Influence of infarct-zone viability on left ventricular remodeling after acute myocardial infarction

BACKGROUND: The relation between residual myocardial viability after acute myocardial infarction (AMI) and ventricular remodeling has yet to be fully elucidated. We hypothesized that the presence of residual viability would favorably influence left ventricular remodeling after AMI and that serial changes in left ventricular dimensions might be related to the extent of myocardial viability in the infarct zone. METHODS AND RESULTS: Ninety-three patients with a first AMI successfully treated with primary coronary angioplasty underwent two-dimensional echocardiography within 24 hours of admission and low-dose dobutamine echocardiography at a mean of 3 days after AMI. Two-dimensional echocardiography and coronary angiography were obtained in all patients 1 and 6 months after coronary angioplasty. On the basis of dobutamine echocardiography responses, patients were divided in two subsets: those with (n=48; group I) and those without (n=45; group II) infarct-zone viability. There was no difference in minimal lesion diameter and infarct-related artery patency at 1 and 6 months between the two groups. Group II patients had significantly greater end-diastolic (76+/-18 versus 53+/-14 mL/m2; P<.0003) and end-systolic (42+/-17 versus 22+/-11 mL/m2; P<.0003) volumes at 6 months than did patients in group 1. The extent of infarct-zone viability was significantly inversely correlated with percent changes in end-diastolic volumes at 6 months (r=-.66; P<.000001) and was the most powerful independent predictor of late left ventricular dilation. CONCLUSIONS: After reperfused AMI, the degree of left ventricular dilation, when it occurs, is inversely related to the extent of residual myocardial viability in the infarct zone. Thus, the absence of residual infarct-zone viability discriminates patients who develop progressive left ventricular dilation after reperfused AMI from those who maintain normal left ventricular geometry.     

Effects of transdermal nitroglycerin on left ventricular function after acute myocardial infarction

Progressive left ventricular dysfunction in acute myocardial infarction patients is associated with a poor prognosis. It has been shown that some therapeutic measures which have the potential for limiting the infarct size and preserving ventricular function, are also able to reduce the incidence of congestive heart and improve survival. The aim of this protocol was to assess the effects of transdermal nitroglycerin administered within 72 hours after the onset of acute myocardial infarction and for the following 6 months, on left ventricular function. A total of 98 consecutive acute myocardial infarction patients were randomly allocated, within 72 hours of onset of symptoms, to a double-blind 6-month-therapy with either 10 mg/24 hour transdermal nitroglycerin or placebo. Patients underwent two-dimensional echocardiography at entry, after 2 weeks, 3 months and 6 months. In the nitroglycerin group, end-diastolic volume increased during the follow-up (+6.7%, p < 0.05) while end-systolic volume remained nearly unchanged; ejection fraction and stroke volume increased progressively (+6.3%, p < 0.05, +14.2%, p < 0.05, respectively) and a important reduction of percent of dyssynergic segments was present (-19.2%, p < 0.005). In the placebo group end-diastolic volume and end-systolic volume slightly increased during the follow-up (+2% and +4.9% respectively); ejection fraction and stroke volume remained nearly unchanged during the study; percent of dyssynergic segments showed an important decrease after 2 weeks and 6 months (-21.3%, p < 0.005). A clinically relevant increase (> 20%) in ejection fraction was present more frequently in the nitroglycerin than in the placebo group (p < 0.001). In conclusion, the early (within 72 hours) and prolonged (6 months) administration of transdermal nitroglycerin in acute myocardial infarction improves ejection fraction and stroke volume but does not modify ventricular remodeling.     

