The prognostic significance of first myocardial infarction type (Q wave versus non-Q wave) and Q wave location. The Multicenter Diltiazem Post-Infarction Research Group

The prognostic significance of the type of first acute myocardial infarction (Q wave versus non-Q wave) and Q wave location (anterior versus inferoposterior) was determined from a multicenter data base involving 777 placebo-treated patients who were participants in the Multicenter Diltiazem Post-Infarction Trial. There were 224 patients (29%) with a non-Q wave infarction, 326 (42%) with an inferoposterior Q wave infarction and 227 (29%) with an anterior Q wave infarction. Mean left ventricular ejection fraction was significantly (p less than 0.001) lower in patients with an anterior Q wave infarction than in the other two groups (anterior Q wave 0.39; inferior Q wave 0.52; non-Q wave 0.53). Nevertheless, the total cardiac mortality rate during the follow-up period (average 25 months per patient) was only marginally higher (p = 0.42) in the anterior Q wave group (8.4%) than in the other two groups (inferoposterior Q wave 7.1%; non-Q wave 6.3%). The total first recurrent cardiac event was somewhat higher (p = 0.08) in the anterior Q wave group (18.1%) than in the other two groups (inferoposterior Q wave 11.7%; non-Q wave 15.6%). Survivorship analyses extending over 3 years revealed that electrocardiographic classification of the type of first infarction and Q wave location did not make significant independent contributions to the risk of postinfarction cardiac death or first recurrent cardiac event, either before or after adjustment for baseline clinical variables.     

Functional impact of remodeling during healing after non-Q wave versus Q wave anterior myocardial infarction in the dog.

OBJECTIVES. This study was undertaken to compare changes in left ventricular remodeling and function during healing after a first anterior non-Q wave versus a Q wave myocardial infarction in the dog. BACKGROUND. Whether ventricular remodeling is more severe after anterior Q wave than after anterior non-Q wave infarction has not been studied systematically. METHODS. Serial remodeling and functional variables (two-dimensional echocardiography), electrocardiography and hemodynamic data were recorded over 6 weeks in 58 instrumented dogs subjected to left anterior descending coronary artery ligation or ligation plus collateral obliteration. Postmortem topography and transmurality (by planimetry) and infarct collagen (hydroxyproline) were measured at 6 weeks. RESULTS. At 6 weeks, infarct collagen was similarly increased in both groups, but the Q wave group had greater infarct size (7.2% vs. 4.5%, p less than 0.025) and greater transmurality (88% vs. 58%, p less than 0.001), higher left atrial pressures, more infarct expansion (expansion index 2.62 vs. 2.31, p less than 0.001), more thinning (thinning ratio 0.62 vs. 0.72, p less than 0.001), greater cavity dilation (diastolic volume 88 vs. 72 ml, p less than 0.001), more regional bulging in the short-axis view (depth 4.9 vs. 1.9 mm, p less than 0.001), more regional asynergy (18% vs. 7%, p less than 0.001), lower global ejection fraction (40% vs. 48%, p less than 0.001), more endocardial and epicardial bulging in the long-axis view and greater incidence of aneurysm (82% vs. 36%, p less than 0.005), left ventricular thrombus (64% vs. 0%, p less than 0.0005) and ventricular arrhythmias. Echocardiograms obtained during a 6-week period indicated that left ventricular topographic deterioration and dysfunction were present in the earliest postinfarction study at 2 days in both groups but were more frequent in the Q wave group. Regional myocardial blood flow (24 dogs) was lower in the Q wave than in the non-Q wave group. Scanning electron microscopy (10 dogs) revealed preservation of the epicardial collagen matrix in the non-Q wave but not the Q wave group. CONCLUSIONS. Anterior Q wave infarction is associated with greater transmurality and more postinfarction left ventricular remodeling and dysfunction than is non-Q wave infarction.     

