Angiographic assessment of the culprit coronary artery lesion before acute myocardial infarction

Serial angiographic studies of patients with myocardial infarction and unstable angina suggest that the culprit plaque underlying a thrombus need not have produced severe luminal obstruction before onset of the event. An atherosclerotic coronary artery lesion can, therefore, have 2 important characteristics. First, it may be obstructive. Second, it may be "vulnerable" in that it has the potential to become thrombogenic if exposed to the appropriate triggering stimulus. A lesion need not be obstructive to become thrombogenic, nor do all obstructive lesions have thrombogenic potential. The cause of an infarction may thus be rupture of a nonobstructive plaque leading to occlusive thrombus formation. Because it may be difficult to predict the site of a subsequent occlusion from a coronary angiogram, coronary bypass surgery or angioplasty directed only at discernible stenotic lesions may not be effective for preventing subsequent myocardial infarctions. Appropriate therapy may need to be directed at the entire coronary tree. Such therapy might include cholesterol lowering, beta blockade and aspirin.     

Angiographic investigation of the pathophysiology of perioperative myocardial infarction

Background: The study of the pathophysiologic mechanism of perioperative myocardial infarctions is limited to two small autopsy studies suggesting a major role for plaque rupture and thrombosis. However, the perioperative period is characterized by increased cardiac metabolic demand that may lead to infarction in patients with otherwise stable obstructive coronary artery disease. The purpose of this study is to investigate the pathophysiology of perioperative myocardial infarctions. Methods: Hospital records and coronary angiograms from patients from 1998 to 2006 who underwent noncardiac surgery complicated by a perioperative myocardial infarction (MI) were reviewed. The culprit lesion was identified based on ECG, left ventriculography, and coronary angiography. Degree of stenosis, TIMI flow, ACC thrombus grade, calcification score, and lesion morphology were evaluated. Based on these criteria, MIs were categorized as thrombotic, demand, or nonobstructive. Results: Sixty‐six patients (average age, 71 years and 44% male), 77% of whom underwent an intermediate risk surgery with a 2% perioperative mortality, were identified. The distribution of demand, thrombotic, and nonobstructive MI was 55%, 26%, and 19%, respectively. There was neither statistical difference in the occurrence of prolonged hypotension or tachycardia between groups nor was there any difference in the use of antiplatelets, β‐blockers, or statins. Conclusion: This study identified demand ischemia as the predominant etiology of perioperative MIs in this cohort. An improved understanding of the pathophysiologic mechanism of perioperative MIs may facilitate the evaluation and management of preoperative patients. © 2012 Wiley Periodicals, Inc.     

Acute myocardial infarction and underlying stenosis severity.

OBJECTIVES: The objective of this study was to investigate the underlying stenosis severity of the culprit lesion in acute myocardial infarction. BACKGROUND: It is widely believed that myocardial infarction often occurs in angiographically mild luminal stenosis. This, however, is in contradiction with experience from interventional practice in primary PCI. METHODS: We performed quantitative coronary angiography (QCA) in 250 consecutive patients referred for acute percutaneous coronary intervention (PCI) because of acute myocardial infarction (AMI). Fundamental for analysis was that a realistic estimate of underlying luminal narrowing before the infarction could be made angiographically that QCA could be performed and that one of two criteria was met: (1) spontaneous reflow allowing assessment of the lumen proximal and distal to the culprit lesion, or (2) coronary artery closed at arrival but reflow after uncomplicated wiring allowing assessment of the lumen proximal and distal to the culprit lesion. RESULTS: Of 250 consecutive patients (mean age 61.7 +/- 12.7 years, 48 women) referred for acute PCI, 156 patients (62%) fulfilled at least one of the above criteria for reliable QCA. In 151 of these patients (96%) the severity of the underlying stenosis was >50% and in 103 (66%) it was >70%. There were no differences in stenosis severity between the left anterior descending [LAD, (72 +/- 13)%, n = 57], left circumflex [Cx, (74 +/- 10)%, n = 20], and right coronary artery territory [RCA, (74 +/- 12)%, n = 76] (ANOVA, P = 0.76). There were no differences in stenosis severity between women [(73 +/- 13)%, n = 36] and men [(75 +/- 11)%, n = 120; P = 0.35]. CONCLUSION: In contrast to what is often believed, the majority of myocardial infarctions occurs in significant stenosis.     

