Large ventricular aneurysms occurring after myocardial infarction

We have studied 33 patients with a large ventricular aneurysm complicating an anterior myocardial infarction. The features of myocardial infarction progressing towards an aneurysm were no previous history of coronary disease, severe infarction as shown by the severity of pain and the presence of pericardial rub and heart failure, and large increase in serum levels of cardiac enzymes. A large aneurysm usually follows a large infarction resulting from the total or partial occlusion of the left anterior descending artery, which is involved alone in about half the patients and is associated with lesions of the circumflex and right coronary arteries in the other half. In most cases, standard radiography showed an abnormal cardiac configuration, but in 7 patients (21%) there was no radiological evidence of aneurysm. ST segment elevation (mean 2.7 mm) was reported in all subjects but one. Heart failure was present in most patients and was an indication for surgical treatment in one-third of the patients. A large aneurysm was not a contraindication to operation even when at angiography the aneurysm seemed to occupy almost all the left ventricle. Twenty-one patients were operated upon for resection of the aneurysm with a mortality rate of 14 per cent.     

Coincidence of true and false left ventricular aneurysms after myocardial infarction.

False aneurysm of the left ventricle is a rare complication of myocardial infarction. In this case cross sectional echocardiography demonstrated the presence of both true and false left ventricular aneurysms. This was confirmed at operation when both aneurysms were successfully resected.     

Prognosis following sustained ventricular tachycardia occurring early after myocardial infarction

Eighty-seven patients with sustained ventricular tachycardia (VT) between 3 and 90 days after acute myocardial infarction (AMI) were evaluated to define factors associated with a high risk of arrhythmia recurrence or death. Most patients had poor left ventricular function (mean ejection fraction 29 +/- 12%), multivessel coronary artery disease (71%) and inducible sustained VT with programmed stimulation (87%). During a mean follow-up of 26 months, 36 patients (41%) died and 21 patients had arrhythmia recurrence (with 19 sudden deaths). Factors independently associated with mortality included: (1) treatment before 1981 (p less than 0.01); (2) anterior AMI (p less than 0.05); (3) short time from AMI to first episode of VT (p less than 0.06); and (4) multivessel coronary artery disease (p less than 0.07). Factors independently associated with arrhythmia recurrence were: (1) medical treatment (as opposed to surgical) (p less than 0.01); (2) greater than or equal to 3 episodes of spontaneous VT (p = 0.01); (3) multivessel coronary disease (p less than 0.05); and (4) anterior AMI (p less than 0.07). Medically and surgically treated patients did not differ significantly in overall survival (49 vs 61%, respectively), although short-term (6 month) surgical survival improved from 31% during the first half of the study to 96% in the latter half (p less than 0.01). For patients with sustained VT early after AMI the risk of death and arrhythmia recurrence can be assessed based on clinical and angiographic characteristics; in addition, surgical treatment is associated with a lower incidence of arrhythmia recurrence than medical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Coincidence of true and false left ventricular aneurysms after myocardial infarction

False aneurysm of the left ventricle is a rare complication of myocardial infarction. In this case cross sectional echocardiography demonstrated the presence of both true and false left ventricular aneurysms. This was confirmed at operation when both aneurysms were successfully resected.     

Mechanisms, prediction and treatment of ventricular tachyarrhythmias occurring late after myocardial infarction

Studies from the 1980s, refined in the intervening years, have examined the milieu for ventricular tachycardia (VT) and ventricular fibrillation (VF) occurring late after acute myocardial infarction (AMI). The arrhythmogenic substrate appears to be patchy areas of fibrous tissue interdigitating with viable bundles of myocardium which have distorted orientation and tortuous interconnections. These promote conduction delay in sinus rhythm. Factors found to promote induction of VT rather than VF are longer conduction delay in sinus rhythm, larger infarct size, a more ragged infarct edge and longer ventricular extrastimulus coupling intervals. Predictors of spontaneous VT and VF late after AMI include inducible VT at electrophysiological studies (EPS), delayed conduction in sinus rhythm detected as late potentials on signal-averaged surface electrocardiogram (ECG), and low left ventricular ejection fraction (LVEF). Treatments of propensity for VT or VF after AMI include insertion of a defibrillator (ICD), which has the best track record, antiarrhythmic medication (less reliable), and ablation or excision of arrhythmogenic substrate (for refractory VT and VF).     

Left ventricular pseudoaneurysm after myocardial infarction

In this report, a case of a left ventricular (LV) pseudoaneurysm due to a previous myocardial infarction, which was repaired successfully, is described. A 62-year-old man, with a history of acute anterior wall myocardial infarction 6 months previously, was admitted with the complaints of acute dyspnea and palpitation. Echocardiography revealed an LV aneurysm, and ventriculography showed ventricular dysfunction and an LV pseudoaneurysm. Coronary angiography showed total occlusion of the proximal segment of the left anterior descending artery with a very thin lumen and insufficient retrograde filling. Under cardiopulmonary bypass and beating heart, the pseudoaneurysm was resected and the defect on the ventricular free wall was closed by the remodeling ventriculoplasty method of Dor. Histopathologic examination of the resected material confirmed the diagnosis of pseudoaneurysm. The postoperative course of our patient was uneventful. He was discharged on the ninth postoperative day.     