Complex ventricular arrhythmias in patients with Q wave versus non-Q wave myocardial infarction

We examined whether or not subsets of patients with complex ventricular arrhythmias after myocardial infarction are at high risk with respect to 1 year mortality after hospital discharge. Based on previous studies showing increased risk for those with non-Q wave infarcts, we hypothesized that complex PVCs (premature ventricular complexes) in this group might be associated with a poorer prognosis than complex PVCs in patients with Q wave infarcts. Seven hundred seventy-seven patients entering our study with acute infarction were followed prospectively for 1 year after undergoing a predischarge 24 hr ambulatory electrocardiographic examination. Patients were classified by electrocardiographic criteria into the following groups: Non-Q wave (n = 191), Q wave anterior (n = 261), and Q wave inferior infarction (n = 325). The following arrhythmias were classified as complex: multiform PVCs, couplets, and ventricular tachycardia. Sixty-two percent of patients with non-Q wave infarcts who did not survive 1 year had complex PVCs, compared with 32% of survivors (p less than .01). No differences were seen in the Q wave subgroup. The survival for patients with Q wave and non-Q wave infarction without complex PVCs were nearly identical at 1 year (93% and 90%), whereas in patients with complex PVCs survival for those with Q wave and non-Q wave infarction was 92% and 76%, respectively (p less than .001). Of those with non-Q wave infarction, only 4% of nonsurvivors were free of any PVCs, as compared with 28% of nonsurvivors in the Q wave group (p less than .02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Quantification of antimyosin uptake and infarct size at various stages of myocardial infarction.

We studied with quantitative techniques the clinical efficacy of indium-111 antimyosin at a later stage of myocardial infarction in 18 patients at various stages after infarction. Antimyosin accumulation was detected irrespective of infarct age and size and quantified as an infarct weight with a tomographic technique. Higher intensities in a planar image were observed in anterior Q wave infarct group (36 +/- 5 g) but not in inferior and non-Q wave anterior infarct groups because of the smaller infarct weights (8 +/- 3 g, 13 +/- 6 g, respectively). Infarct area calculated from thallium-201 tomography significantly correlated with left ventricular ejection fraction in both recent (less than 2 weeks) and older (2-week- to 6-month-old) infarct groups (r = -0.969, P less than 0.001; r = -0.860, P less than 0.001, respectively), whereas there was a significant negative correlation between infarct weight and left ventricular ejection fraction in the recent infarct group (r = -0.731, P less than 0.05) but not in the older infarct group. Thus, antimyosin tomography can detect myocardial necrosis with a high sensitivity regardless of infarct age, size, and location. However, the accumulation might be affected by infarct age and correspond to necrotic mass but not necessarily to infarct volume itself at a later stage probably because of the presence of necrosed and scarred tissues in infarcted myocardium.     

Pericarditis in acute myocardial infarction: characterization and clinical significance

To determine the significance of pericarditis following acute myocardial infarction, the hospital course and 12-month follow-up were analyzed in 703 patients enrolled in the Multicenter Investigation of the Limitation of Infarct Size (MILIS). Pericarditis, defined by the detection of a pericardial rub, occurred in 20% of the patients (n = 141) and was more likely to follow Q wave than non-Q wave infarction (25% vs 9%, p less than 0.001). Patients with pericarditis experienced more serious myocardial damage compared to those without pericarditis, as evidenced by a larger infarct size (25 +/- 1 vs 17 +/- 1 MB-CK gm-Eq/m2, p less than 0.001), a lower admission left ventricular ejection fraction (42 +/- 1% vs 48 +/- 1%, p less than 0.001), and a higher incidence of congestive heart failure (47% vs 26%, p less than 0.001) and atrial tachyarrhythmias (16% vs 10%, p less than 0.05). When patients were classified by the presence of Q or non-Q wave infarction, these differences persisted although statistical significance was not always achieved due to smaller sample size. Mortality at 12-month follow-up for patients with pericarditis was 18% compared with 12% for patients without pericarditis (p = 0.055). This mortality difference could be accounted for in part by the lower ventricular ejection fraction in patients with pericarditis (p = 0.20 after adjustment).     