Comparative accuracy of cross-sectional echocardiography and cineventriculography for left ventricular evaluation after myocardial infarction

223 patients with a previous myocardial infarction (MI) 29-68 years old, have been studied in a double-blind manner both by 2D-Echocardiography and cineventriculography. 5 cross-sectional views and 2 angiographic projections have been employed in order to assess the presence of aneurysm and the motion of the left ventricle. The left ventricle has been divided into 5 anatomic regions: interventricular septum, anterolateral, posterolateral, apical and inferior walls. By cineangiography an aneurysm was diagnosed in 89 patients (one pseudoaneurysm); by 2D-Echo in 83 patients an aneurysm was diagnosed, whereas in the 6 remaining patients the Echocardiogram was nondiagnostic (specificity 100%, sensitivity 93%). Concerning regional motion characteristics, 997 (89%) of 1115 regions were visualized and 905 (91%) correctly identified according to the angiographic findings. Of 92 discrepancies (9%): 64 were attributed to 2D-Echo (69%) and 28 (31%) were attributed to cineangiography; most of the discrepancies attributed to echo resulted from minor grades of asynergy which caused unresolved disagreements between the Echo and angiography findings. It is concluded that Cross-sectional echocardiography is a valuable tool for the diagnosis of aneurysm of the left ventricle (specificity 100% and sensitivity 93%) and for the study of wall motion characteristics. In cases with generalized abnormality of left ventricle motion, resulting in a picture of congestive cardiomyopathy, 2D-Echo can be a substitute for cineangiography. In all other instances both techniques can provide more complete information on ventricular wall abnormalities.     

Post-mastectomy seroma: a new look into the aetiology of an old problem

Postmastectomy seroma (PMS) remains an unresolved quandary as the risk factors for its formation have still not been identified. Sixty-four consecutive female patients undergoing Halsted mastectomy were prospectively studied for this purpose. The risk factors that were studied included age and weight, diabetes, hypertension, tumour (size and location) and nodal (positive or negative) status and the use of perioperative blood transfusion. Additionally, the effect of PMS on total hospital drainage (THD), post-operative hospital stay and other wound-related complications were assessed. The incidence of PMS in this study was 28%, and those patients with PMS were designated as group A while the remaining patients were designated as group B. Group A patients were significantly older (P < 0.02) and heavier (P < 0.05) than group B patients; also, there were significantly (P < 0.0001) greater number of hypertensive patients in group A than in group B. In terms of other risk factors the two groups were statistically similar. Group A patients had significantly greater (P < 0.01) amount of THD than group B patients. Although no septic complications were observed as a result of seroma, its presence significantly (P < 0.0001) lengthened the post-operative hospital stay in group A patients. It is concluded that (1) PMS is a common problem, (2) its occurrence significantly increases the post-operative hospital stay, and (3) hypertension is perhaps the most important risk factor for its causation. Hypertension contributes to seroma formation, probably by way of prolonged oozing from the large mastectomy wound.(ABSTRACT TRUNCATED AT 250 WORDS)     

Assessment of regional left ventricular wall stress after myocardial infarction by echocardiography-based structural analysis

OBJECTIVES: The objective of this study was to determine the distribution of regional left ventricular (LV) wall stress after myocardial infarction (MI). BACKGROUND: After a large MI, structural changes occur in the heart that ultimately may lead to alterations in LV size and shape, a process generally referred to as ventricular remodeling. Regional variation in myocardial wall stress may be responsible for initiation of physiologic and cellular changes that result in myocardial hypertrophy, dilatation, and remodeling after MI. Simplified geometric analytic methods of estimating global LV wall stress cannot determine regional variation such as that occurring after MI. METHODS AND RESULTS: To assess regional LV wall stress after MI, we applied the finite element method to patient-specific end-systolic LV models generated from echocardiographic imaging. After validation by comparison with analytic solutions of LV wall stress in idealized ventricles, LV models were constructed from rotated orthogonal apical images from 13 normal volunteers, 16 patients with recent (<4 days) anterior MI, and 7 patients with recent infero-posterior MI. The mean Von Mises stress was calculated for the entire LV and for 5 separate regions of the LV. Von Mises LV wall stress was increased globally in patients with anterior MI (211 +/- 46 kdyne/cm2; P < .002) or infero-posterior MI (175 +/- 23 kdyne/cm2; P = .04) compared with normal patients (144 +/- 57 kdyne/cm2). Global wall stress correlated directly with ejection fraction (P < .0001) and inversely with wall motion index (P < .004) in patients with anterior MI. Wall stress in the apical regions was increased by a factor of 2.3 in patients with anterior MI (P < .0001), whereas other regions did not differ from normal patients. There were no individual regions that were significantly different from normal in patients with infero-posterior MI. CONCLUSIONS: Anterior MI is associated with an increase in apical end-systolic wall stress compared with normal and infero-posterior MI. This may be an important stimulus for LV remodeling after anterior MI.     