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.     

Early treadmill testing after myocardial infarction: Angiographic and hemodynamic correlations.

Twenty-eight patients who were two weeks post acute myocardial infarction walked on a motorized treadmill at 1 MPH 0 percent grade for five minutes (group 1) or to an end-point of symptoms, ST-T wave changes or arrhythmias (group 2). At subsequent cardiac catheterization, 73 percent in group 1 had single vessel coronary artery disease whereas 82 percent group 2 had three or four vessel coronary artery disease. Ejection fraction was better in group 1 as was the slope of a modified left ventricular function curve. We conclude that limited exercise treadmill testing soon after acute myocardial infarction may be useful in predicting the extent of coronary artery disease and the amount of left ventricular dysfunction.     

Angiographic progression of coronary artery disease and the development of myocardial infarction

There are few data on angiographic coronary artery anatomy in patients whose coronary artery disease progresses to myocardial infarction. In this retrospective analysis, progression of coronary artery disease between two cardiac catheterization procedures is described in 38 patients: 23 patients (Group I) who had a myocardial infarction between the two studies and 15 patients (Group II) who presented with one or more new total occlusions at the second study without sustaining an intervening infarction. In Group I the median percent stenosis on the initial angiogram of the artery related to the infarct at restudy was significantly less than the median percent stenosis of lesions that subsequently were the site of a new total occlusion in Group II (48 versus 73.5%, p less than 0.05). In the infarct-related artery in Group I, only 5 (22%) of 23 lesions were initially greater than 70%, whereas in Group II, 11 (61%) of 18 lesions that progressed to total occlusion were initially greater than 70% (p less than 0.01). In Group I, patients who developed a Q wave infarction had less severe narrowing at initial angiography in the subsequent infarct-related artery (34%) than did patients who developed a non-Q wave infarction (80%) (p less than 0.05). Univariate and multivariate analysis of angiographic and clinical characteristics present at initial angiography in Group I revealed proximal lesion location as the only significant predictor of evolution of lesions greater than or equal to 50% to infarction. This retrospective study suggests that myocardial infarction frequently develops from previously nonsevere lesions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prediction of the severity of acute myocardial infarction

In 698 patients with suspected and definite acute myocardial infarction we tried to predict the severity of the infarction from clinical history and simple bedside evaluation soon after arrival in hospital. The severity of the infarction was judged from serum enzyme activity, 2-year survival, incidence and severity of congestive heart failure and incidence of severe ventricular arrhythmias during initial hospitalization. Entry characteristics which were positively associated with the severity of the infarction were intensity of pain, sign of congestive heart failure, high heart rate, ECG signs of acute myocardial infarction and presence of Q waves. Elderly patients and those with a history of hypertension also had a more severe clinical course.     

Angiographic evidence of myocardial squeezing accompanying tachyarrhythmia as a possible cause of myocardial infarction

The coronary arteriogram of a 52-year-old man with Basedow's disease and who was suffering from myocardial infarction following rapid atrial fibrillation, showed severe myocardial squeezing without organic stenosis. Angiographically, the functional obstructive lesion was always observed both at systole and diastole during atrial pacing, 150 beats per minute, and suggests that myocardial squeezing may be the cause of myocardial infarction following tachyarrhythmia.     

5993 Survivors of suspected myocardial infarction. 10 year incidence of later myocardial infarction and subsequent mortality

Aims To evaluate the 10-year incidence of later infarction and subsequentmortality, as well as predictors of later infarction, in patientswith suspected myocardial infarction and alive on day 15 afteradmission. Methods and Results 5993 patients admitted with suspected myocardial infarctionand alive on day 15 after admission were registered in The FirstDanish Verapamil Infarction Trial database in 1979–81.2586 had definite infarction, 402 probable infarction and 3005no infarction as they fulfilled 3, 2 and 1 criteria for infarction.They were followed for 10 years with respect to later infarctionand death, i.e. including death after later infarction.The 10year infarction rate after index admission was 48·8%in definite, 47·3% in probable and 24·6% in noinfarction patients (P<0·0001). The subsequent 10-yearmortality was 82·3% in primary definite, 74·7%in primary probable, and 77·9% in primary no infarctionpatients (ns). Cox regression analysis with sex, age group,and definite, probable or no infarction as independent variablesshowed that females aged <50 years without a primary infarctionhad the lowest hazard ratio (0·13 relative to males,aged 50–65 years with definite/probable infarction atindex admission) for a later infarction, in contrast to thehighest hazard ratio (1·17) for males aged >65 yearswith definite or probable infarction. Conclusion The 10-year infarction rate in patients with suspected myocardialinfarction in whom the diagnosis is ruled out is lower thanin those with definite or probable infarction, but the mortalityafter a later infarction is similar in all three groups.     