Acute non-Q wave myocardial infarction associated with early ST segment elevation: evidence for spontaneous coronary reperfusion and implications for thrombolytic trials

The clinical significance of early ST segment elevation in patients with non-Q wave infarction is unknown. Therefore, 150 consecutive patients with creatine kinase isoenzyme-confirmed acute uncomplicated myocardial infarction who had ST segment elevation of 1 mm or more in at least two contiguous leads on the admission electrocardiogram were analyzed. None received thrombolytic therapy or acute coronary angioplasty. Predischarge angiography, radionuclide ventriculography and exercise thallium-201 scintigraphy were performed 10 +/- 3 days after myocardial infarction. Based on serial electrocardiograms (on days 1, 2, 3 and 10), all 150 infarcts were classified as Q wave (n = 115 [77%]) or non-Q wave (n = 35 [23%]). Although patients with Q wave infarction exhibited greater ST elevation, the amount observed in the non-Q wave group was appreciable, as reflected by the number of leads with ST elevation (3.8 +/- 1.8 versus 3.1 +/- 1.2, p = 0.007) and the sum of the ST elevation (9.6 +/- 7.4 versus 6.2 +/- 6.2 mm, p = 0.016). When compared with the Q wave group, patients with non-Q wave infarction had a shorter time to peak creatine kinase (23.0 +/- 9.1 versus 15.8 +/- 7.9 hours, p = 0.0001), a higher infarct vessel patency rate (24 versus 57%, p = 0.001), lower peak creatine kinase values based on 4 hour sampling (1,372 +/- 964 versus 664 +/- 924 IU/liter, p = 0.0002) and a higher left ventricular ejection fraction (46 +/- 12% versus 54 +/- 9%, p = 0.0003).(ABSTRACT TRUNCATED AT 250 WORDS)     

Short- and long-term clinical outcome after Q wave and non-Q wave myocardial infarction in a large patient population

Prognosis for patients with non-Q wave myocardial infarction is controversial although a number of studies have shown a less favorable outlook after hospital discharge for patients with non-Q wave than for those with Q wave infarction. Therefore, the in-hospital and 1-year prognosis was investigated in a sufficiently large patient population (n = 2,024) to allow stratification by subgroups, in particular by age and previous myocardial infarction. Patients with non-Q wave infarction (n = 444; 22% of the total study population) were somewhat older (65 vs. 63 years, p less than 0.001) and had an increased incidence of previous myocardial infarction (46% vs. 24%, p less than 0.001) and congestive heart failure (21% vs. 8%, p less than 0.001) than patients with Q wave infarction. In-hospital mortality of patients with non-Q wave infarction was lower (8.1% vs. 11.5%; p less than 0.06), whereas their 1-year mortality after hospital discharge was significantly higher (13.7% vs. 9.2%, p less than 0.05) than for patients with Q wave infarction. However, total mortalities at 1 year were nearly equal. When patients were subgrouped by presence or absence of a previous myocardial infarction, patients in both subgroups exhibited mortality patterns typical of the entire population with Q wave or non-Q wave infarction. However, when stratified by age and previous infarction, in-hospital mortality for patients with non-Q wave infarction was significantly lower only in patients older than 70 years of age. Similarly, the higher mortality after hospital discharge in patients with non-Q wave infarction occurred only in patients older than 70 years of age without previous myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

The relationship between 1-year mortality and infarct location in patients with non-Q wave myocardial infarction.

