LEFT-VENTRICULAR ECHOCARDIOGRAPHIC AND HISTOLOGIC-CHANGES - IMPACT OFCHRONIC UNLOADING BY AN IMPLANTABLE VENTRICULAR ASSIST DEVICE

Objectives. We studied the effects of chronic left ventricular unloadi ng by a ventricular assist device and assessed left ventricular morpho logic and histologic changes. Background. The implantable left ventric ular assist device has been effective as a ''bridge'' to cardiac trans plantation. Although there are reports documenting its circulatory sup port, little is known about the effects of chronic left ventricular un loading on the heart itself. Methods. We performed intraoperative tran sesophageal echocardiography at the insertion and explantation of a He artMate left ventricular assist device in 19 patients with end-stage h eart failure. They were supported by the assist device for 3 to 153 da ys (mean [+/-SD] 68+/-33). Measurements were taken retrospectively to obtain left atrial and ventricular diameters and interventricular sept al and posterior wall thickness. Histologic examinations were made fro m the left ventricular myocardial specimens of 15 patients at the time s of insertion and explantation for heart transplantation. Insertion a nd explantation specimens were compared qualitatively (0 to 3 scale) f or wavy fibers, contraction band necrosis and fibrosis, with quantitat ive measurement of minimal myocyte diameter across the nucleus. Result s. Left atrial and left ventricular diastolic and systolic diameters d ecreased immediately after insertion of the left ventricular assist de vice (from 46 to 35, 63 to 41 and 59 to 36 mm, respectively, all p < 0 .001). Left ventricular wall thickness increased from 10 to 14 mm (p < 0.001) for the interventricular septum and from 10 to 13 mm for the p osterior wall (p < 0.001). No echocardiographic measurements showed si gnificant subsequent changes at the chronic stage. Myocardial histolog ic findings demonstrated a reduction in myocyte damage (from 1.9 to 0. 5, p < 0.001, for wavy fiber and from 1.3 to 0.2, p < 0.01, for contra ction band necrosis) and an increase in fibrosis (from 1.3 to 1.9, p < 0.05), but without significant change in myocyte diameter (from 15.6 to 16.8 mu m, p = 0.065). Conclusions. Left ventricular unloading with the implantable assist device induces an immediate increase in wall t hickness, consistent with the reduction in chamber size, thereby decre asing wall stress. Chronic unloading allows myocardial healing and fib rosis without evidence for ongoing myocyte damage or atrophy. Left ven tricular assist device insertion may have a role in ''resting'' the ve ntricle for selected patients with heart failure.