Histopathologic correlates of myocardial improvement in patients supported by a left ventricular assist device

Background: Left ventricular assist devices unload the failing heart and improve hemodynamic function and tissue architecture. In some patients improvement allows for left ventricular assist device removal. We retrospectively compared histologic features in patients who were weaned off left ventricular assist device support with those who remained on support without evidence of clinical remission. Methods: We graded left ventricular core samples taken at implantation on a scale we designed for evaluating severity and extent of fibrosis and hypertrophy. We correlated the grades with a computerized semiquantitative analysis of picrosirius-red and Masson's trichrome-stained sections. We evaluated interstitial (10x), perivascular (20x), and replacement (4x) fibrosis. Hypertrophy was assessed by myocyte diameter, cytoplasmic area, and nuclear/cytoplasmic ratio. Results: All patients (N=17) underwent left ventricular assist device implantation for heart failure. In eight patients improvement allowed left ventricular assist device removal. The groups did not differ in age (24.1 vs. 25 years, P=.4) or mean time on left ventricular assist device support (506 vs. 414 days, P=.24). All mean measures showed significantly less hypertrophy in the left ventricular assist device-removal group than in the nonremoval group, respectively (cytoplasmic area, 58.00 vs. 77.18 mu m(2), P=.021; myocyte diameter, 20.32 vs. 25.35 mu m, P=.004; nuclear/cytoplasmic ratio, 11.04 vs. 8.69, P=.053). Although not statistically significant, the left ventricular assist device-removal group tended toward less overall fibrosis than the nonremoval group (11.57 vs. 13.24, P=.214). Conclusions: Left ventricular assist device-removal patients had less hypertrophy and fibrosis overall than did nonremoval patients. These findings may help identify patients with a higher probability of left ventricular assist device removal and myocardial recovery. (C) 2011 Elsevier Inc. All rights reserved.