The association between 1-year mortality and infarct location was evaluated in 544 patients with acute non-Q wave myocardial infarction. Infarcts were anterior (alone or including other locations) in 51.1% (n = 278) of cases, localizable but not anterior 29.6% (n = 161) of the time, and nonlocalizable in 19.3% (n = 105) of patients. One-year actuarial mortality (73 deaths) was 16.9% in the anterior group, 13.3% in the nonanterior group, and 6.8% in nonlocalizable patients (p = 0.037). Anterior and localizable nonanterior mortality were similar (p = 0.367). However, there were differences when mixed location infarcts were excluded. Mortality in the inferior infarction only group (2.8%, n = 36) was less than in the lateral infarction only group (16.8%, n = 79, p = 0.041) and almost significantly less than in the anterior only group (15.1%, n = 62, p = 0.064). The positive prognosis in the inferior infarction only group may be associated with the low rate of ST depression among these patients compared with those with other infarct locations (p less than 0.0001). Mortality among localizable infarcts (15.5%) was greater than among those that were nonlocalizable (6.8%, p = 0.021). Despite the low overall risk of the nonlocalizable infarcts, 41.9% (n = 44) of these patients developed at least one important risk factor while in hospital.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic implications of an early peak in plasma MB creatine kinase in patients with acute myocardial infarction

To determine the prognostic implications of an early peak in plasma MB creatine kinase (MB CK) in patients with acute myocardial infarction who were not treated with an acute intervention, 342 patients with myocardial infarction confirmed by MB CK were retrospectively studied. The patients were classified into those with an early peak MB CK (less than or equal to 15 hours after the onset of symptoms, n = 84) and those with a late peak MB CK (greater than 15 hours after the onset of symptoms, n = 258). Patients with an early peak MB CK were slightly older, were more frequently female and had a higher incidence of prior myocardial infarction, congestive heart failure and arrhythmias compared with patients with a late peak MB CK. Patients with an early peak MB CK more frequently presented with ST segment depression (23 versus 11%, p less than 0.01), with anterior location of ischemia or infarction (71 versus 52%, p less than 0.01) and with a lower mean left ventricular ejection fraction (41.4 versus 47.4%, p less than 0.01). Despite more extensive left ventricular dysfunction at initial presentation, patients with an early peak MB CK had a smaller mean MB CK infarct size index (12.6 versus 18.9 g-Eq/m2, p less than 0.01), with no difference in the incidence of in-hospital complications, including death. The early left ventricular dysfunction improved in the patients with an early peak MB CK, evidenced by a 4.5% increase in ejection fraction from admission to 10 days after infarction, whereas the ejection fraction did not improve in patients with a late peak MB CK. However, the patients with an early peaking MB CK had myocardium in jeopardy as reflected by a higher incidence of ST segment depression and a decrement in the global left ventricular ejection fraction with exercise. The 4 year life table estimate for the rate of recurrent myocardial infarction after hospital discharge was higher in patients with an early peak MB CK (33 versus 22%, p less than 0.05), with an even more striking difference in the 4 year estimate for the rate of fatal recurrent infarction (20 versus 8%, p less than 0.001). The 4 year mortality estimate was markedly higher in hospital survivors with an early peak MB CK than in those with a late peak (47 versus 19%, p less than 0.0001) and, even after adjustment for differences in baseline characteristics, the residual excess mortality in those with an early peak was still significant (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)     

Intravenous nitroglycerin therapy to limit myocardial infarct size, expansion, and complications. Effect of timing, dosage, and infarct location

