Cineangiographic assessment of left ventricular function in the acute phase of transmural myocardial infarction.

One hundred fifteen patients underwent hemodynamic investigation including left cineangiography during the acute phase of transmural myocardial infarction. Patients were classified into two groups: those with anterior myocardial infarction (48 patients) and those with inferior myocardial infarction (67 patients). There was a good correlation between the electrocardiographic site of infarction and the location of ventricular dyssynergy. The extent of abnormally contracting segment was 39.3 ± 2 percent (mean ± standard error of the mean) in anterior infarction and 28 ± 1.7 percent in inferior infarction. Left ventricular end-diastolic volume was normal in inferior infarction and slightly increased in anterior infarction. Left ventricular end-diastolic pressure was significantly increased in both groups. The increase in left ventricular end-diastolic pressure was related to (1) depressed contractility as demonstrated by the significant reduction of ejection fraction and mean velocity of circumferential fiber shortening; and (2) changes in left ventricular compliance with a large scatter to the left as well as to the right of the pressure-volume curve.There was no correlation between the extent of dyssynergy and changes in left ventricular end-diastolic compliance but there was a good linear correlation between ejection fraction and the extent of abnormally contracting segment. In the group with anterior infarction, for the same extent of dyssynergy, patients with a decreased end-diastolic compliance had a better ejection fraction than those with an increased end-diastolic compliance. Finally, the extent of infarction seems to be the principal factor determining the degree of ventricular functional impairment because patients with anterior or inferior myocardial infarction carefully matched for similar extent of infarction demonstrated no significant differences in the variables of ventricular performance.     

The QRS scoring system for estimating myocardial infarct size: clinical, angiographic and prognostic correlations

The relation between a QRS score derived from the routine electrocardiogram and left ventricular function was investigated in 181 patients after myocardial infarction. Patients with left ventricular hypertrophy and conduction defects were excluded. The QRS score correlated closely with the severity of wall motion abnormalities and left ventricular ejection fraction. The more severe the dyssynergy, the higher the QRS score (hypokinesia = 3.0; akinesia = 5.4; dyskinesia = 9.1). The left ventricular ejection fraction (percent) = 66 - (3.3 x QRS score) (correlation coefficient [r] = -0.81, probability [p] less than 0.001). With use of this regression equation, the QRS score predicted angiographic left ventricular ejection fraction to within 12% of the angiographic ejection fraction in 29 of 30 additional patients studied prospectively. The QRS score was also related to clinical functional class. The worse the clinical manifestation of left ventricular dysfunction, the higher the QRS score (Killip class I = 3.5; class II = 6.5; class III = 7.1). A QRS score greater than or equal to 7 had a specificity of 97% and a sensitivity of 59% for predicting an ejection fraction of less than 45%. Patients with a QRS score of 7 or greater had severe wall motion abnormalities, higher peak serum creatine kinase levels, higher prevalence of multivessel coronary disease, poor clinical functional class and an unfavorable outcome. The QRS score provides an inexpensive, clinically useful estimate of left ventricular function after myocardial infarction and can identify patients at high risk.     

Left ventricular functional alterations at rest and during submaximal exercise in patients with recent myocardial infarction

