Punishment of doctors must fit their crime.
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Biomedical subjects
Publications and source records attributed to J F Goodwin.
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Cardiomyopathies are defined as 'heart muscle diseases of unknown cause' and classified into hypertrophic, dilated and restrictive types, respectively. Hypertrophic cardiomyopathy is notable for massive ventricular hypertrophy without obvious cause, impaired diastolic and systolic function, a tendency for sudden death and a familial propensity. Dilated cardiomyopathy by contrast, demonstrates severe systolic failure progressing to congestive heart failure, with usually no familial tendency. Restrictive cardiomyopathy and diastolic heart disease represent syndromes with restriction to ventricular filling due to restrictive forces in the endomyocardium (and in constrictive pericarditis in the pericardium). The commonest cause of restrictive cardiomyopathy is endomyocardial fibrosis now usually known as hypereosinophilic endomyocardial disease. Specific heart muscle diseases are those conditions in which myocardial disease is due to a known cause: they usually produce systolic failure though occasionally a restrictive syndrome is evident. Amyloid heart disease occupies a place intermediate between cardiomyopathies and specific heart muscle diseases. The major features of the above conditions are described and current and future advances noted. Examples are the identification of the gene probably responsible for hypertrophic cardiomyopathy located on chromosome 14, and the identification of virus RNA particles in the myocardium in both myocarditis and in dilated cardiomyopathy, which strengthens the growing evidence suggesting that some cases of dilated cardiomyopathy may be due to previous myocarditis.
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The cardiomyopathies are defined and classified into hypertrophic, dilated and restrictive types. In hypertrophic cardiomyopathy the major abnormalities of structure (massive ventricular hypertrophy, myofibrillar disarray, and narrow intramural coronary arteries) and of function (excessive ventricular contraction, systolic pressure gradients, increased ventricular stiffness with impaired relaxation and a tendency for sudden death) are used as the basis for selective and rational treatment with beta-blocking, calcium blocking, or antiarrhythmic agents, or a combination. Treatment is aimed at relieving symptoms, improving prognosis and slowing the progress of disease. Additional methods of treatment involving pacemakers and defibrillators are covered, and the place of septal resection, mitral valve replacement and cardiac transplantation discussed. General management and advice to the patient, and the treatment of complications such as atrial fibrillation, congestive heart failure and infective endocarditis, are also covered. In dilated cardiomyopathy measures to improve ventricular function by vasodilator therapy and the place of antiarrhythmic and anticoagulant drugs are discussed. The controversial treatment with beta-adrenergic blocking agents is reviewed, and the place of immunosuppressive therapy assessed. The possible use of antiviral agents in the future is commented upon, and cardiac transplantation is emphasised as the most effective, although radical, means of improving prognosis in intractable cases. In restrictive cardiomyopathy due to endomyocardial fibrosis, treatment of the initial inflammatory stage with steroids or sulphonylurea, and of the later fibrotic and thrombotic stage with anticoagulants and endocardectomy, is surveyed. The possible place of cardiac transplantation both for endomyocardial fibrosis and amyloid heart disease is mentioned, caution being urged when either of these conditions involves organs other than the heart.