To determine 1) whether the effect of intravenous nitroglycerin (NG) therapy during acute myocardial infarction on creatine kinase infarct size is influenced by infarct location (anterior vs. inferior), timing (therapy less than 4 hours vs. greater than or equal to 4 hours after onset of pain), and dose response (mean blood pressure greater than or equal to 80 mm Hg vs. less than 80 mm Hg during the first 12 hours) and 2) whether NG therapy modifies infarct expansion, 310 patients were randomly allocated to NG (n = 154) and control (n = 156) groups. NG infusion was titrated to lower mean blood pressure by 10% in normotensive and 30% in hypertensive patients, but not below 80 mm Hg, and was maintained for 39 hours. Measurements included clinical variables, creatine kinase infarct size (geq) as well as left ventricular (LV) asynergy, LV ejection fraction, expansion index, and thinning ratio on serial two-dimensional echocardiography. Compared with controls, creatine kinase infarct size was less in the NG group (41 vs. 55 geq, p less than 0.001), in anterior (44 vs. 58 geq, p less than 0.05), and inferior (39 vs. 53 geq, p less than 0.025) NG subgroups, and in early than late NG subgroups (43% vs. 22% decrease). Other indexes of infarct size also improved (p less than or equal to 0.05) with NG compared with controls. Thus, by 10 days, LV asynergy was 40% less, LV ejection fraction was 22% more, and Killip class score was 41% less. A negative effect of mean blood pressure less than 80 mm Hg with NG was reflected in these indexes. In addition, expansion index increased (p less than 0.001) by 31% and thinning ratio decreased (p less than 0.001) by 17% in controls by 10 days but remained unchanged with NG. Infarct-related major complications were less frequent in the NG than the control groups: infarct expansion syndrome (2% vs. 15%, p less than 0.0005), LV thrombus (5% vs. 22%, p less than 0.0005), cardiogenic shock (5% vs. 15%, p less than 0.005), and infarct extension (11% vs. 22%, p less than 0.025). Mortality was less in NG than in control groups in-hospital (14% vs. 26%, p less than 0.01), at 3 months (16% vs. 28%, p less than 0.025) and 12 months (21% vs. 31%, p less than 0.05), but this advantage was only found in the anterior subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Natural history of left ventricular size and function after acute myocardial infarction. Assessment and prediction by echocardiographic endocardial surface mapping

To investigate the natural history of regional dyssynergy and left ventricular size after myocardial infarction, 57 patients with a first Q wave myocardial infarction (18 anterior, 35 inferior, and four apical by echocardiography) were studied by two-dimensional echocardiography and compared with 30 control patients. Measurements from the echocardiograms were used to construct maps of the left ventricular endocardial surface from which the endocardial surface area index (ESAi) and the percent of the endocardial surface area involved by abnormal wall motion (%AWM) were calculated. The maps from entry and 3-month echocardiograms were used to classify patients based on changes in ESAi and abnormal wall motion. Two subgroups of patients were identified at entry--those with a normal ESAi (group 1, n = 50) and those with an increased ESAi (group 2, n = 7). Group 1 patients was subdivided at 3 months by changes occurring in ESAi (1A, 5% increase [n = 19]; 1B, no change [n = 23]; 1C, 5% decrease [n = 8]). The increase in ESAi (64.9 +/- 5.2 to 75.4 +/- 7.5 cm2/m2, p less than 0.0001) in group 1A was associated with global ventricular dilatation (n = 11) and clinically silent infarct extension (n = 8). Groups 1B and 1C were composed predominantly of patients with inferior infarctions, and all exhibited either no change or a significant decrease in infarct size (infarct regression). Group 2 patients demonstrated a continued increase in ESAi by 3 months (88.2 +/- 10.0 to 101.4 +/- 15.5 cm2/m2, p less than 0.007). This group comprised only patients with anterior infarctions, and all exhibited infarct expansion at the left ventricular apex. The changes in left ventricular size and functional infarct size are heterogeneous after acute myocardial infarction and relate to the initial endocardial surface area, infarct location, and functional infarct size.     

Progressive changes in ventricular structure and function during the year after acute myocardial infarction.

