients evaluated within 6 hours after the onset of AMI; Group II, 28 patients, between 6 and 12 hours after the onset; Group III, 12 patients, between 12 and 24 hours after the onset; Group IV, 11 patients, between 2 and 13 days after infarction; Group V, 46 patients, between 14 and 44 days after infarction; and Group VI, 13 patients, more than 45 days after infarction. Collateral vessels were applied a numerical score between 0 and 3 according to the degree of opacification of the native vessel distal to the occlusion. In 58%, 79%, 67%, 73%, 89%, and 92%, patients of Groups I to VI had evidence of collateral vessels, respectively. Well-developed collaterals were observed in 24% of Group I compared with 50%, 58%, 55%, 73% and 69% of patients in Groups II to VI, respectively. The mean coronary collateral scores were 0.9 +/- 0.1, 1.4 +/- 0.2, 1.4 +/- 0.3, 1.6 +/- 0.4, 2.0 +/- 0.2 and 2.2 +/- 0.3 for Groups I to VI, respectively. Patients with preinfarction angina had more well-developed collateral circulations than did patients without it, however, there was no significant correlation between the duration of previous angina and extent of coronary collaterals.     

Left ventricular hemodynamics and contractile pattern after aortocoronary bypass surgery. Factors affecting reversibility of abnormal left ventricular function

Left ventricular hemodynamics and contractile patterns were evaluated in 104 patients before and after aortocoronary bypass surgery. Patients were selected on the basis of referral for surgery because of angina pectoris and the demonstration, postoperatively, of all grafts being patent. Group I consisted of 47 patients with single grafts (LAD 33 and RCA 14). Mean left ventricular end-diastolic pressure, volume, and ejection fraction revealed no change after surgery. Twenty-four patients had asynergy prior to surgery; of these 24, 16 patients had a normal contractile pattern after surgery. Group II consisted of 47 patients with double vein grafts. Postoperatively, there was a significant decrease in left ventricular end-diastolic pressure (p < 0.005) and increase in ejection fraction (p < 0.001). Asynergy in 29 patients preoperatively revealed synergy after surgery in 15 patients. Group III consisted of ten patients with triple vein grafts. Ejection fraction increased postoperatively (p < 0.01). All but two of the eight patients with asynergy preoperatively showed synergy after surgery. In the entire group of patients, 43 with synergy preoperatively, with but one exception, had synergy after surgery. Asynergesis in 41 instances preoperatively revealed postoperatively that 38 patients (93 per cent) had normal wall movement. In 29 instances of preoperative akinesia of one wall, only 8 patients (28 per cent) showed a return to normal wall movement. Unstable angina pectoris alone did not influence reversibility of abnormal contractile patterns. Unstable angina pectoris with absence of abnormal Q-waves in the ECG was noted in 23 patients with asynergy; all but one of these patients had a normal contractile pattern after surgery. Patients with infarction pattern on the ECG, when accompanied by asynergy, were unlikely to have a normal contractile pattern after surgery (4 out of 23 patients). Reversibility of left ventricular function after surgery is common, not related to number of grafts, but is related to type of wall abnormality noted prior to surgery as well as the ECG and clinical state of the patient.     

Hemorrhagic myocardial infarction associated with aortocoronary bypass revascularization.

Experimentally, hemorrhage and extension of myocardial infarction occur commonly when there is reperfusion after coronary artery occlusion. To investigate this hazard in a clinical setting, we compared the histopathologic picture of myocardial infarction in 44 patients who had undergone aortocoronary bypass: 14 (Group I) had myocardial infarction that predated aortocoronary bypass by 1 to 7 days; 13 (Group II) had infarction 1 to 14 days after the surgery; and 17 (Group III) had infarction 15 to 90 days postoperatively. All 44 patients had two or more coronary arteries with luminal narrowing of more than 75 per cent and patent vein grafts to arteries supplying areas of infarction. Hemorrhagic infarcts were present in 57 per cent of patients (eight of 14) in group I and 38 per cent of patients (five of 13) in Group II, contrasting with 6 per cent of patients (one of 17) in Group III (P < 0.005 and P < 0.05, respectively). In hemorrhagic infarcts, the extravasated blood formed irregular intramural dissecting tracts beyond the area of infarction, and foci of myocardial necrosis were present in the border zones. Infarcts affected more than 50 per cent of the left ventricular muscle in 64 per cent of cases of hemorrhagic infarction and in 13 per cent of cases of nonhemorrhagic infarction (P < 0.05). The prevalence of hemorrhagic infarction after revascularization may account for the high mortality of evolving and perioperative myocardial infarction associated with aortocoronary bypass, and this finding militates against wholesale immediate revascularization in patients who have uncomplicated myocardial infarction.     