Submaximal exercise testing with radionuclide ventriculography was performed in 117 patients prior to hospital discharge 16.7 ± 6.7 days (SD) following acute myocardial infarction. The hypothesis tested in this study was that patients with different locations and types of infarction have different functional responses to submaximal exercise prior to discharge. The distribution of the myocardial infarctions were anterior transmural in 33, Inferior transmural in 39, anterior nontransmural in 23, inferior nontransmural in 19, and indeterminant in three. Patients with transmural infarction generally had significantly larger resting left ventricular volumes at enddiastole and end-systole and lower ejection fractions and systolic blood pressure/end-systolic volume Indexes than patients with nontransmural infarctions (p < 0.05). During submaximal exercise, the change in end-systolic volume was significantly different in these two groups. When patients were separated further into anterior and inferior transmural subgroups, the patients with anterior transmural infarction had significantly lower left ventricular ejection fractions and higher right ventricular ejection fractions than the group with inferior transmural Infarction (p < 0.05). In response to exercise, the group with anterior transmural infarction had a significant decrease in left ventricular ejection fraction and a blunted systolic blood pressure/left ventricular end-systolic volume index, in comparison to patients with inferior myocardial infarction (p < 0.05); this was the only group to have a significant increase in end-systolic volume. The group variance for the parameters studied was large, particularly during exercise when the individual responses were frequently directionally opposite from the group means. The group with anterior transmural infarction was the most homogenous, with 26 of 33 having a directionally abnormal response to submaximal exercise. It was concluded that the group with anterior transmural infarction generally displayed the most abnormal left ventricular function. However, despite significant group differences in resting ventricular function with different infarcts, the intragroup variability at rest and in response to exercise was too great to permit an accurate prediction of the subject's resting ventricular performance or to permit a prediction of exercise response based solely on location of the infarct.     

Simultaneous assessment of segmental and global left ventricular function by two-dimensional echocardiography in acute myocardial infarction

Both segmental and global left ventricular performance were assessed simultaneously in 29 patients with acute myocardial infarction using two-dimensional echocardiography. Comparisons were made between left ventricular wall motion versus peak CK-MB, site of infarction, and occurrence of heart failure. Two-dimensional echocardiography identified areas of dyssynergy which corresponded to electrocardiographic areas of infarction in 89% of all cases. Patients with heart failure had more dyssynergic segments, and these segments manifested more severe dyssynergy than patients without heart failure. Patients with severe global dysfunction manifested higher peak CK-MB values, and those with anterior infarction had more global dyssynergy than did those patients with inferior infarction. These observations suggest that two-dimensional echocardiography is a useful technique for localization and assessment of segmental and global dyssynergy in acute myocardial infarction. Information so derived correlates with the clinical status of patients with acute myocardial infarction, and may offer important insights into both prognosis and treatment.     

Left ventricular performance in coronary artery disease evaluated with systolic time intervals and echocardiography

Simultaneous determinations of systolic time intervals (preejection period index [PEPI], left ventricular ejection time index [LVETI] and ratio of preejection period to left ventricular ejection time [PEP/LVET]) and echographic measures of left ventricular performance (percent change in minor axis diameter [%ΔD], circumferential shortening rate [Vcf] and end-diastolic diameter [Dd]) were obtained in 25 normal subjects and 37 patients with previously documented transmural myocardial infarction. The group with previous infarction demonstrated significant (P < 0.001) differences from the normal group in each of the noninvasive measures. PEP/LVET and %ΔD were the most sensitive measures of left ventricular dysfunction. Deviation from the normal range in these measures occurred, respectively, in 70 and 65 percent of patients without dyspnea or fatigability (20 patients) and in 85 percent of those without angina pectoris (13 patients). Abnormalities in systolic time interval and echocardiographic measures were related to the severity of dyspnea and fatigability but not to that of angina. Neither the presence of phonocardiographically documented third or fourth sound gallops nor an abnormal cardiothoracic ratio by chest roentgenogram reliably detected patients with abnormal left ventricular performance. The range of abnormality in left ventricular performance did not differ between patients with prior anterior or diaphragmatic myocardial infarction. The frequency of abnormal performance was greatest among patients with combined sites of prior infarction. Among 26 patients studied by coronary arteriography, abnormal left ventricular performance as determined by values for PEP/LVET and %ΔD occurred in fewer than 30 percent of those with 70 percent or greater obstruction of one coronary artery and in more than 80 percent of those with two or three vessel involvement. There was a high correlation between systolic time intervals, %ΔD and Vcf, the closest correlation occurring between PEP/LVET and %ΔD (r = ?0.93). These data document the sensitivity of the noninvasive systolic time intervals and echographic measures and their superiority over current clinical bedside methods in evaluating left ventricular performance in patients with prior myocardial infarction.     