Acquired left ventricular to right atrial intracardiac shunt after myocardial infarction: a case report and review of the literature

A patient without a history of heart disease was seen in our institution after 3-week history of progressive weakness, dyspnea, and orthopnea. Transthoracic echocardiography demonstrated inferoposterobasal akinesis and a left ventricular to right atrial shunt through the coronary sinus, which was confirmed on cardiac catheterization. This is only the second case reported in the English-language literature documenting this rare shunt after a myocardial infarction.     

Comparison of left and right ventricular function in acute myocardial infarction

Pulmonary arterial end-diastolic and mean right atrial pressures were compared in 25 patients with acute myocardial infarction and in one patient with unstable angina. No consistent relationship was observed between these pressures. Simultaneous ventricular function curves relating the stroke work of each ventricle to its respective filling pressure were constructed on 34 occasions, dextran infusion or diuresis being used to alter the filling pressure. The curves from each ventricle were described mathematically by a quadratic (parabolic) function as well as by a straight line function and then compared by canonical correlation analysis. Alterations in the left ventricular function curves occurred with and without depression or right ventricular function curves. These hemodynamic measurements demonstrate that acute myocardial infarction can alter the relationship between left and right ventricular function.     

Heterogeneous fate of perfusion and contraction after anterior wall acute myocardial infarction and effects on left ventricular remodeling

After acute myocardial infarction, patency of infarct vessel and extent of left venticular (LV) dysfunction are major determinants of ventricular remodeling. Spontaneous, delayed reperfusion in the infarct zone occurs in a sizeable number of patients well after the subacute phase. The aim of this study was to determine the relation between the occurrence of this spontaneous, delayed reperfusion and LV remodeling. In 84 patients, resting LV volumes, topography, regional function, and perfusion were quantitatively evaluated by 2-dimensional echocardiography and sestamibi tomography 5 weeks (study 1) and 7 months (study 2) after anterior Q-wave infarction. At study 2, LV end-diastolic volume increased by > 15% in 17 patients (20%, LV remodeling); they had already had at study 1 significantly larger LV volumes, more severe hypoperfusion and wall motion abnormalities, and greater regional dilation than patients with stable LV volumes. Delayed reperfusion occurred in 8 of 17 patients with and in 42 of 67 patients without LV remodeling (47% vs 63%; p=NS). At study 2, LV regional dilation and end-diastolic volumes were stable in patients with, but increased in patients without, spontaneous reperfusion (from 25+/-24% to 29+/-26% at study 2 [p<0.05] and from 65+/-14 to 68+/-18 ml/m2 [p <0.05]). At multivariate analysis, however, regional ventricular dilation at study 1 was the sole predictor of further LV remodeling. Thus, after acute myocardial infarction, spontaneous reperfusion occurring after 5 weeks plays only a minor role in influencing LV remodeling. Benefits from delayed reperfusion seem limited to patients with preserved LV volumes; patients with an enlarged left ventricle 5 weeks after acute infarction are prone to further LV remodeling, irrespective of delayed reperfusion.     