Perioperative myocardial infarct following aortocoronary bypass. Clinical aspects, causes, consequences

Perioperative infarction is a significant factor of morbidity of coronary bypass surgery. The aim of this study was to review peri-operative infarction and its complications over a 10 year period (1974 to 1984) and to determine its consequences on left ventricular function and life expectancy. The material included 514 patients who underwent coronary bypass surgery. Perioperative infarction was defined as the association of a postoperative Q wave and increase in creatinine phosphokinase after the 24th postoperative hour: this diagnosis was made in 31 cases (Group A), 6 per cent of the series; 483 patients (Group B) had no signs of infarction. The necrosis involved the revascularised zone in 26 cases and other zones in 5 cases. The acute phase of infarction was associated with major complications in 9 patients of Group A. In 22 patients (70 per cent of cases) the initial evolution was uncomplicated. There was no significant difference in the number of patients with unstable angina between Groups A and B (52 per cent vs 67 per cent), with single vessel disease (25 per cent vs 28 per cent), double vessel disease (45 per cent vs 34 per cent) or with triple vessel disease (30 per cent vs 38 per cent). The average number of bypasses was higher in Group A (2.06 per cent vs 1.4 per cent, p less than 0.05), as was the duration of cardiopulmonary bypass (117 min vs 91 min, p less than 0.05) and of aortic clamping (45 min vs 31 min, p. less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

The occurrence of angiographically detected intracoronary thrombus in patients with unstable angina pectoris

To examine the role of intracoronary thrombus (ICT) in unstable angina, we reviewed the coronary arteriograms of 83 patients with unstable angina (group I) and 37 patients with stable angina (group II) for angiographic evidence of ICT. Group I and group II patients were similar with respect to mean age, presence of single and multiple vessel disease, and past history of myocardial infarction. Group I patients had no ECG or creatine kinase enzyme evidence of acute myocardial infarction. The angiographic criteria for ICT included an intracoronary filling defect, intraluminal staining, and total coronary artery occlusion with convex dye outline. ICT was found in 10 of 83 patients in group I (12.0%) vs 0 of 37 patients in group II (p less than 0.05). These findings suggest that in some patients coronary artery thrombosis plays an important role in the pathogenesis of unstable angina.     

Clinical and hemodynamic evaluation of coronary collateral vessels in coronary artery disease

To appraise the functional significance of coronary collateral vessels, 78 consecutive patients with angina pectoris and at least 75 per cent obstruction in a major coronary vessel were studied clinically, hemodynamically, and angiographically and by stress testing. Forty-eight of them (62 per cent) had coronary collateral vessels. When patients with collaterals were compared with those without, the severity of angina pectoris and the number of positive treadmill ECG's were not statistically different. The patients with collaterals had a greater incidence of past myocardial infarction, $\text{33}\text{48}$ (68 per cent) vs. $\text{8}\text{30}$ (27 per cent) (P = 0.001); more extensive obstructive disease angiographically, 8.0 ± 0.4 vs. 6.3 ± 0.5 (P = 0.05); more abnormal pacing ventricular function curves, $\text{22}\text{23}$ (96 per cent) vs. $\text{9}\text{15}$ (60 per cent) (P = 0.01); and a greater incidence of left ventricular contraction abnormalities, $\text{43}\text{48}$ (90 per cent) vs. $\text{16}\text{30}$ (53 per cent) (P = 0.025).Patients who have coronary artery disease and collateral vessels cannot be distinguished from their counterparts without collaterals on a clinical basis except for a greater incidence of myocardial infarction in the former. Present evidence implies that collateral vessels may protect the patient by delaying the onset of angina pectoris, but when angina occurs these patients have more extensive coronary artery disease and greater myocardial dysfunction. In addition, collaterals, although not preventing, may limit the extent of myocardial infarction and reduce immediate mortality. The prognosis from the onset of angina pectoris may be worse in those patients with collateral vessels, however, because of their more extensive disease.     

Clinical predictors of angina following myocardial infarction.

To determine if angina following myocardial infarction could be predicted before hospital discharge we prospectively evaluated 219 consecutive patients admitted to the coronary care unit with acute myocardial infarction. Of the 166 who survived to one year, angina was present before infarction in 53 per cent and after infarction in 61 per cent. Angina did not recur postinfarction in 26 per cent of the patients who had angina before infarction. However, in 47 per cent of those without previous angina it developed postinfarction. Although postinfarction angina correlated with the presence of angina before infarction (p < 0.0005), it did not correlate significantly with age, sex, site of infarction, Killip class on admission nor the presence of a previous infarction.To improve our ability to predict angina after infarction we performed exercise tests to 5 metabolic equivalents (METS), or 70 per cent of age-predicted maximal heart rate, before hospital discharge on all patients less than 70 years old who were without chest pain within four days or without overt heart failure. Of the 105 patients exercised, 31 (86 per cent) of the 36 with positive tests had angina during the subsequent year compared to only 25 (36 per cent) of the 69 with negative tests (p < 0.001). Postinfarction angina occurred in 96 per cent (23 of 24) of the patients who had both angina before infarction and a positive test, but in only 26 per cent (10 of 39) of the patients with neither finding (p < 0.001).We conclude that the presence of angina prior to infarction and a positive limited exercise test performed before hospital discharge are predictive of angina following infarction. Myocardial infarction abolishes angina in a quarter of the patients, but angina develops postinfarction in nearly half of the patients who did not have angina previously.     

