Aortic valve replacement in patients with severe aortic stenosis significantly increased left ventricular myocardial stiffness from 13.2 to 25.2 (p<0.02), unlike in patients with aortic insufficiency.
Observational (n=31)
How does aortic valve replacement affect diastolic stiffness and myocardial structure in patients with aortic valve disease?
Regression of myocardial hypertrophy after aortic valve replacement for aortic stenosis is accompanied by an increase in myocardial stiffness and relative interstitial fibrosis, a phenomenon not observed in eccentric hypertrophy from aortic insufficiency.
Absolute Event Rate: 25.2% vs 13.2%
p-value: p=<0.02
Passive diastolic properties were determined in 10 control patients and 21 patients with aortic valve disease before and 17.5 months after successful valve replacement. Ten patients had severe aortic stenoses (AS), five had combined aortic valve lesions (AS + aortic insufficiency AI), and six patients had severe AI. Left ventricular endomyocardial biopsies were obtained before and after surgery in patients with AS, AS + AI, and AI. Simultaneous echocardiographic and high-fidelity pressure measurements were made in all patients, and left ventricular chamber stiffness was calculated from a viscoelastic pressure-circumference relationship and left ventricular myocardial stiffness from a viscoelastic stress-strain relationship. The constant of chamber stiffness, beta', was slightly although not significantly increased in patients with AS (0.27 before and 0.24 after surgery), but was normal in those with AS + AI (0.22 before and 0.17 after surgery) and slightly decreased in those with AI (0.18 before and 0.16 after surgery) when compared with in control subjects (0.21). The constant of myocardial stiffness beta was normal in patients with AS (13.2), AS + AI (11.5), and AI (11.7) before surgery compared with in the control group (12.5). beta increased, however, significantly in those with AS (25.2; p less than .02), but not in those with AS + AI (16.3; NS) and AI (12.8; NS) after surgery. Myocardial morphologic characteristics showed a significant decrease in muscle fiber diameter in patients with AS, AS + AI, and AI, as well as a significant increase in interstitial fibrosis from 15% to 26% (p less than .05) in those with AS and a slight increase from 15% to 22% (NS) in those with AS + AI and from 19% to 24% (NS) in those with AI. Left ventricular fibrous content (left ventricular muscle mass index multiplied by interstitial fibrosis) remained, however, unchanged in all three groups after aortic valve replacement. In conclusion, left ventricular chamber stiffness is increased in AS but decreased in AI, whereas LV myocardial stiffness is normal in patients with aortic valve disease before surgery. After surgery, left ventricular myocardial stiffness increased significantly in AS patients but remained unchanged in those with AI. Postoperative changes in myocardial structure were characterized by a decrease in muscle fiber diameter and a relative increase in interstitial fibrosis, whereas fibrous content remained unchanged. Thus, regression of myocardial hypertrophy in aortic valve disease is accompanied by an increase of myocardial stiffness in concentric hypertrophy that is not seen in eccentric hypertrophy.
Hess et al. (1984) conducted an observational in Aortic valve disease (n=31). Aortic valve replacement vs. Before surgery and control patients was evaluated on Left ventricular myocardial stiffness (constant beta) in severe aortic stenosis (p=<0.02). Aortic valve replacement in patients with severe aortic stenosis significantly increased left ventricular myocardial stiffness from 13.2 to 25.2 (p<0.02), unlike in patients with aortic insufficiency.