ORTHOTOPIC CARDIAC TRANSPLANTATION REVERSES ABNORMAL REFLEX REGULATION OF THE MICROVASCULATURE IN THE LOWER LEG

Objective: The aim was to investigate the effect of cardiac transplant ation on reflex control of lower leg subcutaneous blood flow. Methods: The reflex regulation of subcutaneous blood flow of the lower leg was studied in 11 patients following orthotopic cardiac transplantation, in 11 patients with severe congestive heart failure (New York Heart As sociation functional class III or IV), and in 11 healthy subjects. Fou r patients were studied before and after cardiac transplantation. Caus e of heart failure was classified as idiopathic dilated cardiomyopathy in all heart failure patients and in all the cardiac transplant patie nts before transplantation. Blood flow was measured by the local (133) xenon washout method in the supine position and during 45 degrees head up tilt. Results: When performing head up tilt without activation of the local nervous venoarteriolar axon reflex in patients with congesti ve heart failure, the relative subcutaneous blood flow increased abnor mally, by 50(SD 25)%, but in patients after cardiac transplantation a normal decrease was seen [-28(13)%, p < 0.001]. The responses in the t ransplant group were similar to those observed in normal controls with a decrease in blood flow [-32(15)%; NS]. Head up tilt with simultaneo us activation of the local venoarteriolar axon reflex increased blood flow [31(22)%] in patients with heart failure as compared to the decre ase in blood flow found in the transplants [-44(17)%, p < 0.001]. The decrease of blood flow was not significantly different between the tra nsplant group and control subjects [-53(19)%; NS]. Conclusion: These r esults indicate that abnormal reflex regulation in severe congestive h eart failure with peripheral vasodilatation of the lower leg during or thostasis is reversed and even normalised after cardiac transplantatio n. The haemodynamic consequence may be a regaining of an oedema-protec tive mechanism that eliminates the stress (capillary hypertension) on the microcirculation seen in severe heart failure.