Diagnostic value of Q-waves in inferior myocardial infarction

Forty-eight patients with proved, healed, inferior myocardial infarction were studied to determine the electrocardiographic characteristics of this syndrome, the correlation between electrocardiographic abnormalities and angiographic findings, and to determine the value of recording Lead III during inspiration to identify abnormal Q-waves.The diagnosis of inferior myocardial infarction (IMI) was established by the presence of two of the following three criteria: (1) past history of acute infarction, associated with typical acute electrocardiographic changes and compatible clinical data, (2) total occlusion or more than 80 per cent occlusion of the right coronary artery, and (3) contraction abnormalities of the inferior left ventricular wall.Fifteen per cent of patients with inferior myocardial infarction had diagnostic Q-waves in all the three limb Leads II, III, and aV_F, and 29 per cent of patients had no diagnostic Q-waves in any of the three limb leads. Relative frequency of diagnostic Q-waves in inferior myocardial infarction were found to be 70, 43, and 15 per cent in Leads III, aV_F, and II, respectively.One hundred per cent correlation was noted between left ventricular inferior wall asynergy and presence of diagnostic Q-waves in all the limb Leads II, III, and aV_F, but the correlation was low (54 per cent) when none of the limb Leads II, III, and aV_F revealed diagnostic Q-waves.Obtaining Lead III in deep inspiration to differentiate an abnormal Q-wave due to inferior myocardial infarction from a benign Q-wave was not found to be a reliable measure and could result in false-negative diagnosis of inferior myocardial infarction in a significant number of patients.     

Clinical characteristics of unstable angina before acute myocardial infarction

Four hundred and seventy-six patients with acute myocardial infarction (AMI) were interviewed to evaluate the clinical features of angina before AMI. Two hundred and sixty-six of the 476 patients had angina before AMI, of which 137 had new onset of angina within 2 months before AMI, and 129 had chronic angina of more than 2 months before AMI. Forty of the 129 chronic angina patients noted worsening of symptoms within 2 months before AMI. Of the 177 patients with new onset angina or worsening angina such as unstable angina, the incidence of new onset angina was higher than that of worsening angina. Twenty-eight (70%) of the 40 patients with worsening of symptoms had started with effort angina, 16 of whom turned to resting angina from effort angina at the onset of unstable angina in spite of the fact that 12 had worsening of effort angina. Of the 137 patients with new onset angina, 65 (40%) started with resting angina and 72 (53%) with exertional angina. In the former group, 43 (66%) developed AMI within 1 week after the onset of angina, which was greater than 19 (26%) in the latter group. These results may suggest that the appearance of the resting angina would herald AMI in both groups of unstable angina. The onset of resting angina in the group of new onset angina could be the warning of AMI development within a shorter interval than those of exertional angina.     

Propranolol withdrawal in angina pectoris: a prospective study.

In a prospective study, 100 consecutive patients (mean age 51.3 years) with angina pectoris had propranolol abruptly discontinued 24 to 144 hours (mean 39.0 hours) prior to elective coronary arteriography. The mean duration of therapy was 8.2 months and the mean daily propranolol dose was 216.1 mg. New York Heart Association Class II, III and IV symptoms were present in 30, 41, and 29 patients and one, two, or three coronary arteries were more than 50 per cent narrowed in 37, 29, and 34 cases, respectively. Three patients experienced minor increases in chest pain and two suffered non-transmural myocardial infarctions prior to the time of scheduled cessation of therapy. The same number of minor and major complications occurred in the post-withdrawal period. All four patients who developed non-transmural myocardial infarction in this study had pre-existing Class IV symptoms. The course of the remaining 90 patients was uneventful. These findings do not support the concept of a rebound propranolol withdrawal reaction.     

