[Hemodynamic compensatory mechanisms of impaired left ventricular contraction in coronary artery disease (author's transl)].
The effect of chronic coronary insufficiency on the hemodynamics, the geometry and muscle mass of the left ventricle were studied in 30 patients and compared to 13 controls. In these patients the cardiac output was normal in spite of impaired contractility and left ventricular wall movement. The impaired cardiac performance was compensated by 1. hypertrophy and 2. dialatation of the left ventricle. In one-vessel disease of the the coronary arteries left ventricular muscle mass was modestly, but not significant increased. Hypertrophy decreased from +20% in one vessel disease to +10% in three vessel disease. In contrast, left ventricular dilatation increased from +23% in one vessel disease to 43% in two vessel disease and to 70% in patients with sclerotic lesions in three vessels. Left ventricular dilatation seems to be the main hemodynamic compensatory mechnism resulting in a relative increase of the pump function of the heart compared to non dilated hearts. However, dilatation leads in the end-phase to left ventricular failure. By increased wall tension in the presence of impaired coronary blood flow dilatation bears the risk of deterioration of left ventricular function.
D000328:Adult; D000368:Aged; D000790:Angiocardiography; D001795:Blood Pressure Determination; D006328:Cardiac Catheterization; D002302:Cardiac Output; D006332:Cardiomegaly / Q000503:physiopathology; D002908:Chronic Disease; D003327:Coronary Disease / Q000503:physiopathology*; D004106:Dilatation; D004562:Electrocardiography; D005260:Female; D006333:Heart Failure / Q000503:physiopathology; D006352:Heart Ventricles; D006439:Hemodynamics; D006801:Humans; D000860:Hypoxia; D008297:Male; D008875:Middle Aged; D009119:Muscle Contraction; D009203:Myocardial Infarction / Q000503:physiopathology*; D010101:Oxygen Consumption
Haemodynamische Kompenastionsmechanismen der Kontraktionsstörungen bei der chronischen Koronarsklerose