Angiographic diagnosis of true and false LV aneurysms after inferior wall myocardial infarction

False aneurysms of the left ventricle are rare complications of myocardial infarction. In this unusual case, a 57-year-old male patient had a false aneurysm, that took origin from a true aneurysm in the inferior wall, both discovered 7 years postinfarct. The aneurysms were demonstrable by ventriculography and were resected because of ventricular tachycardia. © 1995 Wiley-Liss, Inc.     

Hyperthyroidism-associated coronary vasospasm with myocardial infarction and subsequent euthyroid angina.

A 40-year-old African-American woman presented with atypical chest pain, an acute non-ST segment elevation myocardial infarction, and angiographic evidence for severe ostial vasospasm of the left main and right coronary arteries. Subsequently, she was diagnosed with hyperthyroidism and treated with antithyroid therapy and oral nitrates. Repeat angiography revealed resolution of the vasospasm; however, the chest pain recurred in the euthyroid state. Hyperthyroidism-associated coronary vasospasm is a rare disorder that characteristically causes angina in young Asian women and resolves with correction of hyperthyroidism. We present an atypical case of an African-American woman presenting with a myocardial infarction who developed recurrent angina while euthyroid.     

Angiographic assessment of prospectively determined non-invasive reperfusion indices in acute myocardial infarction

OBJECTIVE—To investigate the value of non-invasive reperfusion indices in acute myocardial infarction, avoiding the possible need for acute coronary angiography and subsequent angioplasty.
DESIGN—In a prospective angiographic study, seven potential ECG or clinical markers of reperfusion were analysed in 230 patients with acute myocardial infarction. In all patients two 12 lead ECGs were used: the ECG on admission and the ECG immediately before coronary angiography. Non-invasive markers of reperfusion determined just before coronary angiography were prospectively correlated to thrombolysis in myocardial infarction (TIMI) flow. Data analysis correlated these non-invasive indices with coronary flow (analysis A: TIMI 2-3 v TIMI 0-1 flow; analysis B: TIMI 3 v TIMI 0-2 flow).
RESULTS—A sudden decrease in chest pain was the most common sign of reperfusion (36%), followed by reduction in ST segment elevation by  50% (30%), and the development of a terminal negative T wave (20%) in the lead with the highest ST segment elevation. Reduction in ST segment elevation by  50% and the appearance of an accelerated idioventricular rhythm (AIVR) had the highest positive predictive value for reperfusion. For analyses A and B, the positive predictive values were 85% and 66% for resolution of ST segment elevation, and 94% and 59% for AIVR, respectively. The presence of three or more non-invasive markers of reperfusion predicted TIMI 3 flow accurately in 80% of cases.
CONCLUSIONS—The prospective use of non-invasive indices of reperfusion is simple, practical, and can be of value in assessing coronary patency in patients admitted with acute myocardial infarction. Using these indices, discrimination between TIMI 0-1 and TIMI 2-3 flow can be made with good accuracy. However, TIMI 3 flow cannot be determined reliably. The use of such non-invasive indices depends on the goal of reperfusion.


Keywords: reperfusion indices; acute myocardial infarction     

Acute coronary thromboembolization in unstable angina without subsequent myocardial infarction

A 58 year old man underwent coronary arteriography for unstable angina. During the catheterization, distal embolization of a nonoccluding intracoronary thrombus formed at the site of a subtotal atherosclerotic occlusion of the left anterior descending coronary artery and was documented angiographically. This event, which appears unique, was not associated with subsequent myocardial infarction or any apparent morbidity.     

Transatrial repair of ventricular septal defect subsequent to myocardial infarction

We describe successful transatrial repair of a ventricular septal defect occurring secondary to myocardial infarction. This approach avoids the need for ventriculotomy and may be technically simpler and safer than repair across the zone of infarction in a subset of patients with posterior defects and right ventricular dysfunction who survive the early period subsequent to their infarct.