A. Klipstein et al., LEFT-VENTRICULAR FUNCTION IN PATIENTS WIT H POST-ENDOCARDITIC AORTIC REGURGITATION AND AORTOANNULLAR DILATATION, Schweizerische medizinische Wochenschrift, 125(31-32), 1995, pp. 1469-1476
Background: The duration of valvular regurgitation is an important det
erminant of left ventricular function in the presence of severe volume
overload. Purpose: To evaluate the effect of aortic regurgitation (ao
rtoannullar dilatation vs. history of bacterial endocarditis) on left
ventricular (LV) function. Patients: Between February 1976 and January
1993 45 patients (mean; age 45+/-12 years) underwent diagnostic evalu
ation for clinical purposes. Patients were divided into three groups:
group 1 consisted of 17 patients with normal LV function (controls), g
roup 2 of 11 patients with severe aortic regurgitation due to aortoann
ullar dilatation (AAD) and group 3 of patients with severe aortic regu
rgitation and a history of bacterial endocarditis (BE). Methods: LV fu
nction was assessed by biplane LV-angiography and simultaneous pressur
e recordings. The ejection fraction and peak systolic wall stress were
calculated in all patients. Systolic and diastolic LV function was de
termined and compared within the three groups. Results: Heart rate, me
an aortic pressure and cardiac index were similar in the three groups.
The mean aortic diameter was significantly increased in group 2 when
compared to the other two groups (p <0,001). Systolic function was sig
nificantly reduced in both groups with aortic regurgitation when compa
red to the control patients. The enddiastolic pressure-volume relation
ship was shifted to the right in patients with aortic regurgitation, b
ut only 3 patients with a history of bacterial endocarditis showed sev
ere diastolic dysfunction. Conclusions: No hemodynamic differences wer
e observed in patients with severe aortic regurgitation with regard to
the etiology or time course of LV volume overload. However, 17% of th
e patients with a history of bacterial endocarditis had severe diastol
ic dysfunction, which is probably due to the faster development of vol
ume overload after bacterial endocarditis.