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Eur J Cardiothorac Surg 2007;32:588-595. doi:10.1016/j.ejcts.2007.07.003
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Left ventricular mass: impact on left ventricular contractile function and its reversibility in patients undergoing aortic valve replacement

^a Department of Cardiovascular Surgery, Osaka Rosai Hospital, Sakai, Japan
^b Department of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Suita, Japan

Received 9 January 2007; received in revised form 27 June 2007; accepted 2 July 2007.

^_* Corresponding author. Address: Department of Cardiovascular Surgery, Labor Health and Welfare Organization Osaka Rosai Hospital, 1179-3 Nagasone-cho, Sakai, Osaka 591-8025, Japan, Tel.: +81 72 252 3561; fax: +81 72 255 5492. (Email: kazuhiro{at}orh.go.jp).

Background: We examined the relationships of left ventricular (LV) contractile state with LV geometry and hypertrophy in patients with aortic valve disease, and investigated the reversibility of LV hypertrophy and contractility following aortic valve replacement. Methods: Preoperative data from quantitative cineangiography and pressure measurements in 132 patients with chronic aortic valve disease, of whom 82 aortic regurgitation (AR), 41 aortic stenosis (AS), and 9 had mixed stenosis and regurgitation (AS-AR), were reviewed. Late after surgery, 59 of the patients (39 with AR, 20 with AS) were studied to elucidate the postoperative reversibility of LV performance and regression of LV hypertrophy. Results: Preoperatively, multiple comparison tests found significant changes in the variables of LV volumes and dimensions in relation to LV contractile state. In stepwise regression analysis, the LV mass index was initially incorporated into a multivariate regression model as an important correlate of LV contractile state. LV geometric variables showed either no or a poor correlation with contractile state. Following aortic valve replacement, improvement of LV contractile dysfunction and regression of LV hypertrophy were limited in many of the patients who had severe preoperative hypertrophy (LV mass index 200% of normal or greater). Further, a close association between LV hypertrophy and LV contractility persisted postoperatively. Conclusion: Our results suggest that the development of LV hypertrophy in terms of an increase in LV mass index, in contrast to changes in geometric patterns, is significantly associated with deterioration in contractile function. LV hypertrophy may become irreversible and pathological at equivalent degrees of hypertrophy (LV mass index 200% of normal), regardless of the type of aortic valve lesion.

Abbreviations: LV = left ventricular • AR = aortic regurgitation • AS = aortic stenosis • AS-AR = mixed aortic stenosis and regurgitation • EDV(I) = end-diastolic volume (index), cc (cc/m²) • ESV (I) = end-systolic volume (index), cc (cc/m²) • EDD = end-diastolic minor-axis dimension, mm • ESD = end-systolic minor-axis dimension, mm • EF = ejection fraction • ESS = end-systolic stress, kdyn/cm² • EDS = end-diastolic stress, kdyn/cm² • PSS = peak systolic stress, kdyne/cm² • CS = contractile state • EOA (I) = effective orifice area (index), cm² (cm²/m²)

Key Words: Left ventricular hypertrophy • Left ventricular contractility • Aortic valve disease • Left ventricular mass

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