Left ventricular asynergy in patients with impending myocardial infarction: two-dimensional echocardiographic assessment

To determine the clinical significance of regional left ventricular asynergy in patients with impending myocardial infarction, we recorded two-dimensional echocardiograms (2DE) serially and performed coronary angiography immediately after the hospital admission in nine patients with initial impending infarction and their last anginal attacks were within 48 hours. Left ventricular asynergy on the first 2DE was observed in six of nine patients during symptom-free periods (Group A: LV asynergy group). Five of the six patients had significant coronary artery lesions (greater than or equal to 75% stenosis) in at least one major coronary artery. Intracoronary filling defects were detected in four of the five patients. Another three patients without asynergy (Group B) had significant fixed stenosis. Coronary artery spasm was observed in two patients during coronary angiography, but no patient had intracoronary filling defects. Intracoronary nitroglycerin (0.1-0.3 mg) reduced the severity of coronary artery narrowing in two patients. In addition, urokinase (240,000-480,000 IU) via the corresponding vessel (PTCR) in the remaining seven patients resulted in reduction in the severity of coronary artery stenosis in four patients, but not in the remaining three patients. Left ventricular wall movement in the asynergy group improved rapidly and no asynergy was observed by the seventh hospital day in five of the six patients. Successful PTCR treatment resulted in improvement of left ventricular wall movement. No asynergy was found in the non-asynergy group throughout their hospitalizations. These findings indicated that abnormal left ventricular wall movement is found in patients with impending myocardial infarction, even during symptom-free periods, but the wall movement gradually improves. The 2DE observations are useful for estimating the clinical status and for planning precise therapy for impending myocardial infarction.     

Criteria for electrocardiographic differentiation of right ventricular hypertrophy from true posterior myocardial infarction

Electrocardiograms recorded from patients with true posterior myocardial infarction show an abnormal anterior shift in the QRS forces. Differentiation of these records from those of right ventricular hypertrophy has been recognized as a difficult problem for a long time. An attempt was made to establish criteria for separating electrocardiograms of posterior myocardial infarction from those of right ventricular hypertrophy exhibiting a similar pattern. Frank lead electrocardiograms obtained from 81 patients with posterior myocardial infarction were compared with electrocardiograms recorded from 71 patients with right ventricular hypertrophy.With two measurements that can be easily obtained, 70 percent of the posterior myocardial infarction records were classified correctly with 15 percent of the right ventricular hypertrophy records being misclassified. A set of three measurements for right ventricular hypertrophy correctly identified 55 percent of cases of right ventricular hypertrophy; however, 13 percent of the posterior myocardial infarction records were misclassified as right ventricular hypertrophy.With seven measurements obtained on the basis of multivariate analysis, 78 percent of the posterior myocardial infarction and 79 percent of right ventricular hypertrophy cases were correctly classified. These measurements were found to be useful in classifying records that could not be categorized by hand measurements. Classification procedures were also tested in 23 autopsy cases with results equal to or slightly better than those obtained in clinical samples.Several measurements on the QRS vector loop previously considered useful in the differentiation of right ventricular hypertrophy from posterior myocardial infarction gave disappointing results when tested in our samples.     

Left ventricular thrombus and myocardial infarction

The aim of our study was to determine whether a relationship existed between echocardiographic evidence of left ventricular thrombus (LVT) and clinical course of myocardial infarction. We followed 143 patients who had had typical myocardial transmural infarction (82 with "anterior") and 61 with "inferior" myocardial infarction) over a three month period. Incidence of LVT, detected by Two-Dimensional Echocardiography (TDE) was significantly greater in subjects affected by "anterior" myocardial infarction (p less than 0.05). Furthermore, the occurrence of LVT was more frequent in the presence of left ventricular a-, dys-kinesis detected by TDE (p less than 0.01). No significant relationship was demonstrated either with the occurrence of severe ventricular arrhythmias (Lown 3-4-5) or with an abnormal stressing test performance. Thus certain clinical and laboratory features such as anterior site of infarction, higher serum level of CPK and CPK-MB and severe alterations of left ventricular kinesis proved to be useful in identifying a subset of patients most likely to have LVT who may benefit from early anticoagulant therapy.     

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.     

Left posterior hemiblock in acute myocardial infarction.

Fifteen cases of left posterior hemiblock associated with acute myocardial infaction were studied. In 5 cases the left posterior hemiblock was the only intraventricular conduction defect, while in the other 10 cases it was associated with complete right bundle-branch block. Left posterior hemiblock proved to be an early complication, appearing within a few hours from the onset of the acute episode, and an ominous sign, since hospital mortality rate was 87 per cent. Cause of death was mainly pump failure. In most of these cases ther was electrocardiographic evidence of infarction involving both anterior and inferior ventricular walls. Infarction of most or all of the ventricular septum was a common finding in the cases examined anatomically. Histologically, acute changes involving mainly the posterior septal and midseptal fibres were observed in 6 of the 8 cases studied. On the basis of these findings and of other published findings an alternative physiopathological mechanism for so-called left posterior hemiblock is proposed.     

Left posterior hemiblock in acute myocardial infarction.

