Abstract 15154: Effect of Continuous-Flow Mechanical Support on Microvasculature Remodeling may Contribute Adversely to Bridge to Recovery in the Failing Heart
Introduction: Left ventricle (LV) unloading using a left ventricular assist device (LVAD) has been shown to enhance reverse LV remodeling. Despite the increasing need for its usage, the direct effect of continuous-flow LVAD with decreased pulsatility and shear stress on microvasculature is unknown. We examined that pulseless continuous flow may affect myocardial microvasculature and remodeling of the failing heart.
Methods: The study included 24 patients with chronic heart failure who underwent LVAD implantation. Pulsatile-flow LVAD was used in 11 patients (P group) with a median support period of 954 days, whereas continuous-flow LVAD was used in 13 patients (C group) with a median support period of 709 days. Serial echocardiograms were compared between the 2 groups. Transmural LV tissues were sampled during both the implantation and explantation of the LVAD in all patients for histopathological assessment including immunolabeling for CD31 and α-smooth muscle actin (SMA).
Results: Echocardiography showed that the LV systolic dimension and LV ejection fraction improved to a significantly greater extent in the P group (63 ± 2 mm to 46 ± 9 mm and 15 ± 8% to 34 ± 4%) than in the C group (65 ± 2 mm to 59 ± 3 mm and 17 ± 2% to 22 ± 4%; P = 0.008 and P = 0.05). Histological analysis showed significantly increased microvasculature density and decreased cardiomyocyte size during LVAD support in the P and C groups, without significant difference between the 2 groups. Further, microvessel thickness of the SMA-positive layer significantly increased during LVAD support in the C group (9 ± 0.4 μ m to 14 ± 0.6 μ m, P = 0.0002), but did not change in the P group (10 ± 1.7 μ m to 12 ± 0.7 μ m, P = 0.28).
Conclusion: Even though, mechanical unloading may enhance the reverse remodeling of cardiomyocytes and result in increased microvascular density, continuous-flow LVAD induced smooth muscle cell hypertrophy of myocardial microvasculature, suggesting its adverse effect for bridge to recovery in the failing heart.
- © 2012 by American Heart Association, Inc.