Acute myocardial infarction in a young man with dilated cardiomyopathy: clinicopathological correlation

Cardiac involvement is commonly described in autopsy examinations of patients infected with human immunodeficiency virus (HIV). However, only a small percentage have clinically significant cardiac disease. Dilated cardiomyopathy is one of the most common HIV-related heart diseases. Cardiovascular complications of HIV infection are likely to become more common with improvements in treatment and survival. Coronary thromboembolism has rarely been reported in the setting of dilated cardiomyopathy. Coronary thromboembolism should be suspected in a patient presenting with acute myocardial infarction, normal coronary arteries at subsequent angiography and a potential source of embolus. A patient presenting with acute myocardial infarction subsequently diagnosed as a coronary artery embolism due to HIV cardiomyopathy is reported. Coronary artery embolism and HIV cardiomyopathy are briefly discussed.     

The clinical course of idiopathic dilated cardiomyopathy. A population-based study.

OBJECTIVE: To describe the prognosis of individuals with idiopathic dilated cardiomyopathy in a population-based sample and to compare this with the prognosis of patients in a previous referral center case series of idiopathic dilated cardiomyopathy. DESIGN: Cohort study. SETTING: Population-based in Olmsted County, Minnesota. PATIENTS: Forty residents of Olmsted County, Minnesota with idiopathic dilated cardiomyopathy initially diagnosed between 1975 and 1984 who were followed through 1 July 1989 and 104 patients from a Mayo Clinic referral case series from 1960 to 1973. MEASUREMENTS: Survival for the population-based cohort at 1 year and 5 years. RESULTS: Survival at 1 year differed dramatically between the population-based cohort and the referral case series at 1 year (95% compared with 69%, respectively) and at 5 years (80% compared with 36%, respectively) (P less than 0.001). Long-term survival for the population-based cohort was nonetheless impaired when compared with an age- and sex-matched cohort, that is, the 1980 Minnesota white population (8-year survival: observed, 58% compared with expected, 83%; P less than 0.001). Among community patients, older age (adjusted Cox model hazard ratio for 10-year increase in age, 1.59; 95% CI, 1.08 to 2.35) and lower left ventricular ejection fraction (adjusted hazard ratio for 10% decrease, 1.90; CI, 1.04 to 3.50) were independently associated with impaired survival. CONCLUSIONS: These population-based data challenge the clinical perception of the clinical course of idiopathic dilated cardiomyopathy based on referral practice prognostic studies and suggest that the clinical course of this condition may be more favorable than previously recognized.     

Acute myocardial infarction in toxic cardiomyopathy without coronary obstruction.

Confluent left ventricular scar without significant coronary obstruction has been found in alcoholic subjects at autopsy. To evaluate the pathogenesis, 12 patients with chronic alcoholism and severe precordial pain persisting 4-24 hours were observed clinically. Cardiac isoenzymes of lactic dehydrogenase rose in serum. ST segment was elevated in anterior or posterior ECG leads, and abnormal Q waves appeared. Hypertnesion and hypercholesterolemia were present in two (group B) but not in the ten (group A). The latter exhibited no significant obstructive disease, based on coronary angiography in seven survivors and postmortem examination of the remaining three. Clinical evidence, as well as the quantitative assessment of platelets, made arterial thromboembolism an unlikely cause for the symptoms. Neither hemotologic or systemic disease affecting myocardium was present. The morphology of the left ventricle in three autopsies was compared with that of patients with alcoholism who had no cardiac disease, cardiomyopathy, or an asymptomatic scar. All had accumulation of Alcian positive glycoprotein in the interstitium. The patients with cardiac disease also had interstitial fibrosis which was characterized, particularly in the acute infarction group, by concentric periarterial fibrosis. Restriction of coronary vasodilation by this process during periods of high blood flow requirements was postulated as a basis for infarction.     

Acute myocardial infarction in the diabetic patient: pathophysiology, clinical course and prognosis.

Although there have been significant advances in the care of many of the extrapancreatic manifestations of diabetes, acute myocardial infarction continues to be a major cause of morbidity and mortality in diabetic patients. Factors unique to diabetes increase atherosclerotic plaque formation and thrombosis, thereby contributing to myocardial infarction. Autonomic neuropathy may predispose to infarction and result in atypical presenting symptoms in the diabetic patient, making diagnosis difficult and delaying treatment. The clinical course of myocardial infarction is frequently complicated and carries a higher mortality rate in the diabetic than in the nondiabetic patient. Although the course and pathophysiology of myocardial infarction differ to some degree in diabetic patients from those in patients without diabetes, much more remains to be known to formulate more effective treatment strategies in this high risk subgroup.     

Case report: Acute myocardial infarction complicating a viper bite.