Fifteen cases of left posterior hemiblock associated with acute myocardial infaction were studied. In 5 cases the left posterior hemiblock was the only intraventricular conduction defect, while in the other 10 cases it was associated with complete right bundle-branch block. Left posterior hemiblock proved to be an early complication, appearing within a few hours from the onset of the acute episode, and an ominous sign, since hospital mortality rate was 87 per cent. Cause of death was mainly pump failure. In most of these cases ther was electrocardiographic evidence of infarction involving both anterior and inferior ventricular walls. Infarction of most or all of the ventricular septum was a common finding in the cases examined anatomically. Histologically, acute changes involving mainly the posterior septal and midseptal fibres were observed in 6 of the 8 cases studied. On the basis of these findings and of other published findings an alternative physiopathological mechanism for so-called left posterior hemiblock is proposed.     

Masking of electrocardiographic features of right ventricular infarction by true posterior left ventricular infarction

An echocardiographically documented case of right ventricular infarction is reported. Electrocardiographic diagnosis was masked by concomitant true posterior left ventricular infarction. This case highlights an important limitation of electrocardiography in diagnosing right ventricular infarction.     

Relation system of electrocardiographic parameters in posterior myocardial infarction]

The polarcoordinates of the electrical heart vector in the groups of posterodiaphragmatic, postero-basal and extensive posterior myocardial infarctions were determined by the triaxicardiometer analogue computer. The ecg leads of Franks' system were numerically and graphically reconstructed from the digitalized polarcoordinates using formulas of connection between spherical polarcoordinates and rectangular Cartesian coordinates. Then the 12 conventional leads, by the use of coefficients were synthetized from the reconstructed leads of Franks' system and of the conventional leads were performed by the ODRA 1204 computer. So was created the connection system of the electrocardiological parameters, where the informative value of the polarcoordinates and the Cartesian coordinates-also mathematically-is exactly alike.     

Left ventricular diastolic function following myocardial infarction

An acute myocardial infarction causes a loss of contractile fibers which reduces systolic function. Parallel to the effect on systolic function, a myocardial infarction also impacts diastolic function, but this relationship is not as well understood. The two physiologic phases of diastole, active relaxation and passive filling, are both influenced by myocardial ischemia and infarction. Active relaxation is delayed following a myocardial infarction, whereas left ventricular stiffness changes depending on the extent of infarction and remodeling. Interstitial edema and fibrosis cause an increase in wall stiffness which is counteracted by dilation. The effect on diastolic function is correlated to an increased incidence of adverse outcomes. Moreover, patients with comorbid conditions that are associated with worse diastolic function tend to have more adverse outcomes after infarction. There are currently no treatments aimed specifically at treating diastolic dysfunction following a myocardial infarction, but several new drugs, including aldosterone antagonists, may offer promise.     

Left ventricular pseudoaneurysm following acute myocardial infarction

We describe a case of 57-year-old man who presented with acute myocardial infarction (AMI) and heart failure with rapid progression of cardiomegaly. Cardiac multislice computed tomography and echocardiography showed the ventricular pseudoaneurysm, probably due to cardiac free wall rupture caused by AMI. Cardiac CT is another useful tool for the non-invasive diagnosis of cardiac rupture.     

Left ventricular restoration devices post myocardial infarction

Even in the era of percutaneous reperfusion therapy, left ventricular (LV) remodeling after myocardial infarction (MI) leading to heart failure remains a major health concern. Contractile dysfunction of the infarcted myocardium results in an increased pressure load, leading to maladaptive reshaping of the LV. Several percutaneous transcatheter procedures have been developed to deliver devices that restore LV shape and function. The purposes of this review are to discuss the spectrum of transcatheter devices that are available or in development for attenuation of adverse LV remodeling and to critically examine the available evidence for improvement of functional status and cardiovascular outcomes.     

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 lipomatous metaplasia following myocardial infarction

We present 3 cases of left ventricular lipomatous metaplasia after myocardial infarction evaluated with cardiovascular magnetic resonance (CMR). Delayed enhancement CMR alone cannot differentiate lipomatous metaplasia from scar. T1-weighted images with and without fat suppression are needed to identify this condition. The aetiology, pathophysiology, and possible clinical significance of lipomatous metaplasia in infarcted myocardium are still unknown. The multi-parametric capabilities of CMR make it the ideal modality to identify non-invasively, and without exposure to radiation, individuals with lipomatous metaplasia.     

Left ventricular apex-dimension loops in acute myocardial infarction

Apex-dimension loops may provide useful information in patients with acute myocardial infarction because incoordinate contraction and relaxation can be demonstrated. The method could allow assessment of the effects of therapeutic interventions. Fifty consecutive patients with AMI in the coronary care unit within 48 hours after the onset of their symptoms were studied. Simultaneous recordings of the echocardiogram and apexcardiogram, which were of an adequate quality for analysis, were obtained in only 7 patients (success rate 14%). In all these patients, incoordinate relaxation was demonstrated. A major practical drawback of the method is the time needed for recording the basic data requiring 2 investigators. Therefore, because of the low success rate and difficulties in obtaining simultaneous recordings, apex-dimension loops are not practical in most patients with acute myocardial infarction.     

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.