EFFECT OF ORTHOTOPIC CARDIAC TRANSPLANTATION ON PERIPHERAL VASCULAR FUNCTION IN CONGESTIVE-HEART-FAILURE - INFLUENCE OF CYCLOSPORINE THERAPY

The objective of this study was to examine peripheral vascular functio n before and after cardiac transplantation and to assess the effect of immunosuppressive therapy on peripheral vascular reactivity. Peripher al vascular function abnormalities present in congestive heart failure may be reversed with cardiac transplantation, but immunosuppressive t herapy may alter these changes in the peripheral vasculature. Venous o cclusion plethysmography was used to study peripheral vascular functio n in nine patients with severe congestive heart failure who underwent cardiac transplantation. Forearm blood flow and forearm vascular resis tance were measured:in patients with congestive heart failure in respo nse to cold stimulation, maximal hyperemia, and hand grip exercise (1) before transplantation; (2) 24 to 36 hours posttransplantation before the commencement of cyclosporine; (3) 6 to 8 days posttransplantation in the presence of therapeutic cyclosporine levels; and (4) 6 weeks p osttransplantation. Venous capacitance was also measured. After cardia c transplantation, mean arterial pressure increased and remained eleva ted. Forearm blood flow initially increased after transplantation but subsequently decreased with cyclosporine. Cold-induced reflex sympathe tic activation decreased immediately after transplantation but was sig nificantly enhanced with cyclosporine. The maximal vasodilatory respon se following ischemic cuff occlusion and with 5 minutes of isometric h and grip exercise increased significantly after transplantation and re mained improved at 6 weeks. Thus after cardiac transplantation, periph eral vasodilator function improves and is not altered by cyclosporine. However, with cyclosporine therapy resting forearm vascular resistanc e increases and reflex sympathetic vasoconstriction is enhanced, sugge sting that cyclosporine may potentiate adrenergic-mediated peripheral vasoconstriction and thus may contribute to posttransplant hypertensio n.