Early angiotensin converting enzyme inhibitor therapy after experimental myocardial infarction prevents left ventricular dilation by reducing infarct expansion: a possible mechanism of clinical benefits

OBJECTIVE: To examine the effects of early angiotensin-converting enzyme (ACE) inhibitor therapy after myocardial infarction on infarct expansion in an experimental rat model. BACKGROUND: ACE inhibitor therapy within 24 h of acute myocardial infarction (AMI) reduces mortality by unknown mechanism(s). METHODS: Rats underwent permanent coronary artery occlusion. A treated group received enalapril (1.9+/-0.2 mg/kg) daily in drinking water beginning 2 h after coronary artery occlusion, a time too late to reduce infarct size. Rats were sacrificed 2 days or 2 weeks after myocardial infarction. Hearts were arrested and fixed at a constant pressure, then sectioned and photographed for morphometric analysis. RESULTS: Infarcts in the control group expanded between 2 days and 2 weeks after myocardial infarction (expansion index 0.7+/-0.1 versus 2.5+/-0.4, P< 0.05). However, infarct expansion remained unchanged in the enalapril group between 2 days and 2 weeks after myocardial infarction (expansion index 0.8+/-0.1 versus 1.3+/-0.1, NS). Two weeks after myocardial infarction, the enalapril group had fewer expanded infarcts than the control group (expansion index 1.3+/-0.1 versus 2.5+/-0.4, P< 0.05). While left ventricular volume increased in the control group between 2 days and 2 weeks after myocardial infarction (0.17+/-0.01 ml versus 0.36+/-0.03 ml, P< 0.05), it remained constant in the enalapril group (0.22+/-0.02 ml versus 0.25+/-0.03 ml, NS). Two weeks after myocardial infarction, the left ventricles were larger in the control group than in the enalapril group (0.36+/-0.03 ml versus 0.25+/-0.03 ml, P< 0.05). CONCLUSIONS: Treatment with enalapril initiated 2 h after AMI prevented left ventricular dilation by limiting infarct expansion. This may explain the mechanism by which ACE inhibitor therapy started within 24 h of an AMI improves survival 5-6 weeks after infarction.     

Serial measurements of left ventricular ejection fraction by radionuclide angiography early and late after myocardial infarction

1-Acyl-2-succinyl glycero-3-phosphorylcholine (GPC) was synthesized and its properties described. Although 1-acyl-2-succinyl GPC is a good substrate for succinate dehydrogenase, experiments on the incorporation of [2,3-14C] succinate into mitochondrial lipids gave no evidence to indicate that it is an intermediate in the enzymic oxidation of succinate to fumerate, as has been suggested earlier.     

The heart rate performance curve and left ventricular function during exercise in patients after myocardial infarction

PURPOSE: The aim of the study was to investigate the heart rate turn point (HRTP) in the time course of the heart rate performance curve (HRPC) in patients after myocardial infarction, and the relationship between the HRTP, the left ventricular function, and the second lactate turn point (LTP2). METHODS: We studied the degree and the direction of the HRPC and the left ventricular ejection fraction (LVEF) in 49 male patients 57 +/- 8 d after their first posterior wall infarction (MI). An incremental cycle ergometer test was performed and three phases of energy supply were defined (I: aerobic; II: aerobic-anaerobic transition; III: anaerobic) via blood lactate LA concentration. HRTP and LVEF-turn points (LVEFTP) were assessed by linear turn point analysis. The degree and direction of the deflection of HRPC were described as factor k (k > 0.1: downward deflection; -0.1 < k < 0.1: linear time curse; k < -0.1: upward deflection). The LVEF was determined by RNA. The difference between Pmax and LTP2 was calculated for LVEF (delta LVEF). RESULTS: An HRTP could be found in 44 and a LVEFTP in 47 cases. The HRTP occurred at 85 +/- 17 Watt (W), which correlated (r = 0.95; P < 0.001) with the LTP2 (84 +/- 17 W) and the LVEFTP (84 +/- 17 W, r = 0.93; P < 0.001). From LTP2 to Pmax a significant decrease in LVEF was found. There was a correlation between the percentage of HRmax at the HRTP and k (r = 0.70), as well as delta LVEF (r = 0.56). CONCLUSIONS: To prevent myocardial overloading, it seems to be useful to determine the HRTP, which indicate the workload where LVEF decreases.     