Myocardial infarction is a rare complication of snakebite. The present report describes a 40-year-old Jordanian farmer who developed an acute myocardial infarction several hours after a snakebite. The diagnosis of myocardial infarction was confirmed by a typical history of retrosternal chest pain, characteristic electrocardiographic changes, and elevated serum creatinine kinase (MB-CK). The patient had no risk factors for coronary artery disease and the coronary arteries were normal on cardiac catheterization. The possible mechanisms leading to myocardial infarction following snakebite are discussed.     

The course of idiopathic dilated cardiomyopathy in New Zealand.

The course of dilated cardiomyopathy in New Zealand was studied in 72 cases that were followed up for less than or equal to 10 years after cardiac catheterisation and coronary angiography. Eighty one per cent were male and 86% were white; the remainder were Maori. The mean age of patients at the time of investigation was 50 X 15 years. Most patients were unskilled labourers. The commonest presenting symptom was dyspnoea and the commonest physical sign was cardiomegaly. Mean survival time from first hospital presentation was 85 months; half the deaths were sudden. Factors predicting a poor survival included cardiomegaly, age, arrhythmias, cigarette smoking, and subclinical thiamine deficiency. The syndrome of dilated cardiomyopathy in New Zealand appears to be identical with that seen in other European populations.     

扩张型心肌病的心肌组织细胞凋亡的研究

目的：研究扩张型心肌病（DCM）的心肌细胞凋亡及其与心功能的关系。方法：DCM组21例,其心肌组织14例来自右室心内膜心肌活检（EMB）亚组,7例来自死后尸检（尸检组）;对照组为5例死于非心血管疾病的尸检心肌组织。用原位细胞凋亡检测心肌组织凋亡细胞,计算凋亡指数（AI）。结果（1）DCM组的AI明显高于正常组（P＜0．01）,EMB亚组的AI明显低于尸检亚组（P＜0．01,但明显高于对照组（P＜0．01）。（2）DCM组中,心胸比（HTR）＜0．6、左室舒张末期内（LVDd)＜65mm和左室射血分数（LVEF）≥40％的患者AI均分别明显于低于HTR≥0．6、LVDd ≥65mm和LVEF＜40％的患者（P值均＜0．01）,但仍分别显著高于对照组（P值均＜0．01）。结论：DCM存在明显心肌细胞凋亡并随心功能恶化而程度加重,提示凋亡是DCM的心肌细胞丢失和心功能不全的重要机制。     

Hypertrophic cardiomyopathy in childhood: studies of the clinical picture and course

30 children with hypertrophic cardiomyopathy and a mean age of 4.9 +/- 4.4 years, 11 infants and 19 children, were followed up for an average of 6.6 +/- 5.6 years. Apart from a systolic murmur in nearly all patients, only a few had symptoms. 7 patients from 5 families had a positive family history. The ECG often showed left ventricular hypertrophy, twice a deep Q wave, and no cases of giant T wave. A subaortic pressure gradient greater than or equal to 40 mm Hg was measured in 6 children, a secondary cardiomyopathy was excluded by biopsy in 8. Associated lesions were coarctation (n = 2) and patent ductus arteriosus (n = 2). 7 children died: 1 infant in congestive heart failure, 3 children suddenly, and 3 postoperatively. The annual mortality rate was 3.5%. Also in childhood, beta-blocker therapy may not prevent sudden cardiac death, nor may operation prevent late complications. In spite of the lack of pressure gradients, the children did not fulfil the criteria of hypertrophic non-obstructive cardiomyopathy.     

Clinical course of idiopathic dilated cardiomyopathy in children

Previous studies in adults with dilated cardiomyopathy suggest that the presence of arrhythmia, especially ventricular tachycardia, correlates with increased mortality. We performed a retrospective analysis of 63 children with idiopathic dilated cardiomyopathy to determine the prognostic significance of arrhythmias and other findings with respect to mortality. The mean age at diagnosis of the cardiomyopathy was 4.96 +/- 5.3 years. The overall mortality rate was 16% over a 10 year follow-up period. Persistent congestive heart failure and ST-T wave changes correlated with increased mortality (p less than 0.05). No other variables affected outcome. Arrhythmias were found in 46% of the patients; of the arrhythmias, 48% were atrial arrhythmias. Ventricular tachycardia was present in six patients. Death occurred in 4 (14%) of 29 patients with known arrhythmia; 1 of the 5 died suddenly. The remaining 6 deaths in the series occurred in the 34 patients without a documented arrhythmia. It is concluded that 1) arrhythmias are frequently seen in children with dilated cardiomyopathy but are not predictive of outcome; 2) sudden death in children with this disease is rare; and 3) persistent congestive heart failure portends a poor prognosis.     

Mitral insufficiency complicating acute myocardial infarction.