Cellular basis of ventricular remodeling after myocardial infarction.

To determine whether acute left ventricular failure associated with myocardial infarction leads to architectural changes in the spared nonischemic portion of the ventricular wall, large infarcts were produced in rats, and the animals were sacrificed 2 days after surgery. Left ventricular end-diastolic pressure was increased, whereas left ventricular dP/dt and systolic pressure were decreased, indicating the presence of severe ventricular dysfunction. Absolute infarct size, determined by measuring the fraction of myocyte nuclei lost from the left ventricular free wall, averaged 63%. Transverse midchamber diameter increased by 20%, and wall thickness diminished by 33%. The number of mural myocytes in this spared region of the left ventricular free wall decreased by 36% and the capillary profiles by 40%. Thus, side-to-side slippage of myocytes in the myocardium occurs acutely in association with ventricular dilation after a large myocardial infarction. In order to analyze the chronic consequences of myocardial infarction on ventricular remodeling, a second group of experiments was performed in which the left coronary artery was ligated and the functional and structural properties of the heart were examined 1 month later. In infarcts affecting an average 38% of the free wall of the left ventricle (small infarcts), reactive hypertrophy in the spared myocardium resulted in a complete reconstitution of functioning tissue. However, left ventricular end-diastolic pressure was increased, left ventricular dP/dt was decreased, and diastolic wall stress was increased 2.4-fold. After infarctions resulting in a 60% loss of mass (large infarcts), a 10% deficit was present in the recovery of viable myocardium. Functionally, ventricular performance was markedly depressed, and diastolic wall stress was increased 9-fold. The alterations in loading of the spared myocardium were due to an increase in chamber volume and a decrease in the myocardial mass/chamber volume ratio that affected both infarct groups. Thus, decompensated eccentric ventricular hypertrophy develops chronically after infarction and growth processes in myocytes are inadequate for normalization of wall stress when myocyte loss involves nearly 40% or more of the cells of the left ventricular free wall. The persistence of elevated myocardial and cellular loads may sustain the progression of the disease state toward end-stage congestive heart failure.     

Reproducibility of exercise-induced ventricular arrhythmia after myocardial infarction.

To evaluate the reproducibility of exercise-induced ventricular arrhythmia, 155 men with a mean age of 53 +/- 8 years underwent serial exercise testing 3 to 52 weeks after myocardial infarction. The reproducibility of categorical test responses, that is, the presence or absence of ventricular arrhythmia, was evaluated with the kappa coefficient, which considers negative as well as possible test responses and expresses reproducibility above the chance level. Reproducibility was highest at an intertest interval of 1 to 5 days and was not enhanced by further categorizing premature ventricular complexes as simple or complex based on their frequency or configuration. Continuous response measures such as frequency of premature ventricular complexes yielded higher reproducibility than categorical responses. Continuous response measures appear preferable to categorical responses for evaluating the clinical significance and response to antiarrhythmic therapy of ventricular arrhythmias.     

Management of intractable ventricular tachyarrhythmias after myocardial infarction.

Twenty-five patients with recent or old myocardial infarction were studied because they had life-threatening ventricular arrhythmias that required repeated cardioversions and were intractable to medical management. All patients had had a large anterior infarction a mean of 4.6 weeks before the emergence of the arrhythmias and all had severe left ventricular dysfunction. Cardiac catheterization or autopsy revealed a left ventricular aneurysm in 18 of 18 patients and obstruction of the left anterior descending coronary artery in 20 of 20 patients. Of 16 patients treated surgically with aneurysm resection or coronary bypass grafting, or both, 10 (62 percent) were alive after 3 to 39 (mean 26) months of follow-up. The perioperative mortality rate was 31 percent and only one patient died during the postoperative follow-up period 4 months after discharge from the hospital. By contrast, all nine medically treated patients died either in the hospital (four patients) or suddenly within 2 months of discharge (five patients). Ventricular fibrillation was documented as the cause of death in five of these patients. Surgical intervention was found to improve significantly the survival of these patients (P less than 0.02). The perioperative mortality rate was lower when at least 4 weeks had elapsed from acute infarction to surgery (10 versus 67 percent) and when the procedure included coronary bypass grafting (13 versus 50 percent), although these differences were not statistically significant (P greater than 0.05).     