To investigate the long-term changes in left ventricular structure and function after myocardial infarction, 51 patients with a first myocardial infarction (17 anterior, 23 inferior, and 11 non-Q wave) were studied by two-dimensional echocardiography at the time of entry into the hospital, at 3 months, and 1 year after infarction. The left ventricular endocardial surface was reconstructed from these echocardiograms, and the endocardial surface area (ESA) index (in cm2/m2) and area of abnormal wall motion (AWM in cm2) were quantitated. Despite different trends in the ESA index between entry and 3-month values in those with and without early infarct expansion, a decrease in the ESA index from 3 months to 1 year was noted in anterior and non-Q wave infarctions (anterior with early expansion: 96.3 +/- 8.6 to 81.5 +/- 4.2 cm2/m2, p less than 0.05; anterior without early expansion: 59.7 +/- 2.0 to 54.7 +/- 2.0 cm2/m2, p less than 0.01; non-Q wave: 64.1 +/- 3.5 to 57.9 +/- 4.4 cm2/m2, p less than 0.01). The mean decline in ESA from 3 months to 1 year of 8.9 +/- 2.5 cm2 was independent of initial infarct size. Regional function, as represented by the area of AWM, was also improved but the timing of the improvement was related to the location and size of the infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Post-myocardial infarction exercise testing. Non-Q wave versus Q wave correlation with coronary angiography and long-term prognosis

BACKGROUND. The presence or absence of baseline diagnostic Q waves has been believed to compromise the accuracy of standard exercise electrocardiography in identifying severe coronary artery disease (three-vessel and/or left main disease); therefore, a retrospective analysis was performed using a personal computer data base of exercise test responses and cardiac catheterization results to evaluate this premise, and follow-up was performed to observe how Q waves and/or severe coronary disease impacted on survival. METHODS AND RESULTS. Two hundred fifty-three male patients who had survived a myocardial infarction were studied. Patients on digitalis, those with left bundle branch block or left ventricular hypertrophy on their baseline electrocardiogram, those with previous revascularization procedures, and those with significant valvular or congenital heart disease were excluded. All patients performed either a low-level predischarge or a sign/symptom limited exercise test and underwent diagnostic coronary angiography within 32 days of each test (range, 0-90 days). Long-term follow-up on patients was performed for an average of 45 months (+/- 17 months). Group NQMI comprised 103 post-myocardial infarction patients lacking Q waves at the time of exercise testing and group QMI comprised 150 patients who developed Q waves with their myocardial infarction. The cut points of greater than or equal to 1 mm (chi 2 = 14.39, p less than 0.001) and greater than or equal to 2 mm (chi 2 = 26.11, p less than 0.001) of exercise-induced ST segment depression were reliable markers of severe coronary disease in Q wave infarct survivors. This was also true for non-Q wave infarct survivors as greater than or equal to 1 mm (chi 2 = 6.02, p = 0.01) and greater than or equal to 2 mm (chi 2 = 4.37, p = 0.04) of ST segment depression were reliable markers of severe coronary disease. Receiver operating characteristic curve analysis revealed that exercise-induced ST segment depression had discriminating power for the identification of severe coronary artery disease in both the Q wave myocardial infarction patients (area = 0.735, z = 4.47, p less than 0.001) and the non-Q wave infarct patients (area = 0.700, z = 3.20, p less than 0.001). After 4.4 years of cumulative follow-up, patients with severe coronary disease had an infarct-free survival rate of 72% (95%, CI, 50.0-86.0%), whereas those without severe disease had an 86% (95% CI, 76.5-91.5%) infarct-free survival rate (Cox chi 2 = 4.00, p = 0.045). Non-Q wave patients had an infarct-free survival rate of 81% (95% CI, 66.0-89.5%), whereas those with Q waves had an infarct-free survival rate of 85% (95% CI, 73.9-91.3%) (Cox chi 2 = 0.0005, p = NS). CONCLUSIONS. The presence or absence of diagnostic Q waves has no significant effect on the ability of the exercise electrocardiogram to identify severe coronary artery disease in survivors of myocardial infarction. Long-term infarct-free survival of patients with myocardial infarction is more related to the presence of severe coronary disease rather than if they suffered a non-Q wave or Q wave infarction.     

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.     

Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic dysfunction, infarct size and location

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.     

