Medium-term determinants of left ventricular mass index after stentless aortic valve replacement

This study aimed to investigate the risk factors for elevated left ventricular mass index 3 to 5 years after stentless aortic valve replacement, and to elucidate the underlying physiologic mechanisms.

Eighty-nine patients (age, 76 +/- 6 years, 51 males) having a stentless porcine valve for aortic stenosis (n = 76) or regurgitation (n = 13) were prospectively studied by Doppler echocardiography 3 to 5 years after operation. Left ventricular systolic function, mass index, blood pressure, cardiac rhythm, and New York Heart Association function class were all determined. Stentless valve effective orifice area, mean pressure drop, and the presence and degree of aortic regurgitation were quantified.

The mean stentless aortic valve size was 24 +/- 2 mm. At follow-up time of 45 +/- 9 months, effective orifice area index was 1.2 +/- 0.35 cm2 x m(-2), and mean pressure drop was 5.7 +/- 3.8 mm Hg. Left ventricular mass index was 128 +/- 47 g x m(-2), and ejection fraction was 63% +/- 14%. Multivariant analysis showed a greater left ventricular mass index to be associated with nonsinus rhythm (versus sinus) (163 +/- 8 versus 131 +/- 7 g x m(-2)), greater pulse pressure (> 84 mm Hg) (161 +/- 7 versus 133 +/- 7 g x m(-2)), New York Heart Association class II or III (versus class I) (166 +/- 10 versus 128 +/- 5 g x m(-2)), and male sex (versus female) (160 +/- 7 versus 134 +/- 8 g x m(-2)), all p < 0.01. Mean pressure drop (> 8 mm Hg), effective orifice area index (< 1.0 cm2 x m(-2)), the presence of mild regurgitation of the stentless valve, or the type of previous valve disease were insignificant determinants of left ventricular mass index.

Three to five years after the implantation, stentless aortic valve hemodynamics remain excellent. Left ventricular hypertrophy caused by previous native aortic valve disease had largely regressed. However, patient-related factors, particularly systemic blood pressure, cardiac rhythm, and function, are significant causes of late residual left ventricular hypertrophy. Thus, continued medical care and earlier surgical intervention may further improve the outlook for these patients.