Heart and vessels. Supplement最新文献

Both the clinical and the biopsy diagnoses of myocarditis are prone to false-positive and false-negative interpretations. False-positive clinical diagnoses probably most commonly result from a failure to recognize other disorders, such as cardiomyopathy and myocardial infarction, that may mimic myocarditis. False-negative clinical diagnoses may occur in patients with myocarditis in whom the signs and symptoms are atypical, absent, or misinterpreted. The two most common errors made by pathologists that produce false-positive tissue diagnoses appear to be a failure to recognize the number of lymphocytes that occupy the normal myocardial interstitium and a misinterpretation of noninflammatory interstitial cells as lymphocytes. Sampling error may be the most usual cause of false-negative tissue diagnoses. Since myocarditis is characterized by leukocytic and reparative responses, the most important features to evaluate in endomyocardial biopsy tissues are the type, distribution, and extent of the inflammatory infiltrate and the presence and extent of interstitial and endocardial fibrosis. Although no single histopathologic criterion is both sensitive and specific for myocarditis, it appears that quantitative evidence of an interstitial leukocytic infiltrate is currently the best available hallmark for myocarditis in biopsy specimens. It is suggested that a mean lymphocyte count greater than 5.0/high-power (X 400) microscopic field be considered indicative of lymphocytic myocarditis and that a mean count less than this be interpreted as myocarditis only if discrete clusters of lymphocytes are identified, since differentiation of low-grade diffuse infiltrates from expected normal lymphocytic populations is problematic at levels less than 5.0.

Fifty-seven patients with unexplained dilated hearts and congestive heart failure were studied clinically and by endomyocardial biopsy of the left ventricle. Of the patients, 61% had histologic evidence of active lymphocytic myocarditis. The sudden onset of heart failure, often with arrhythmias, if preceded by a viral-like illness indicated a high chance of finding inflammatory infiltration in the biopsy material. No abnormal accumulation of immunoglobulin was found in these patients with dilated cardiomyopathy and myocarditis. Immunosuppressive therapy did not always bring about improvement.

The accuracy of a newly developed nuclear magnetic resonance-computed tomography (NMR-CT) technique in diagnosing idiopathic cardiomyopathy was assessed and compared with other procedures such as echocardiography, coronary angiography, left ventriculography, myocardial biopsy, and electrocardiography. In case 1, the NMR-CT clearly revealed thickening of the lateral ventricular free wall and ventricular septum, which strongly suggested hypertrophic cardiomyopathy. Catheterization showed a pressure gradient of 54 mm Hg and this patient was diagnosed as having hypertrophic obstructive cardiomyopathy. In case 2, the NMR-CT showed dilatation of the ventricular cavity indicative of dilated cardiomyopathy. This was confirmed by echocardiography, which revealed the enlarged cavity of the ventricle and poor movement. In case 3, the patient had marked hypertension; the cardiac silhouette was enlarged, but the NMR-CT revealed that the ventricular free wall and septum were of normal thickness. This study shows that NMR-CT is of value in the differential diagnosis of idiopathic cardiomyopathy.

This light- and electron-microscopic study using monoclonal antibody and anti-immunoglobulin antibodies in murine Coxsackie B3 virus myocarditis provides an immunohistochemical demonstration of surface antigens of lymphocytes. On the 7th and 9th days after inoculation, many necrotic cardiocytes were surrounded by numerous cellular infiltrates, in which macrophages and T lymphocytes predominated, whereas immunoglobulin-bearing B lymphocytes represented a minority. Immuno-electron microscopy showed some T lymphocytes in close contact with other lymphocytes, macrophages, and the sarcolemma of cardiocytes. After the 30th day, significant numbers of T lymphocytes and macrophages were still identifiable in and around the fibrotic foci. Our study suggests that cell-mediated immunity plays a protective role by lysing and scavenging virus-infected cardiocytes and cell debris at least in the early stage of myocarditis. The residual T lymphocytes in the chronic stage suggest their involvement in sustained cardiocyte injury.

The relationship of infection to dilated cardiomyopathy is reviewed on the basis of 200 patients seen at University College Hospital, Ibadan. Evidence of infection with Toxoplasma and Coxsackie B viruses is presented. Clinically detectable myocarditis is rare in children, and the preponderance of dilated cardiomyopathy is in patients above the age of 30 years, possibly because there is a long latent period between the initial infection and the development of frank cardiomyopathy. This paper concluded that infections are probably the most important cause of dilated cardiomyopathy in Nigeria.

Ten patients with previous myocarditis were evaluated to determine cardiac conditions by T1-201 myocardial perfusion imaging and stress radionuclide ventriculography during the follow-up of 18-102 (average 56) months; the results were compared with those from ten sex- and age-matched controls. Exercise capacity by supine bicycle ergometer was reduced in patients with myocarditis. Their resting left ventricular ejection fraction (LVEF) was 57.5% +/- 3.9%, similar to that of controls. LVEF response to stress in myocarditis was abnormal with an increment of end-systolic volume, while in the controls LVEF increased significantly during stress. Seven of the eight patients with an abnormal ejection fraction response had constant T1-201 perfusion defects. This study indicates that latent left ventricular dysfunction is present in patients with prior myocarditis and that nuclear study is useful for long-term follow-up.

