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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