Temporal response of left ventricular performance to mitral valve surgery

Abstract

The temporal changes in left ventricular performance and hypertrophy after valve replacement for mitral regurgitation (MR) or stenosis (MS) are unclear. We studied 16 patients with MR and 17 patients with MS using echocardiography before and serially after surgery for an average of 15 months. Before surgery, average end-diastolic and end-systolic dimension (EDD and ESD, respectively) and left ventricular muscle cross-sectional area (CSA), an index of left ventricular mass, were significantly greater than normal in subjects with MR. After surgery, EDD fell significantly, from 6.40 ± 1.00 (SD) cm to 5.40 ± 1.44 cm (p < 0.01); ESD (3.94 ± 0.93 cm) remained essentially unchanged postoperatively; CSA (25.9 ± 6.9 cm2) decreased significantly to 22.0 ± 6.7 cm2 (p < 0.01). In patients with MS, EDD, ESD and CSA were normal and did not change significantly at any time after surgery. The left ventricular ejection fraction (EF) was normal in both groups preoperatively (MR group 0.68 ± 0.07, MS group 0.63 ± 0.11). After surgery, EF was significantly reduced in patients with MR, while in patients with MS it was unchanged. We separated MR patients into two subgroups. In 12 subjects (group 1) with preoperative EDD = 5.94 ± 0.42 cm, ESD = 3.55 ± 0.43 cm, and EF = 0.70 ± 0.05, EF fell slightly by 6 months after surgery to 0.59 ± 0.10 (p < 0.01), but remained within the normal range. Concomitantly, left ventricular hypertrophy regressed, as CSA was 24.2 ± 6.5 cm2 before and 18.6 ± 2.4 cm2 after surgery (p < 0.01). In contrast, in four subjects (group 2) with preoperative EDD = 8.07 ± 0.35 cm, ESD = 5.69 ± 0.70 cm, and EF = 0.57 ± 0.05, left ventricular function progressively deteriorated after surgery, with EF falling to 0.26 ± 0.06 (p < 0.01). In the latter group left ventricular hypertrophy did not regress (CSA = 31.5 ± 4.5 cm2 before and 31.9 ± 3.4 cm2 after surgery, NS). Techniques for myocardial preservation during mitral valve surgery did not differ between the MR and MS groups. In group 2 MR subjects, there was no evidence of intraoperative myocardial infarction. We conclude that in patients with MR who have moderate left ventricular dilatation and a normal EF preoperatively, there is regression of myocardial hypertrophy and only minimal reduction of left ventricular percent shortening after mitral valve replacement. However, in patients with MR who exhibit before surgery an EDD > 7.00 cm, an ESD > 5.00 cm and a low normal or depressed EF, left ventricular shortening likely has become partially dependent on systolic afterload reduction through a low impedance leak; after mitral valve replacement, left ventricular EF becomes markedly impaired and chamber dilatation and myocardial hypertrophy persist.