Predictors of left ventricular thrombus formation in patients with anterior myocardial infarction: role of activated protein C resistance

BACKGROUND: Left ventricular mural thrombus formation is a well-recognised consequence of acute anterior myocardial infarction. The vast majority of left ventricular thromboses occur in patients with anterior myocardial infarction and depressed left ventricular function. OBJECTIVE: To evaluate the factors predicting left ventricular thrombus formation in patients similar for left ventricular function and left ventricular score indexes. METHODS: We evaluated 45 consecutive patients who met the inclusion criteria of anterior myocardial infarction resulting in apical, anterior or septal asynergy (akinesia, dyskinesia), without non-Q-wave myocardial infarction, dilated cardiomyopathy, or renal or hepatic dysfunction. Patients were divided into two groups: group I with, and group II without, left ventricular mural thrombus. The groups were compared for clinical, echocardiographic and hematologic parameters (activated protein C resistance (APC-R), protein S and antithrombin III). RESULTS: Smoking and ACP-R were significantly greater in group I than in group II (P < 0.05 and P < 0.005 respectively). Multivariate regression analysis showed that APC-R was an independent risk factor for left ventricular thrombus formation in the patient group selected. Antithrombin III and protein S concentrations were not statistically different between two groups. All other clinical and echocardiographic characteristics of the patients were similar in both groups. CONCLUSION: APC-R is an independent risk factor for left ventricular thrombosis in patients with anterior myocardial infarction resulting in septal or anterior and apical akinesia or dyskinesia.     

Clinical significance of exercise-induced ST segment elevation. Correlative angiographic study in patients with ischaemic heart disease.

We have examined the relation between electrocardiographic ST elevation during treadmill exercise (greater than or equal to 1 mm, using the conventional 12 leads), the severity of coronary artery disease, and left ventricular wall motion abnormalities in 680 patients. They were divided into three groups: (1) 218 patients with clinically significant coronary artery disease, (2) 178 patients with clinically significant coronary artery disease, and (3) 284 patients with clinically significant coronary artery disease and previous myocardial infarction. ST elevation during exercise (predominantly in lead V2) was seen in two patients (1%) in group 1, three patients (2%) in group 2, and 147 patients (52%) in group 3. Coronary artery disease (number of vessels involved and severity of stenoses) was comparable in groups 2 and 3. All the patients in group 1 showed a normal left ventricular contraction pattern; 64% of the patients in group 2 showed wall motion abnormalities (predominantly hypokinesia) and 95% of group 3 (mainly akinesia, dyskinesia, or aneurysm). A strongly positive correlation was seen between the ST elevation and left ventricular dysfunction in patients belonging to group 3. The overall sensitivity and the specificity of the stress test in detecting wall motion abnormalities was 55% and 100% respectively. The sensitivity increased with deterioration in left ventricular function, reaching 81% and 90% in patients with dyskinesia and aneurysm, respectively. Maximal ST elevation (greater than or equal to 3 mm) was confined to the patients with dyskinesia or aneurysm. The incidence of ST elevation during exercise was also related to the location of previous infarction, showing a positive response in 85% of patients with anterior myocardial infarction and in only 33% with inferior myocardial infarction. We conclude that ST segment elevation during exercise in patients with previous myocardial infarction is a sensitive and a specific indicator of advanced left ventricular asynergy. The ST segment response during exercise in patients with previous infarction and with angiographically demonstrated myocardial asynergy appears to be a continuous spectrum. A normal ST segment response or elevation alone usually signifies involvement of only one vessel supplying the infarcted myocardium, ST elevation with concomitant ST depression indicates additional coronary artery disease, and ST depression alone indicates overwhelming myocardial ischaemia resulting from multiple vessel disease. The employment of multiple leads is essential to obtain this information.     

