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What are possible etiologies for dilated cardio-myopathy?
Dilated (congestive) cardiomyopathies exist in both inflammatory and non-inflammatory forms. The inflam-matory variety, or myocarditis, is usually the result of infec-tion or parasitic infestation. Myocarditis presents with the clinical picture of fatigue, dyspnea, and palpitations usually in the first weeks of the infection, progressing to overt congestive heart failure (CHF) with cardiac dilatation, tachycardia, pulsus alternans (regular alternation of pressure pulse amplitude with a regular rhythm), and pul-monary edema. Complete recovery from infectious myocarditis is usually the case, but there are exceptions such as myocarditis associated with diphtheria or Chagas’ disease. The non-inflammatory variety of dilated car-diomyopathy also presents with the picture of myocardial failure, but in this case secondary to idiopathic, toxic, degenerative, or infiltrative processes in the myocardium.
Alcoholic cardiomyopathy is a typical hypokinetic, non-inflammatory cardiomyopathy associated with tachycardia and premature ventricular contractions (PVC) that progresses to left ventricular failure with incompetent mitral and tricuspid valves. This cardiomyopathy is proba-bly due to the direct toxic effect of ethanol or its metabo-lite, acetaldehyde, which releases and depletes cardiac norepinephrine. In chronic alcoholics, acute ingestion of ethanol produces decreases in contractility, elevations in ventricular end-diastolic pressure, and increases in systemic vascular resistance.
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