Different clinical and prognostic aspects of angina pectoris in unstable phase

The purpose of this study was to focus on the clinical and angiographic characteristics of 113 patients with crescendo angina (Group I) as compared to 187 patients with angina of new onset (Group II), selected from a series of 474 consecutive subjects, admitted to our clinic between January 1976 and July 1983 because of recurrent episodes of spontaneous angina, who underwent cardiac catheterization and coronary angiography within one month of hospitalization. Group I patients showed a greater incidence of prior transmural myocardial infarction (p less than 0.01), arterial hypertension (p less than 0.01), multivessel disease (p less than 0.01) and a lower value of left ventricular ejection fraction (p less than 0.01) than Group II patients. In the latter group of patients anginal episodes were more frequently associated with S-T segment elevation than with S-T segment depression (p less than 0.001), while the opposite was found in patients with crescendo angina. Survival curves up to five years showed that medically treated patients with crescendo angina had a worse long-term prognosis than patients with unstable angina of new onset (p less than 0.01). On the contrary no difference was found between the surgically treated patients of the two groups. Our data suggest that the more diffuse involvement of the coronary tree associated with a more depressed left ventricular function may result in an unfavorable long-term prognosis in patients with crescendo angina as compared to those with unstable angina of new onset. Such a difference between the two groups was abolished by surgical treatment.     

Relation between QRS changes and left ventricular function after coronary artery bypass grafting

Preoperative and serial postoperative electrocar-diograms (ECGs) were reviewed in 104 patients undergoing rest and exercise radionuclide angiocardiography before and 1 to 12 months after coronary artery bypass grafting (CABG). Five patient groups were defined by ECG findings before and after CABG: Group I—normal ECG before and no ECG change after CABG; Group II—prior myocardial infarction by ECG before but no QRS change after CABG; Group III—all patients with a minor QRS change (< 0.04-second Q wave, loss of R-wave amplitude) after CABG; Group IV—all patients with a major QRS change (≥ 0.04-second Q wave) after CABG; Group V—all patients without new Q waves or loss of R-wave amplitude but with a major QRS change (conduction disturbance) after CABG. Mean resting ejection fraction changed little after CABG in all groups, although the 0.03 increase in Group I was significant (p < 0.05). Group IV had the largest decrease in resting ejection fraction after CABG (0.04), but this was not statistically significant. Mean exercise ejection fraction increased significantly (p < 0.0001) in Groups I, II and III but not in Groups IV and V. QRS changes do not consistently reflect impairment of left ventricular (LV) function after CABG.     

Effects of preceding stable or unstable angina on hospital morbidity-mortality of myocardial infarction. Results of a continuous series of 1,910 patients

The aim of this study was to determine the effect of preceding unstable angina on the short-term prognosis of myocardial infarction based on early complications: cardiac failure, cardiac rupture, ventricular septal defect, sustained ventricular tachycardia ventricular fibrillation and hospital mortality. A continuous series of 1,910 patients admitted with 7 days of myocardial infarction was analysed retrospectively. The patients were divided into two groups according to their previous coronary history: Group A (myocardial infarction preceded by unstable angina) and Group B (myocardial infarction without preceding unstable angina). Group B was subdivided into Group B1 (myocardial infarction de novo) and Group B2 (myocardial infarction with previous stable angina). The results showed that patients with previous unstable angina (Group A) had a lower hospital mortality (7.9%) than those without (Group B) (13.3%) (p = 00017), fewer cardiac ruptures (1.1 versus 2.9%, p = 0.03) and less ventricular fibrillation (2.6 versus 4.5%, p = 0.053). Subgroups analysis showed that patients with de novo myocardial infarction (Group B1) had more sustained ventricular tachycardia than those with previous stable angina (Group B2) (5.3 versus 2.7%, p = 0.04). The authors conclude that pre-infarction unstable angina, possibly by ischaemic pre-conditioning, is an independent factor of a better prognosis in myocardial infarction.     

The clinical presentation of acute myocardial infarction predicts the severity of the lesion in the infarct-related artery

The purpose of this study was to correlate the clinical presentation of acute myocardial infarction with the patency rate and degree of residual stenosis of the infarct-related artery. One hundred and forty-five patients who underwent angiography after acute myocardial infarction were divided into two groups according to the time of onset of anginal pain prior to infarction. Group A comprised 119 patients, (109 men, 10 women, aged 53 +/- 9 years) who did not experience any symptoms before infarction or with anginal pain of less than 5 days preceding myocardial infarction, and group B 26 patients (all men, aged 54 +/- 12 years) with previous stable angina for greater than or equal to 1 year. Twenty-two days after acute myocardial infarction, 68 of the 145 patients (47%) had a patent infarct-related artery: 64 patients in group A (54%) and four patients in group B (15.4%) (P less than 0.006). Furthermore, 19 patients in group A (16%) and none in group B had less than 70% stenosis in the infarct-related artery (P less than 0.02). The mean residual stenosis in group A was 83.3 +/- 27% whereas in group B it was 98.1 +/- 4% (P less than 0.001). These results indicate that a long-standing history of angina before acute myocardial infarction is often related to a severe pre-existing atheromatous obstruction, which would account for the higher incidence of total coronary occlusion observed in group B. Thus angina of recent onset preceding acute myocardial infarction is associated with a higher patency rate of the infarct-related artery and frequent less than 70% residual lesions.