Accuracy of systolic time intervals in detecting abnormal left ventricular performance in coronary artery disease

Sixty-six consecutive patients with a history of previous myocardial infarction and 48 patients with angina pectoris without evidence of previous myocardial infarction, all of whom had diagnostic coronary arteriography and left ventriculography, were studied in a prospective analysis of the accuracy of noninvasively determined systolic time intervals as a measure of global left ventricular performance. Forty-one patients who were evaluated for atypical chest pain and found to have normal coronary arteries and left ventricular performance served as control subjects. Six methods of statistical analysis were employed in assessing the accuracy of systolic time intervals in relation to the left ventricular ejection fraction: (1) analysis of variance, (2) cumulative distribution analysis, (3) correlation, (4) sensitivity and specificity, (5) percent agreement, and (6) logistic regression analysis. These tests permitted comparison between the systolic time intervals and the angiographic left ventricular ejection fraction. Analysis of variance revealed identical discriminating power for the ratio of the preejection period to left ventricular ejection time (PEP/ LVET) and left ventricular ejection fraction in separating the normal group and patients without previous myocardial infarction from the patients with previous myocardial infarction. The preejection period and left ventricular ejection time corrected for heart rate were less discriminating than left ventricular ejection fraction or PEP/LVET. The cumulative distribution plots for the left ventricular ejection fraction and PEP/LVET in the three groups of patients were remarkably similar. The correlation of PEP/LVET and left ventricular ejection fraction for all three groups of patients was 0.84. The sensitivity and specificity of the PEP/LVET in relation to the left ventricular ejection fraction were 88 and 96 percent, respectively. The overall agreement between the two measures in detecting the prevalence of abnormality in global left ventricular performance in subgroups of patients was 92 percent. By logistic regression analysis the two measures had equal capacity in discriminating the patients with previous myocardial infarction from the control group.The multiple strategies of comparison employed in this study document the close relation of measures of the timing of the left ventricular contraction cycle by systolic time intervals and estimates of the extent of left ventricular contraction by ejection fraction in patients with coronary artery disease. It is concluded that these measures afford independent and complementary methods of defining the presence of abnormal left ventricular performance in the resting supine patient with coronary artery disease.     

Vectorcardiographic, electrocardiographic, and angiographic correlations in apparently isolated inferior wall myocardial infarction.

Twenty-six patients with ECG evidence of localized inferior myocardial infarction and poor ejection fraction (less than 50 per cent) were compared with 26 patients with similar ECG's, but with normal ejection fraction (over 50 per cent). The poor ejection fraction group had significantly more frequent and more severe disease in left anterior descending artery and a higher incidence of triple coronary obstruction than the normal ejection fraction group. The poor ejection fraction group had a significantly greater incidence of ventricular asynergy in the anterior and apical segments of left ventricle. Vectorcardiography was available in 35 of the 52 patients studied and frequently supplied diagnostic information not available in the scalar ECG's. Of 18 patients with scalar ECG patterns of isols, vectorcardiography identified five cases with anterior infarction, three with left ventricular hypertrophy, and one with left anterior hemiblock. Vectorcardiography is a valuable supplementary tool in the clinical assessment of patients with apparently isolated inferior infarction. When extensive coronary and poor ventricular function exist, VCG clues may be expected in about half the patients.     

Differences in left ventricular function between anterior and inferior myocardial infarction of equivalent enzymatic size