The pathological processes underlying the symptom of mitral insufficiency appearing during the course of acute myocardial infarction are reviewed. The mitral valve apparatus can be considered as being composed of fibrous elements (the annulus fibrosus, the valve leaflet and the chordae tendineae), the left atrial endocarduim and the muscular elements (the papillary muscles together with their supporting myocardium). Since the fibrous elements are avascular, it is concluded that they are unlikely to be directly affected by ischemia. For this and other reasons dilatation of the mitral annulus is not considered a cause of incompetence. It is suggested that muscular involvement is the most likely cause of mitral incompetence during acute myocardial infarction. The syndrome of 'papillary muscle dysfunction' is therefore reviewed under the headings of (1) conditions producing abnormal spatial orientation of the muscles, (2) conditions producing abnormal or absent contraction of the muscles and (3) conditions producing improper timing of muscular contraction. Cases are illustrated which demonstrated generalized dilatation of the left ventricle, localized dilatation and both complete and imcomplete papillary muscle rupture. Mitral insufficiency under these circumstances may ensue from either improper orientation or improper functioning of the muscular elements of the mitral valve apparatus, or from both. It is also emphasized that direct involvement of the papillary muscles by the ischemic process is not necessary for incompetence to occur, and that most cases of mitral incompetence complicating the acute stage of myocardial infarction are of transient nature, resolving during the recovery phase.     

Atrioventricular plane displacement in severe congestive heart failure following dilated cardiomyopathy or myocardial infarction

Echocardiographic recording of the atrioventricular (AV) plane displacement during the cardiac cycle was used to assess left ventricular (LV) global function in patients with congestive heart failure (CHF). The study population consisted of 70 patients with chronic CHF (NYHA functional groups III and IV) following dilated cardiomyopathy (DCM) or myocardial infarction (MI), and 35 age-matched healthy subjects. The AV plane displacement was recorded from the apical 4- and 2-chamber views at four LV sites located about 90 degrees apart and representing the septal, anterior, lateral and posterior parts of the LV wall. A mean value was calculated from the above sites (AV-mean). Patients with CHF showed a significant generalized reduction of AV plane displacement compared to healthy subjects (5.6 mm vs. 14.5 mm, P less than 0.001). Thirty CHF patients also underwent radionuclide angiography in order to determine the ejection fraction (EF). The correlation between AV-mean and EF was good (r = 0.82, P less than 0.001). The selection of an AV-mean of less than 7 mm to define a severely depressed LV function (EF less than 30%) gave a sensitivity of 92% and a specificity of 67%. It is concluded that the AV plane displacement can be used to estimate LV systolic function in patients with CHF.     

Left ventricular trabeculae evaluated with MRI in dilated cardiomyopathy and old myocardial infarction]

The morphological examination of the left ventricular trabeculae was performed using MRI (0.5T) in 14 normal volunteers, 12 patients with dilated cardiomyopathy (DCM), and 9 patients with old myocardial infarction (OMI). Left ventricular trabeculae were observed at the free walls of the left ventricle in all subjects, but not at the septal wall. Left ventricular trabeculae were larger in DCM than in the normals. The trabeculae were scarce in OMI and inner sides of the infarcted myocardium were very smooth. The development of the left ventricular trabeculae was graded as diminished, ordinary, and marked. Ordinary trabeculae were seen in 86% of the normals, whereas; marked trabeculae in 75% of DCM, and diminished trabeculae in 78% of OMI. In patients with DCM, the mean area of the left ventricle with marked trabeculae was greater than that with ordinary trabeculae. The more dilated left ventricle, the thinner the anterior wall was and the lower the ejection fraction was in DCM and OMI, though there were no significant differences in values of these 3 items between DCM and OMI. The MRI findings on the development of the trabeculae were confirmed in patients with DCM at autopsy. Thus, the MRI findings were very useful in the differential diagnosis between DCM and OMI.     

Acute myocardial infarction in the puerperium.

The authors describe the case of a forty-two-year-old patient with acute myocardial infarction (MI) on the third day of puerperium, who underwent direct angioplasty. The authors review the main physiological cardiovascular and hemostatic changes in pregnancy, which are usually well tolerated but which increase the probability of cardiovascular events when risk factors or previous cardiac disease are associated. Blood volume and cardiac output increase by around 50% during pregnancy, hemoglobin concentration falls, and reduced peripheral vascular resistance leads to a fall in arterial blood pressure during the first half of pregnancy. End-diastolic pressure, stroke volume and cardiac output increase in the immediate puerperium, and cardiovascular risk is highest in the perinatal period. The incidence of MI during pregnancy and puerperium is low; however, it is on the increase due to the growing number of pregnancies in women close to the end of their reproductive age.