Survival after hospital discharge in matched populations with inferior or anterior myocardial infarction

Prognostic differences between patients with anterior or inferior myocardial infarction are often related to such variables as previous infarction or the size of the myocardial infarct. We examined the determinants of mortality in 997 hospital survivors of acute Q wave infarction (anterior in 449, inferior in 548) who, although not preselected, were well matched with respect to age, sex and prior infarction or congestive heart failure. Additionally, there was no significant difference in peak serum creatine kinase (CK) between the groups with anterior and inferior infarction (1,459 +/- 1,004 versus 1,357 +/- 1,036). Among the patients with anterior infarction who died during the 1 year follow-up period, 56% died in the first 60 days after hospital discharge compared with 18% of those without inferior infarction (p less than 0.01). Survival curves then became nearly identical at 3 months, and remained so until 1 year when the total mortality rate was 10% for the anterior and 7% for the inferior infarction group (p = NS). Variables associated with heart failure during the hospital phase were more prevalent in anterior infarction, but rales above the scapulae during the hospital stay (p less than 0.0001) and ventricular gallop at the time of discharge (p less than 0.0001) were the top two predictors of 1 year mortality by both univariate and multivariate analysis in inferior infarction. Age (p less than 0.0001) and peripheral edema (p less than 0.0001) were the strongest predictors of mortality in anterior infarction. Previous infarction, although just as common in the group with anterior infarction, was present at 1 year in 48% of nonsurvivors of the group with inferior infarction compared with only 19% of survivors (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of right bundle branch block on short- and long-term survival after acute anterior myocardial infarction

The impact of right bundle branch block on long-term prognosis after anterior wall myocardial infarction is unclear. In 932 patients with Q wave anterior infarction, the short- and long-term prognostic significance of the presence of right bundle branch block was analyzed. Compared with 754 patients without block, 178 patients with right bundle branch block after myocardial infarction showed an increased incidence of left ventricular failure (72% versus 52%, p less than 0.001) and increased in-hospital (32% versus 8%, p less than 0.001) and 1 year after hospital discharge (17% versus 7%, p less than 0.001) cardiac mortality rates. The presence of right bundle branch block was an independent predictor of increased in-hospital and 1-year mortality when entered in a multivariate analysis. However, the absence of left ventricular failure identified a subgroup of patients with right bundle branch block with low in-hospital (4%) and 1 year postdischarge (5%) cardiac mortality rates comparable with those of patients with neither failure nor right bundle branch block (1.7% and 4.8%, respectively). In the presence of left ventricular failure, patients with associated right bundle branch block had higher in-hospital (43% versus 14%, p less than 0.01) and 1 year postdischarge (24% versus 9%, p less than 0.01) cardiac mortality rates than those of patients with failure but no right bundle branch block. Thus, the presence of right bundle branch block after anterior myocardial infarction is an independent marker of poor prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Multicenter trial of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) in acute myocardial infarction: effects on infarct size and left ventricular function

Two hundred thirty-one patients with a first acute myocardial infarction were randomly allocated within 5 h after the onset of symptoms either to treatment with anisoylated plasminogen streptokinase activator complex (APSAC), 30 U over 5 min, or to conventional heparin therapy, 5,000 IU in a bolus injection. Heparin was reintroduced in both groups 4 h after initial therapy at a dosage of 500 IU/kg per day. One hundred twelve patients received APSAC and 119 received heparin within a mean period of 188 +/- 62 min after the onset of symptoms. Both groups were similar in age, location of the acute myocardial infarction, Killip functional class and time of randomization. Elective coronary arteriography was performed on an average of 4 +/- 1.2 days after initial therapy. Follow-up radionuclide angiography and thallium-201 single photon emission computed tomography were performed before hospital discharge. Infarct size was estimated from single photon emission computed tomography and expressed as a percent of total myocardial volume. The patency rate of the infarct-related artery was 77% in the APSAC group and 36% in the heparin group (p less than 0.001). Left ventricular ejection fraction determined from contrast angiography was significantly higher in the APSAC group than in the heparin group. This was true for the entire study group (0.53 +/- 0.13 versus 0.47 +/- 0.12; p = 0.002) as well as for the subgroups of patients with anterior and inferior wall infarction (0.47 +/- 0.13 versus 0.40 +/- 0.11; p = 0.04 and 0.56 +/- 0.10 versus 0.51 +/- 0.11; p = 0.02, respectively). At 3 weeks, the difference remained significant for the anterior myocardial infarction subgroup. A significant 31% reduction in infarct size was found in the APSAC group (33% for the anterior infarction subgroup [p less than 0.05] and 16% for the inferior infarction subgroup [p = NS]). A close inverse relation was found between the values of left ventricular ejection fraction and infarct size (r = -0.73, p less than 0.01). By the end of a 3 week follow-up period, seven APSAC-treated patients and six heparin-treated patients had died. In conclusion, the early infusion of APSAC in acute myocardial infarction produced a high early patency rate, significant limitation of infarct size and significant preservation of left ventricular systolic function, mainly in anterior wall infarction.     