The reasons for the poorer prognosis of anterior versus inferior myocardial infarction of equivalent enzymatic size remain uncertain. We investigated whether there are differences in left ventricular function between patients with anterior and inferior infarctions of equivalent enzymatic size to account for their differing outcomes. Clinical, serum enzyme, and electrocardiographic data were prospectively recorded in a consecutive series of patients less than 70 years of age with their first myocardial infarction. At 29 +/- 6 days following infarction, ejection fraction and left ventricular wall motion were assessed by gated heart scintigraphy and functional capacity by treadmill exercise testing in 19 patients with anterior and in 23 patients with inferior myocardial infarction. Peak creatine kinase and QRS scores were used to estimate total infarct size and left ventricular infarct size respectively. The anterior infarcts were of similar size to the inferior infarcts as determined by peak creatine kinase (1444 [mean] +/- 1161 [SD] U/L versus 1484 [mean] +/- 1182 [SD] U/L, respectively, P = 0.91) and peak aspartate transaminases (174 +/- 112 U/L versus 164 +/- 102 U/L, P = 0.78). The anterior myocardial infarct group had a greater percentage of the left ventricle infarcted on QRS scoring than the inferior infarct group (25.9 +/- 14.4% versus 11.1 +/- 6.0% respectively, P = 0.0004), lower global left ventricular ejection fraction (45.8 +/- 16% versus 54.6 +/- 9.2%, P = 0.04) and greater left ventricular regional wall abnormality. A significant negative correlation existed between left ventricular ejection fraction and peak creatine kinase for both groups, but was more marked with anterior infarction (r = -0.78, P less than 0.01) compared with inferior infarction (r = -0.49, P less than 0.05). Exercise-induced ST segment elevation was more frequent in the anterior than the inferior infarct group (59% versus 18%, P less than 0.02). However, both infarct locations had similar exercise tolerance, exercise-induced angina and ST segment depression. Despite equivalence of infarct size of the two infarct locations on enzyme testing, anterior infarction was associated with greater abnormality of left ventricular function with lower resting global left ventricular ejection fraction; greater resting left ventricular regional wall abnormality and greater exercise-induced ST segment elevation. These differences probably contribute to the poorer prognosis of patients with anterior infarction compared to those with inferior infarction of equivalent enzymatic size, given the previously well-documented prognostic importance of left ventricular function.     

Clinical implications of anterior S-T segment depression in patients with acute inferior myocardial infarction

To assess various factors associated with anterior S-T segment depression during acute inferior myocardial infarction, 47 consecutive patients with electrocardiographic evidence of a first transmural inferior infarction were studied prospectively with radionuclide ventriculography an average of 7.3 hours (range 2.9 to 15.3) after the onset of symptoms. Thirty-nine patients (Group I) had anterior S-T depression in the initial electrocardiogram and 8 (Group II) did not have such “reciprocal” changes. There was no difference between the two groups in left ventricular end-diastolic or end-systolic volume index or left ventricular ejection fraction. Stroke volume index was greater in Group I than in Group II. There were no group differences in left ventricular total or regional wall motion scores. A weak correlation existed between the quantities (mV) of inferior S-T segment elevation and reciprocal S-T depression. No relation between anterior S-T segment depression and the left ventricular end-diastolic volume index could be demonstrated; the extent of left ventricular apical and right ventricular wall motion abnormalities, both frequently associated with inferior infarction, did not correlate with the quantity of anterior S-T depression.These data show that anterior S-T segment depression occurs commonly during the early evolution of transmural inferior infarction, is not generally a marker of functionally significant anterior ischemia and cannot be used to predict left ventricular function in individual patients. Anterior S-T segment depression may be determined by reciprocal mechanisms.     

Correlation of cold pressor response with coronary atherosclerosis and left ventricular performance.

A comparison of cold pressor response with coronary arteriography and left ventriculography was made in 26 consecutive patients having chest pain suggesting coronary heart disease. Patients with normal coronary arteriograms and normal left ventriculograms showed normal cold pressor responses. Patients with coronary atherosclerosis and normal left ventricular performance showed an exaggerated cold pressor response, whereas patients with severe coronary atherosclerosis and poor left ventricular performance did not exhibit an exaggerated cold pressor response. In patients with inferior wall myocardial infarction having dyskinesia or akinesia of the inferior wall, the cold pressor response was not impaired. In contrast, patients with anterior wall myocardial infarction and dyskinesia or akinesia of the anterior wall showed a marked impairment of the left ventricular performance and no exaggeration of the cold pressor response.     