Our recent survey of the Japanese literature, actual case experience, and previous studies revealed the following results. Fifty-three cases were reported in which the main cause of death in sarcoidosis was congestive heart failure (11 of 17 cases, 64.7%) and not sudden death as was previously believed. ECG analysis revealed that third degree AV block, bundle branch block, and ventricular arrhythmias were the most frequent findings indicating the presence of cardiac sarcoidosis. It was recognized that in the Japanese population fatal myocardial sarcoidosis or clinical diagnosed cardiac sarcoidosis occurred most frequently in females over the age of 40 years. It is suggested that myocardial changes progress independently of granulomatous changes. This is due to the detection of a high incidence of basal lamina layering of myocardial capillaries (14 of 18 cases, 77.8%) and is considered to play a significant role in the progression of this disease. Radionuclide studies showed that thallium scintigraphy or technetium ventriculography were positive in those cases where ECG abnormalities are prominent, indicating the presence of myocardial disease. Previous therapeutic studies of cardiac sarcoidosis have shown a decrease in the incidence of sudden death; death due to congestive heart failure occurred more frequently despite pacemaker implantation. Control of congestive heart failure is thus regarded as the most important aspect of improved treatment and prognosis.

Segmental wall motion abnormalities are common in patients with myocarditis. Left ventricular (LV) regional wall motion was assessed in six patients with myocarditis by two-dimensional echocardiography. Some of our patients demonstrated regional thinning of the wall, similar to myocardial infarction. Therefore, segmental wall motion abnormalities with or without regional wall thinning detected by two-dimensional echocardiography cannot be used to differentiate myocarditis from coronary artery disease. Nevertheless, echocardiography can be performed repeatedly and is useful for evaluating the severity of myocarditis by assessing LV regional wall motion abnormalities, changes in LV wall thickness and cardiac pump function during the course of the disease.

Drug-induced toxic changes in the myocardium have become an increasing problem. The effect of drugs on heart morphology may be acute or cumulative. In general, adverse drug reactions manifest themselves as myocarditis (toxic or hypersensitivity), cardiomyopathy with chamber dilatation, or restrictive disease. Drugs affecting embryologic development of the heart will not be discussed. Drugs causing myocarditis can be divided into: toxic myocarditis, e.g., cyclophosphamide. The morphologic changes are dose-related and have lesions of different ages, which include myocyte necrosis with hemorrhage and vasculitis. Fibrous endocarditis, e.g., methysergide. These reactions include thickening of the endocardium and sometimes the cardiac valves with fibrosis. Drugs causing hypersensitivity myocarditis, e.g., thiazide diuretics. In this case, the lesions are not dose-related, are the same age, and there is an eosinophilic infiltrate. Drugs causing cardiomyopathic-like changes of ventricular dilatation and failure, e.g., anthracyclines, particularly adriamycin. This group of drugs cause a gradual myofibrillar loss within cardiac myocytes and a sarcotubular dilatation which is characteristic. The damaged cells are replaced by fibrosis and ventricular failure ensues. With the rapid synthesis of new drugs, the problem of drug cardiotoxicity may be an ever-increasing problem. With the more widespread use of the endomyocardial biopsy, drug-induced heart disease can be documented and the effects of different methods of drug delivery and pharmacologic antagonists studied.

Endomyocardial biopsy provides a safe, reliable, morphologic index of acute rejection and has an important role to play in the management of patients in whom acute rejection occurs. Repeated endomyocardial biopsies are well tolerated, permitting monitoring of acute rejection in cardiac recipients. Some patients have undergone over 30 serial biopsies. Adequate sampling requires at least four pieces of tissue. The biopsies are graded in the following manner: Mild acute rejection is characterized by a perivascular and mild interstitial infiltrate of pyroninophilic lymphoblasts without myocyte necrosis. Moderate acute rejection has an increased infiltrate extending into the interstitium and causing focal myocyte necrosis. This requires augmentation of immunosuppression. Severe acute rejection, which is more difficult to reverse, includes a more prolific infiltrate with the addition of neutrophils, hemorrhage, and increased myocyte necrosis. Ongoing acute rejection implies that the degree of acute rejection is the same, or worse, than the previous biopsy. Resolving or resolved acute rejection shows reparative changes with diminishing or absent inflammatory infiltrate following treatment. Recipients treated with Cyclosporin-A develop rejection and respond to treatment more slowly than with conventional treatment. This group also develops endocardial infiltrates and a dose-related fine perimyocytic cardiac fibrosis. The endomyocardial biopsy is also useful in identifying infectious agents, for example, toxoplasmosis in cardiac recipients.