An ovine model of acute myocardial infarction and chronic left ventricular dysfunction

In order to develop and validate an ovine model of myocardial infarction with subsequent impairement of left ventricular function, 15 instrumented sheep underwent selective microembolization of the left coronary arteries with 0.5 mL 90 microns polystyrene beads. Hemodynamics and plasma hormones were measured preembolization (baseline) and then at hours 2, 4, 6, and 12 and days 1, 2, 3, 5 and 7 postembolization. Of the 15 sheep studied, 2 (13%) died on the day of embolization from arrhythmias. In the remaining sheep, left ventricular systolic pressure and stroke work (both P < 0.001) were reduced promptly and remained below basal levels. Mean arterial pressure (P < 0.001) increased initially, then decreased to below basal levels by hour 6. Heart rate (P < 0.001) and left atrial pressure (P < 0.05) were increased while cardiac output was decreased (P < 0.05). Left ventricular ejection fraction at day 7 was reduced (38.8 +/- 3.5 vs 46.0 +/- 3.9% preembolization; P < 0.05). The cardiac enzymes creatine kinase (P < 0.001) and troponin-T (P < 0.001) were increased following microembolization and returned to basal levels by days 2 and 5 respectively. Plasma atrial and brain natriuretic peptides (both P < 0.001) and plasma renin activity (P < 0.005) were all increased following embolization. This ovine model mimics the hemodynamic and neurohumoral features of acute myocardial infarction, resulting in left ventricular dysfunction, and should prove suitable for the study of interventions in a number of these conditions.     

Plasma N-terminal pro-brain natriuretic peptide and adrenomedullin: new neurohormonal predictors of left ventricular function and prognosis after myocardial infarction

BACKGROUND: Newly discovered circulating peptides, N-terminal pro-brain natriuretic peptide (N-BNP) and adrenomedullin (ADM), were examined for prediction of cardiac function and prognosis and compared with previously reported markers in 121 patients with myocardial infarction. METHODS AND RESULTS: The association between radionuclide left ventricular ejection fraction (LVEF) and N-BNP at 2 to 4 days (r=-.63, P<.0001) and 3 to 5 months (r=-.58, P<.0001) after infarction was comparable to that for C-terminal BNP and far stronger than for ADM (r=-.26, P<.01), N-terminal atrial natriuretic peptide (N-ANP), C-terminal ANP, cGMP, or plasma catecholamine concentrations. For prediction of death over 24 months of follow-up, an early postinfarction N-BNP level > or = 160 pmol/L had sensitivity, specificity, positive predictive value, and negative predictive values of 91%, 72%, 39%, and 97%, respectively, and was superior to any other neurohormone measured and to LVEF. Only 1 of 21 deaths occurred in a patient with an N-BNP level below the group median (Kaplan-Meier survival analysis, P<.00001). For prediction of heart failure (left ventricular failure), plasma N-BNP > or = 145 pmol/L had sensitivity (85%) and negative predictive value (91%) comparable to the other cardiac peptides and was superior to ADM, plasma catecholamines, and LVEF. By multivariate analysis, N-BNP but not ADM provided predictive information for death and left ventricular failure independent of patient age, sex, LVEF, levels of other hormones, and previous history of heart failure, myocardial infarction, hypertension, or diabetes. CONCLUSIONS: Plasma N-BNP measured 2 to 4 days after myocardial infarction independently predicted left ventricular function and 2-year survival. Stratification of patients into low- and high-risk groups can be facilitated by plasma N-BNP or BNP measurements, and one of these could reasonably be included in the routine clinical workup of patients after myocardial infarction.     

Independent impact of thrombolytic therapy and vessel patency on left ventricular dilation after myocardial infarction. Serial echocardiographic follow-up

