Copyright © 2003 by the European Society of Cardiology.
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Regression of left ventricular hypertrophy during 10 years after valve replacement for aortic stenosis is related to the preoperative risk profile
a Department of Thoracic and Cardiovascular Surgery, Aarhus University Hospital in Skejby, Aarhus, Denmark
b Department of Cardiology, University Hospital in Skejby, Aarhus, Denmark
c Department of Clinical Physiology and Nuclear Medicine, Aarhus University Hospital in Skejby, Aarhus, Denmark
* Correspondence: Ole Lund, MD, DSc, Department of Cardiothoracic Surgery, Royal Victoria Hospital, Grosvenor Road, Belfast BT12 6BA, UK.
E-mail address: olelund{at}ntlworld.com
Received 29 December 2002; revised 11 March 2003; accepted 28 May 2003
Background Previous studies have suggested that regression of hypertrophy may be the underlying determinant of longevity and left ventricular function after valve replacement (AVR) for aortic stenosis (AS). The potential for hypertrophy regression could therefore be related to the preoperative risk profile.
Methods Ninety-one consecutive patients with AS had a ‘project’ Doppler-echo and radionuclide ventriculography in addition to the standard investigation programme prior to AVR with a disc valve (19–29mm, n=82), a caged ball valve (26–29mm, n=8), or a stented porcine valve (26mm, n=1); 49 (group A) were selected for a serial follow-up study while 42 served as controls (group B). Forty-two group A patients took part in a 1.5-year examination while 47 (26 group A, 21 group B) patients were studied at 10 years.
Results Groups A and B were comparable as regards all pre- and intra-operative data including left ventricular mass index (LVMi). A previously developed preoperative prognostic index (PI) separated the patients into groups with low (n=23), intermediary (n=19) and high risk (n=49) with 10-year survivals of 87%, 58% and 43% (P<0.01). LVMi dropped from 202±58g/m2preoperatively to 152±45g/m2(P<0.0001) at 1.5 years, and 139±40g/m2(P<0.0001) at 10 years (three and six patients, respectively, with paravalvular leak or mitral regurgitation excluded). PI correlated with preoperative (r=0.51, P<0.001), 1.5-year (r=0.46, P<0.01), and 10-year LVMi (r=0.41, P<0.01). Also preoperative left ventricular ejection fraction correlated with the three LVMi measurements. Patients with systemic hypertension had higher LVMi at 1.5 years (193±42, n=6 vs 144±42, n=33, P<0.05) and 10 years (175±39, n=12 vs 124±31g/m2, n=29, P<0.001). Patients with low, intermediary or high PI, excluding those with hypertension, had 1.5-year LVMi of 110±35 (n=8), 134±43 (n=9) and 164±33g/m2(n=16; P<0.01), respectively, and 10-year LVMi of 116±25 (n=17), 126±27 (n=6), and 146±41g/m2(n=6; P<0.05), respectively. There was no relation between LVMi at 1.5 or 10 years and peak or mean Doppler gradient, prosthetic valve size, or valve size index.
Conclusions Left ventricular hypertrophy regression for patients who survived up to 10 years after AVR for AS is dependent on the preoperative risk profile indicating that irreversible myocardial disease is the underlying factor. Systemic hypertension is an important factor in its own right.
Key Words: Aortic stenosis • Valve replacement • Left ventricularhypertrophy • Prognosis • Hypertension
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