[Ventricular and myocardial function in aortic regurgitation (author's transl)].
The influence of chronic volume load on ventricular function and myocardial load and shortening was investigated in 10 patients with chronic aortic regurgitation by means of biplane ventriculography and simultaneous pressure measurements. The regurgitant fraction was 63 +/- 15 per cent. Enddiastolic volume (EDVI 227 +/- 37 ml/m2), systolic (161 +/- 18 mm Hg) and enddiastolic ventricular pressure (30 +/- 12 mm Hg) were elevated, ejection fraction was reduced (54 +/- 7 per cent). Myocardial mass related to EDV was normal (1.2 +/- 0.2 g/ml). Contractility as measured from dp/dt max (1736 +/- 492 mm Hg s-1) and dp/dtmax/PI (22.2 +/- 4.3 s-1) was slightly reduced. Mean velocity of equatorial midwall fiber shortening VMW 0.45 +/- 0.13 cir X s-1) was significantly diminished, equatorial midwall fiber stress during ejection (sigma tej 267 +/- 44.5 X 10(3) dyn X cm-2) was elevated. In spite of a very high enddiastolic stress (sigma ED 96 +/- 36 X 10(3) dyn X cm-2) mean systolic power (sigma tej X VMX 123 +/- 43.2 X 10(3) dyn X cm-2 X s-1) was normal. Compensation of chronic volume load in aortic regurgitation is not compensated by an increased contractility but by ventricular enlargement and a pronouned increase in preload. Myocardial load and shortening in chronic aortic regurgitation are altered in the same way (increased stress and reduced shortening) as in chronic pressure overload.
D000328:Adult; D001022:Aortic Valve Insufficiency / Q000503:physiopathology*; D001794:Blood Pressure; D003971:Diastole; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium; D013318:Stroke Volume; D013599:Systole
Ventrikel- und Myokardfunktion bei Aortenklappeninsuffizienz.