BACKGROUND: It has been shown that successful reperfusion of the infarct-related artery by thrombolysis can prevent left ventricular dilation after acute myocardial infarction; these beneficial effects were detected from several days to several months after infarction. To date, however, no study has shown that these effects can be demonstrated within hours after the onset of infarction. Furthermore, data are scarce on the independent impact of thrombolytic therapy and late vessel patency on ventricular volume and function. The aim of this study was to assess separate effects of thrombolysis and patency of the infarct-related artery on left ventricular size and function by serial two-dimensional echocardiographic examinations. METHODS AND RESULTS: We evaluated 131 consecutive patients with first acute myocardial infarction by two-dimensional echocardiography in the following sequence: days 1, 2, 3, 7, and after 3 and 6 weeks. Intravenous streptokinase was administered in 81 patients, and 50 patients were treated without thrombolysis. Left ventricular end-diastolic volume, end-systolic volume, and ejection fraction were determined from apical two- and four-chamber views using the Simpson biplane formula and normalized to body surface area. Coronary angiography was performed in 107 patients after a mean of 26.0 +/- 20.2 (mean +/- SD) days after infarction. Patency of the infarct-related artery was assessed using TIMI criteria, with 54 considered patent (TIMI 3) and 53 with TIMI grade < 3. On day 1, end-systolic volume was significantly higher in patients not receiving thrombolysis (37.7 +/- 15.3 versus 33.0 +/- 10.6 mL/m2, P = .045). End-systolic volume (ESVi) was significantly higher in patients treated without thrombolysis throughout the study, whereas significant differences in end-diastolic volume (EDVi) were detected from day 3 (P = .041) onward and in ejection fraction (EF) from day 2 (P = .025) onward, all differences becoming progressively more significant with time (6-week values: EDVi, 78.8 +/- 25.4 versus 65.9 +/- 15.7 mL/m2, P = .001; ESVi, 45.4 +/- 22.6 versus 33.9 +/- 15.1 mL/m2, P = .002; EF, 45.1 +/- 11.6% versus 50.2 +/- 10.1%, P = .018). Patients with an occluded infarct-related artery (TIMI < 3) demonstrated highly significant differences at 6 weeks compared with patients with patent vessels (EDVi, 76.8 +/- 24.7 versus 65.2 +/- 15.6 mL/m2, P = .006; ESVi, 44.6 +/- 23.3 versus 31.9 +/- 12.2 mL/m2, P = .001; EF, 45.0 +/- 11.6% versus 52.1 +/- 9.0%, P < .001), but these differences developed more slowly than that seen among the thrombolytic subgroups. Indeed, multivariate analysis demonstrated that thrombolysis was the major determinant of initial volumes (P = .08, .02, and .08 for EDVi, ESVi, and EF, respectively), while vessel patency was the overwhelming determinant of subsequent changes (P = .0033, .0002, and .0024 for EDVi, ESVi, and EF, respectively). Additionally, ventricular volumes were significantly higher and ejection fractions lower in patients with anterior versus inferior infarction, but even adjusting for these differences as well as those associated with age, sex, and initial ventricular volume, the additive and independent impact of thrombolysis and infarct vessel patency persisted. CONCLUSIONS: These data indicate that the beneficial effect of thrombolysis on left ventricular size and function can be demonstrated in the earliest phases of acute myocardial infarction and that subsequent changes are mediated primarily through patency of the infarct-related artery. Thrombolytic therapy and late vessel patency thus have an additive and complementary impact in reducing ventricular dilation after myocardial infarction.     

Association of calcium channel blocker use with increased rate of acute myocardial infarction in patients with left ventricular dysfunction

The Studies of Left Ventricular Dysfunction (SOLVD) assessed the effect of enalapril in patients with systolic left ventricular dysfunction (LVD). We performed retrospective analyses of the association between calcium channel blocker (CCB) use and fatal and nonfatal myocardial infarction (MI) in these patients. MI occurred in 11.5% of 845 patients receiving CCBs versus 7.5% of 2551 patients not receiving CCBs in the enalapril group and in 14.4% of 874 patients receiving CCBs versus 9.3% of 2527 patients not receiving CCBs in the placebo group. By multivariate Cox regression analysis, adjusting for comorbidity, cause and severity of LVD, heart failure, and concomitant drug use, CCB use was an independent predictor of MI (relative risk [RR] 1.37, confidence interval [CI] 1.14 to 1.63). The increase in MI risk was greater among patients with a higher heart rate (RR 1.46, CI 1.14 to 1.86) and lower blood pressure (RR 1.45, CI 1.14 to 1.86). The adjusted risk ratio for all-cause mortality associated with CCB use was 1.14 (CI 1.00 to 1.28; p = 0.0454). In this analysis of patients with LVD, CCB use was associated with significantly increased risk of fatal or nonfatal MI.     

