Delayed and Incomplete Reversal of Impaired Metabolic Vasodilation in Patients with Heart Failure During Long-term Circulatory Support with Left Ventricular Assist Device

Impaired vasodilation in response to metabolic stimuli in the peripheral circulation is an important determinant of exercise intolerance in patients with congestive heart failure (CHF). The pathogenesis of impaired metabolic vasodilation in patients with CHF is uncertain but may be related in part to chronic reductions in peripheral blood flow in patients with low cardiac output (CO). left ventricular assist device (LVAD) is an implantable mechanical pump that provides non-pharmacologic means to markedly increase CO in patients with severe CHF for long periods of time. Whether long-term mechanical restoration of normal resting CO with an LVAD enhances metabolic vasodilation in the peripheral circulation of patients with CHF is unknown. Accordingly, peak forearm blood flow (FBF, ml/min/100 ml) after 5 minutes of brachial artery occlusion ( maximal metabolic vasodilation stimulus) was measured with venous occlusion plethysmography in 8 patients with NYH Class IV CHF (mean age 52 yrs, mean EF 22%) before, and 1 and 8 weeks (wks) after continuous LVAD support and in 8 normal subjects. Mean arterial pressure (MAP, mmHg) was measured during each FBF measurement in the contralateral arm by cuff method. MAP, peak FBF, and maximum vascular conductance (calculated in arbitrary units as FBF/MAP) after arterial occlusion were as follows: Mean CO increased from 2.3 l/min before LVAD to 5.4 l/min 1 and 8 wks during LVAD support. Despite early normalization of CO and MAP within 1 week after LVAD, the maximum vascular conductance after brachial artery occlusion did not change after 1 week, and remained less than that observed in normal subjects after 8 weeks of LVAD support. The delayed and incomplete reversal of abnormal metabolic vasodilation during long-term continuous LVAD support suggests that mechanisms in addition to reduced CO contribute to decreased metabolic vasodilation in patients with CHF.