Significance of rest technetium-99m sestamibi imaging for the prediction of improvement of left ventricular dysfunction after q wave myocardial infarction: importance of infarct location adjusted thresholds

Objective. The value of rest technetium-99m (Tc-99m) sestamibi scintigraphy under oral nitrate medication to predict myocardial viability was examined in patients with chronic infarcts.Background. The value of rest Tc-99m sestamibi to predict viability in infarct regions has not been fully established because significant underestimation of viability, especially in the inferior myocardial wall, has been reported.Methods. Forty patients with Q wave myocardial infarction underwent Tc-99m sestamibi single-photon emission computed tomography under nitrate medication before revascularization of the infarct-related artery. Wall motion was quantified from paired angiograms before and 4 months after revascularization. Tracer uptake was quantified in the central infarct region identified on the angiogram.Results. The average Tc-99m sestamibi uptake in the central infarct region of patients with anterior infarcts and improvement of left ventricular function was significantly higher (68 ± 12%, mean ± SD) than in patients without improvement of function (40 ± 14%, p < 0.02). The average Tc-99m sestamibi uptake in the central infarct region of patients with improvement of function and inferior infarcts was significantly lower (43 ± 7%) than in patients with anterior infarcts (68 ± 12%, p < 0.003), but was significantly higher than in patients with inferior infarction and no improvement of function (31 ± 7%, p < 0.02). Using an infarct location adjusted optimal threshold (50% for anterior infarcts, 35% for inferior infarcts), Tc-99m sestamibi had a positive predictive value of 90% and a negative predictive value of 91% for improvement of left ventricular function.Conclusion. Quantitative rest Tc-99m sestamibi scintigraphy after oral nitrates reliably predicts improvement of left ventricular function after revascularization if infarct location adjusted thresholds are used.     

High-risk subgroups of patients with non-Q wave myocardial infarction based on direction and severity of ST segment deviation

To determine the significance of the direction of ST segment deviation on admission of patients who evolved non-Q wave myocardial infarction (MI), 97 patients with initial ST segment depression were compared to 207 patients with initial ST segment elevation. Patients with ST segment depression developed smaller infarcts than those with ST segment elevation (creatine kinase MB isoenzyme 8.2 vs 13.3 gmEq/m2, p less than 0.002), but had a lower left ventricular ejection fraction on admission (44% vs 51%, p less than 0.001), more in-hospital complications, and a higher cumulative 1-year mortality (29% vs 11%, p less than 0.001) that could be accounted for by an excess of adverse baseline characteristics. Although a severity index (combining magnitude and extent of the initial ST segment deviation) was not useful for discriminating prognosis of patients with non-Q wave MI who presented with ST segment depression, it was useful in identifying a subgroup of patients with ST segment elevation with an adverse prognosis. The poor outcome of patients with non-Q wave MI presenting with either ST segment depression or severe ST segment elevation on admission suggests that patients in these subgroups should receive close surveillance and should possibly be considered for aggressive therapy.