Nonsurgical transthoracic epicardial catheter ablation to treat recurrent ventricular tachycardia occurring late after myocardial infarction

OBJECTIVES: We sought to evaluate feasibility, safety and results of transthoracic epicardial catheter ablation in patients with ventricular tachycardia occurring late after an inferior wall myocardial infarction. BACKGROUND: Transthoracic epicardial catheter ablation effectively controls recurrent ventricular tachycardia (VT) in patients with Chagas' disease in whom epicardial circuits predominate. Epicardial circuits also occur in postinfarction VT. METHODS: Fourteen consecutive patients aged 53.6 +/- 14.5 years with postinfarction VT related to the inferior wall were studied. The VT cycle length was 412 +/- 51 ms. Two patients had previously undergone unsuccessful standard endocardial radiofrequency energy (RF) ablation. The VT was incessant in one patient. Left ventricular angiography showed inferior akinesia in 13 patients and an inferior aneurysm in 1 patient. Ablation was performed with a regular steerable catheter placed into the pericardial sac by pericardial puncture. RESULTS: The pericardial space was reached in all patients. Electrophysiologic evidence of an epicardial circuit was present in 7 of 30 VTs. Due to a high stimulation threshold, empirical thermal mapping was the only criterion used to select the site for ablation. Three VTs were interrupted during the first RF pulse. Two pulses were necessary to render it noninducible in 3 patients (1 VT per patient). In the remaining 4 VTs, 3, 3, 4 and 5 RF pulses, respectively, were used. The overall success was 37.14% (95% confidence interval, 11.83% to 62.45%). Patients are asymptomatic for 14 +/- 2 months. CONCLUSIONS: Postinfarction pericardial adherence does not preclude epicardial mapping and ablation to control VT related to an epicardial circuit in postinferior wall myocardial infarction.     

Left ventricular dyssynchrony acutely after myocardial infarction predicts left ventricular remodeling.

OBJECTIVES: We sought to identify predictors of left ventricular (LV) remodeling after acute myocardial infarction. BACKGROUND: Left ventricular remodeling after myocardial infarction is associated with an adverse long-term prognosis. Early identification of patients prone to LV remodeling is needed to optimize therapeutic management. METHODS: A total of 178 consecutive patients presenting with acute myocardial infarction who underwent primary percutaneous coronary intervention were included. Within 48 h of intervention, 2-dimensional echocardiography was performed to assess LV volumes, LV ejection fraction (LVEF), wall motion score index, left atrial dimension, E/E' ratio, and severity of mitral regurgitation. Left ventricular dyssynchrony was determined using speckle-tracking radial strain analysis. At 6-month follow-up, LV volumes, LVEF, and severity of mitral regurgitation were reassessed. RESULTS: Patients showing LV remodeling at 6-month follow-up (20%) had comparable baseline characteristics to patients without LV remodeling (80%), except for higher peak troponin T levels (p < 0.001), peak creatine phosphokinase levels (p < 0.001), wall motion score index (p < 0.05), E/E' ratio (p < 0.05), and a larger extent of LV dyssynchrony (p < 0.001). Multivariable analysis demonstrated that LV dyssynchrony was superior in predicting LV remodeling. Receiver-operating characteristic curve analysis demonstrated that a cutoff value of 130 ms for LV dyssynchrony yields a sensitivity of 82% and a specificity of 95% to predict LV remodeling at 6-month follow-up. CONCLUSIONS: Left ventricular dyssynchrony immediately after acute myocardial infarction predicts LV remodeling at 6-month follow-up.     

Left ventricular performance after acute myocardial infarction

Current knowledge concerning the major hemodynamic features of acute myocardial infarction has been reviewed and discussed in relation to present concepts of cardiac pathophysiology. The physical examination provides a great deal of information and new, noninvasive methods promise to supplement the bedside appraisal of left ventricular function. Direct hemodynamic methods of serially monitoring patients with acute myocardial infarction are finding increasing application and recently have added considerably to our understanding of this condition. Certain limitations in the use of the central venous pressure, pulmonary arterial pressure, and cardiac output in appraising left ventricular function have become apparent, but together with direct catheterization of the left ventricle such hemodynamic studies have now provided limited correlations between the clinical picture and various hemodynamic patterns. It is becoming increasingly clear that most of these features, including cardiogenic shock, probably reflect varying degrees of left ventricular failure. These initial findings and interpretations will require confirmation, however, and so far insufficient objective data are available concerning the natural history of acute myocardial infarction and its responses to various forms of therapy. The aims of investigations now being carried in specialized Myocardial Infarction Research Units and other cardiovascular research centers, are to gain such further understanding of the pathophysiology of this disease and to aid in its clinical management by developing accurate indirect monitoring techniques as well as new forms of therapy.     

Left ventricular intra-myocardial dissection after myocardial infarction

Left ventricular (LV) intra-myocardial dissection or dissecting hematoma is a rare complication of myocardial infarction that could occur in the acute phase, during remodeling process and even after coronary revascularization. LV intra-myocardial dissection has a high mortality, and the best management strategy remains controversial. Here, we present a case of dissection of left ventricle late after anterior myocardial infarction diagnosed by multimodality imaging.     

心肌梗死后室性心律失常的治疗

急性心肌梗死（AMI）和陈旧性心肌梗死（OMI）患者易于伴发各种心律失常，其中室性心律失常（vA）发生率较高，也是导致猝死、危及患者生命的重要因素之一。文献报道AMI后室性早搏（PVB）的发生率为10％-93％，室性心动过速（VT）的发生率为3％-39％，心室颤动（VF）的发生率为4％-36％。每年美国有大约32．5万的人发生心脏猝死（sudden cardiac death，SCD），其中由冠心病引起占80％以上。心肌梗死后发生的VA是猝死最常见的原因，60％AMI性死亡的患者发生在发病后1h内，被认为与VA，