Diagnostic value of electrocardiogram and vectorcardiogram in postinfarction ventricular asynergy

The ability of ECG-VCG to predict the severity of postinfarction LV asynergy was evaluated in 152 patients with previous myocardial infarction who underwent left cineventriculography in the right anterior oblique view. Various ECG and VCG signs were examined in order to predict the existence of severe asynergy in general (dyskinesia or akinesia or severe hypokinesia) and of dyskinesia in particular. In patients with inferior myocardial infarction (Group A) persistent ST segment elevation was the only specific ECG sign (100%) of severe asynergy; it had a poor sensitivity (6.2%). Four frontal VCG signs (presence of terminal bite, y- greater than 0.18 mV, maximum early superior vector along x axis = MESV greater than or equal to 1.3 mV, duration of initial superior forces = DISF greater than 50 msec) increased the sensitivity of the ECG-VCG method to 75.8% while maintaining a 100% specificity. Regarding the diagnosis of dyskinesia, only the ECG sign of persistent ST segment elevation and the VCG sign of y- greater than or equal to 0.3 mV had a 100% specificity. The sensitivity of the ECG-VCG method was 33.3% (16.6% ECG and 16.6% VCG). In patients with anterior myocardial infarction (Group B), concerning the diagnosis of severe asynergy, the ECG signs of sigma ST greater than 3 mm in anterior leads; pathologic Q wave in four or more anterior leads (including D1 and aVL); and the presence of LAH or LAH + RBBB, had a 100% specificity and a good sensitivity (60.5%). The VCG sign of a narrow horizontal QRS loop increased the sensitivity of the ECG-VCG method to 71% while maintaining a 100% specificity. As for the diagnosis of dyskinesia, the ECG signs with a 100% specificity were sigma ST greater than or equal to 5 mm in anterior leads, a pathologic Q wave in more than five anterior leads (including I and a VL) and RBBB + LAH; these variables had a sensitivity of 48.3%. The VCG sign of a narrow horizontal QRS loop increased the sensitivity of the ECG-VCG method to 79.3% while maintaining a 100% specificity. In patients with inferior plus anterior myocardial infarction (Group A + B) the signs mentioned above for each group were evaluated, confirming a 100% specificity. Regarding the diagnosis of severe asynergy, the ECG signs had a sensitivity of 61.3%, while VCG increased the sensitivity of the ECG-VCG method to 90.3%.(ABSTRACT TRUNCATED AT 400 WORDS)     

Right ventricular infarction with tricuspid insufficiency and chronic right heart failure.

A patient with chronic right heart failure and probable tricuspid insufficiency associated with an inferior myocardial infartion is described. Angiograms demonstrated total occlusion of the right coronary artery at its origin, a patent venous bypass graft to the mid-right coronary artery and hypokinesia of the inferior wall of both the right and left vebtricles. Clinical data indicated a greater impairment of right than of left ventricular function. It is proposed that infarction of the right ventricle resulted in chronic right heart failure and tricuspid insufficiency.     

Relation of ventricular arrhythmias in the late hospital phase of acute myocardial infarction to sudden death after hospital discharge.

To determine the prognostic significance of ventricular arrhythmias persisting during the hospital ambulatory phase of acute myocardial infarction, 64 patients with acute myocardial infarction underwent continuous 10-hour Holter monitoring an average of 11 days after discharge from the coronary care unit (CCU). Patients were categorized according to the results of ambulatory monitoring: 27 patients had ventricular extrasystoles, which were complicated (multifocal, R on T, paired, more than 5/min), or ventricular tachycardia; 22 had uncomplicated premature ventricular contractions; and 15 exhibited no ventricular arrhythmias. The 64 patients were followed prospectively for an average course of 25.8 months; 12 died suddenly; 8 died of other causes, and 44 survived. In all patients who died suddenly, ventricular ectopy was recorded on Holter monitoring before their discharge from the hospital (complicated premature ventricular contractions, eight patients; uncomplicated premature ventricular contractions, four patients); there were no sudden deaths in the patients without ventricular arrhythmias. Patients who died suddenly and those survived were similar in respect to age (60, 62 years), sex, location of infarction, presence of coronary risk factors, severity of acute myocardial infarction (Q waves, cardiac enzymes), serum cholesterol levels, evidence of cardiomegaly on roentgenograms, presence of ventricular gallop and drug therapy received. The occurrence of acute arrhythmias in the CCU did not separate patients who died suddenly from those who survived; there were no differences in ventricular tachycardia or ventricular fibrillation (3 or 12 patients who died suddenly, 6 of 44 patients who survived) or complicated premature ventricular contractions (4 or 12 patients who died suddenly, 18 of 44 patients who survived). Electrocardiograms obtained late in the hospital course revealed no differences in the extent of Q or T wave changes between these two groups. However, the extent of S-T segment abnormality was greater in patients who died suddenly than in patients who survived (5.6 compared to 1.8 leads/standard tracing, p smaller than 0.02) suggesting that the arrhythmias in the former were related to persistent ischemia or segmental ventricular dyssynergy. Thus, in this relatively small number of patients, ventricular arrhythmias persisting late in the hospital course of patients admitted for acute myocardial infarction are shown to predispose to subsequent sudden death.     