Effect of early enalapril therapy on left ventricular function and structure in acute myocardial infarction

Infarct expansion starts within hours to days after transmural myocardial injury. Previous echocardiographic and left ventriculographic studies demonstrated that angiotensin-converting enzyme (ACE) inhibitor therapy limits left ventricular dilatation, particularly in patients with anterior wall acute myocardial infarction (AMI) or impaired left ventricular function. Forty-three patients with an acute Q-wave AMI were randomized within 24 hours of symptom onset to intravenous enalaprilat (1 mg) or placebo. Patients were then given corresponding oral therapy and followed for 1 month. Predrug and 1-month gated blood pool scans were obtained in 32 patients to evaluate changes in cardiac volumes and ejection fraction. Twenty-three patients underwent magnetic resonance imaging at 1 month to evaluate left ventricular infarct expansion. Blood pressure decreased at 6 hours but returned to baseline in both groups after 1 month of therapy. The change in cardiac volumes from baseline to 1 month differed between the placebo (end-diastolic volume +16 +/- 5 ml, end-systolic volume +8 +/- 6 ml), and enalapril (end-diastolic volume -8 +/- 9 ml and end-systolic volume -14 +/- 7 ml) groups (p < 0.05 vs placebo). Global and infarct zone ejection fractions improved significantly at 1 month in the enalapril group (+6 +/- 3% and 19 +/- 5%, respectively) but did not change over 1 month in the placebo group. Infarct segment length and infarct expansion index by magnetic resonance imaging were significantly less in those treated with enalapril, suggesting less infarct expansion in this group. Thus, early administration of enalaprilat to patients presenting with a first Q-wave AMI prevents cardiac dilatation and infarct expansion.     

Predischarge two-dimensional echocardiographic evaluation of left ventricular thrombosis after acute myocardial infarction in the GISSI-3 study

Left ventricular (LV) thrombosis can be found in patients with acute myocardial infarction (AMI). No wide multicenter trial on AMI has provided information about LV thrombosis until now. The protocol of the GISSI-3 study included the search for the presence of LV thrombosis in patients from 200 coronary care units that did not specifically focus on LV thrombosis. We examined the GISSI-3 database results related to 8,326 patients at low to medium risk for LV thrombi in which a predischarge echocardiogram (9 +/- 5 days) was available. LV thrombosis was found in 427 patients (5.1%): 292 of 2,544 patients (11.5%) with anterior AMI and in 135 of 5,782 patients (2.3%) with AMI in other sites (p <0.0001). The incidence of LV thrombosis was higher in patients with ejection fraction < or = 40% (151 of 1,432 [10.5%] vs 276 of 6,894 [4%]; p <0.0001) both in the total population and in the subgroup with anterior AMI (106 of 597 [17.8%] vs 186 of 1,947 [9.6%]; p <0.0001). Multivariate analysis showed that only the Killip class > I and early intravenous beta-blocker administration were independently associated with higher LV thrombosis risk in the subgroup of patients with anterior AMI (odds ratio 1.75, 95% confidence interval 1.28 to 2.39; odds ratio 1.32, 95% confidence interval 1.02 to 1.72, respectively). In patients with anterior AMI, oral beta-blocker therapy given or not given after early intravenous beta-blocker administration does not influence the occurrence of LV thrombosis. The rate of LV thrombosis was similar in patients treated or not treated with nitrates and lisinopril both in the total population and in patients with anterior and nonanterior AMI. In conclusion, in the GISSI-3 population at low to medium risk for LV thrombi, the highest rate of occurrence of LV thrombosis was found among patients with anterior AMI and an ejection fraction < 40%. Killip class > I and the early intravenous beta-blocker administration were the only variables independently associated with a higher predischarge incidence of LV thrombosis after anterior AMI.