Abstract

The reduced exercise capacity observed in most patients after heart transplantation may be due to treatment with immunosuppressive drugs, deconditioning, cardiac denervation, and graft rejection. Cardiac allograft vasculopathy (CAV) is presently the major factor limiting long-term survival after transplantation. Little information is available with regard to the relationship between CAV and functional impairment in these patients. Prospective. A university hospital and a large transplant center. About 37+/-5 months (range, 2 to 137 months) after orthotopic heart transplantation, 120 patients underwent lung function testing, cardiopulmonary exercise testing, and right and left heart catheterization. Significant CAV was defined as a stenosis > or =70% or severe diffuse obliteration in any of the three main vessels. Group I (n = 28) had a significant CAV; group II (n = 92), without a remarkable CAV, was the control group. Overall, the maximum heart rate was 86+/-2% of what was predicted, and the peak oxygen consumption was 18.8+/-0.7 mL/kg/min (64% of that predicted). Groups I and II did not show significant differences with regard to anthropometric data, hemodynamic measurements, or number of rejection episodes. Group I exhibited significant differences in maximum heart rate (120+/-5 vs. 134+/-3 beats/min; p<0.01), work capacity (47+/-5% vs. 59+/-3%; p<0.05), peak oxygen uptake (16+/-1 vs. 20+/-1 mL/min/kg; p<0.01), and functional dead space ventilation (31+/-2 vs. 26+/-1; p<0.01). Pretransplant status, etiology of heart failure, ischemic time, and the number of rejection episodes did not correlate with any exercise parameter. Following heart transplantation, patients with significant CAV show a diminished exercise capacity, a reduced oxygen uptake, and a ventilation-perfusion mismatch. Thus, CAV may be a major factor limiting exercise capacity in heart-transplant patients.

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