Correlation between body surface isopotential maps and left ventriculograms in patients with old inferoposterior myocardial infarction

In 24 patients with old inferoposterior myocardial infarction, body surface isopotential maps were compared with left ventriculographic findings. In 16 patients with asynergy restricted to the inferior and/or posterolateral segment, surface potential abnormalities due to infarction were observed during specific phases of QRS and in specific portions on the chest surface depending on the location and extent of ventricular severe asynergy (akinesis and dyskinesis). However, the remaining eight patients with coexisting severe asynergy in the anterior, apical, or septal segment showed surface potential maps quite different from those of the former patients. It is suggested that body surface isopotential maps are a useful clinical tool for detecting the location and extent of ventricular severe asynergy in patients with old inferoposterior myocardial infarction.     

Echocardiographic determinants of left ventricular ejection fraction after acute myocardial infarction

OBJECTIVE: This study was performed to determine if factors other than the size of regional dysfunction influence the global left ventricular ejection fraction after acute myocardial infarction. BACKGROUND: Left ventricular ejection fraction is an important prognostic variable after acute myocardial infarction. Although infarct size is known to affect the subsequent global left ventricular ejection fraction, it remains unclear whether other factors such as site or severity of the wall motion abnormality influence the ejection fraction after acute myocardial infarction. METHODS: Sixty-nine consecutive patients (mean age 61 +/- 14 years, 46 [67%] male) who did not receive thrombolytic therapy or undergo early revascularization were studied by echocardiography 1 week after Q-wave myocardial infarction. The absolute size of the region of abnormal wall motion (AWM) and the percentage of the endocardium involved (%AWM) were quantitated along with the wall motion score. A severity index was then derived as the mean wall motion score within the region of AWM. Site of myocardial infarction was classified as either anterior or inferior from the endocardial map. Left ventricular ejection fraction was measured by Simpson's method with 2 apical views. RESULTS: Twenty-nine (42%) patients had anterior and 40 had inferior myocardial infarction. The mean left ventricular ejection fraction was significantly lower in anterior than in inferior myocardial infarction (44.8% +/- 11.5% vs 53% +/- 8.6%; P =. 001). The mean %AWM was greater in anterior than in inferior myocardial infarction (32.1 +/- 15.5 vs 22.4 +/- 14.1; P =.01). The mean wall motion score was greater in anterior than in inferior myocardial infarction (9.8 +/- 6.4 vs 6.4 +/- 4.4; P =.01). The mean severity index did not differ by site. Multiple regression analysis demonstrated that, in descending order of importance, %AWM, extent of apical involvement, and site of myocardial infarction were independent determinants of global left ventricular ejection fraction. CONCLUSIONS: For myocardial infarctions of similar size, left ventricular ejection fraction is lower when apical involvement is extensive and the site of infarction is anterior. This site-dependent difference may be related to characteristics specific to the apex.     

Regional left ventricular function in acute myocardial infarction: Evaluation with quantitative radionuclide ventriculography

Regional and global left ventricular performance was noninvasively assessed with quantitative gated equilibrium radionuclide ventriculography in 43 patients an average of 40 hours after the onset of a first acute transmural myocardial infarction. In all 16 patients with anterior infarction, regional ejection fraction, a quantitative measure of regional left ventricular performance, was uniformly depressed in the infarcted zone. In patients with inferior infarction the abnormalities of regional performance were less severe. Fourteen of 20 patients (70 percent) with inferior infarction had depressed performance in the infarcted zone. Function in noninfarcted zones was abnormal in only 6 of the 20 patients (30 percent) with inferior infarction, but it was abnormal in 11 of the 16 patients (69 percent) with anterior infarction, particularly in those with severe pump failure. As a consequence, global left ventricular ejection fraction was significantly lower in patients with anterior than in those with inferior infarction (mean ± standard error of the mean 31 ± 3 percent versus 51 ± 3 percent, p < 0.005). Prognosis and clinical functional class were related to performance not only in infarcted zones, but also in noninfarcted zones as assessed with electrocardiography.It is concluded that depressed function in apparently noninfarcted left ventricular zones contributes significantly to left ventricular dysfunction after acute myocardial infarction, particularly in patients with anterior infarction.     

Left ventricular dysfunction in acute myocardial infarction due to isolated left circumflex coronary artery stenosis

The characteristics of regional and global left ventricular dysfunction due to isolated left circumflex (LC) artery stenosis were determined from the contrast ventriculograms of 52 patients studied during acute myocardial infarction. In patients with a left dominant coronary circulation (35%), the severity, circumferential extent and location of hypokinesia resembled those of right coronary artery stenosis. However, in patients with a right dominant or balanced circulation (65%), the location of LC artery-related hypokinesia varied over the entire left ventricular contour, overlapping with the territories of the left anterior descending and right coronary arteries. The method for measuring the severity of hypokinesia was adjusted to take into account the wide territory of the LC artery. This enhanced the sensitivity of the method, particularly in the right anterior oblique view, as indicated by the greater severity of hypokinesia measured (-2.5 +/- 0.9 vs -1.8 +/- 1.1 standard deviations by our previously published method, p less than 0.001). However, the overlap of the artery territories may make it difficult to selectively measure the dysfunction due to stenosis of an artery of interest in patients with multiple infarctions. The circumferential extent of hypokinesia due to LC artery thrombosis was greater in the left than the right anterior oblique view. When averaged over both views, the size of the dysfunctional segment approached that due to left anterior descending coronary artery thrombosis, exceeding the size previously reported. These results suggest that current eligibility criteria for thrombolytic therapy select patients with extensive LC artery beds.     

Anterior ST depression in inferior myocardial infarction: correlation with results of intracoronary thrombolysis

Thirty-eight patients underwent left ventricular angiography and coronary arteriography within the first 6 hours of inferior myocardial infarction, in an attempt at intracoronary thrombolysis with streptokinase. Twenty-three of these patients presented with ST segment depression of more than 1 mm on the anterior leads (V1 to V4) of ECGs done immediately before the attempt at thrombolysis (group I), whereas 15 did not (group II). Quantitative analysis of left ventricular angiography showed an ejection fraction significantly lower in group I (51 +/- 10%) than in group II (59 +/- 7%; p less than 0.01). This difference was the result of inferior hypokinesia which was larger both in surface area (group I = 11.5 +/- 6.5 cm2; group II = 4.2 +/- 2.7 cm2; p less than 0.001) and in percentage of ventricular perimeter (group I = 46 +/- 14%; group II = 27 +/- 12%; p less than 0.001). The prevalence of a left anterior descending artery lesion and the degree of stenosis were the same in both groups. The success rate of thrombolysis was not significantly different. However, in cases of persistent success, there was an improvement of regional contraction only in group I, as opposed to absence of change in group II. These results suggest that patients with inferior myocardial infarction and ST anterior depression have an extensive ischemic area rather than anterior wall ischemia. An attempt at coronary thrombolysis seems to be worthwhile only in these patients, as it results in appreciable myocardial salvage when successful.