| dc.description.abstract | Objective: Cardiovascular disease is a major contributor to morbidity and mortality after organ transplantation. Development of cardiovascular risk factors, like hypertension, is common after transplantation. The mechanism of post transplant hypertension is incompletely understood but vasoconstriction and endothelial dysfunction have been suggested to participate.Aims: To describe the prevalence of new-onset cardiovascular risk factors after lung transplantation, identify independent predictors and to investigate possible vascular mechanisms responsible for the development of hypertension after lung transplantation.Materials and methods: I: Lung transplant recipients (Ltx) without pre-transplant cardiovascular risk factors were included in a retrospective descriptive study. Cumulative prevalence of new-onset hypertension, hypercholesterolemia and diabetes were calculated, and independent preoperative predictors were identified. II-IV: Forearm vascular resistance (FVR) and effects on forearm blood flow of endothelial-dependent and independent vasodilators, inhibition of endothelial nitric oxide synthesis and endothelinA-receptor blockade were investigated in Ltx early (II-III) and late after transplantation (IV), and in healthy subjects by means of venous occlusion plethysmography. Plasma levels of endothelin-1 (ET-1) were determined and arterial compliance was measured by echo-tracking. Results: I: Three years after transplantation 90% of Ltx had developed at least one cardiovascular risk factor, and 40% two or more. Independent pre-transplant predictor for hypertension was; diastolic blood pressure, for hypercholesterolemia; serum-cholesterol level and for diabetes; cystic fibrosis and blood glucose level. II: Basal FVR, endothelial-independent vasodilatation and nitric oxide synthesis-inhibition induced vasoconstriction did not differ significantly between Ltx and controls. Ltx had an increased arterial stiffness. III: Ltx had an impaired vasodilatation to endothelinA-receptor blockade and increased plasma levels of ET-1. IV: Basal FVR was lower in Ltx late after transplantation while endothelial-dependent and -independent vasodilatation did not differ between the groups. There was a significant correlation between endothelin-1 levels and FVR in healthy subjects, but not in Ltx. Conclusions: Development of new-onset cardiovascular risk factors is common after lung transplantation and occurs early. No evidence of general vasoconstriction and endothelial dysfunction was detected after lung transplantation and accordingly, the results question this concept as being responsible for post-transplant hypertension. In contrast, alterations in endothelin-1 handling and endothelinA-receptor function were demonstrated in Ltx, which may have importance for the development of post-transplant hypertension. | en |
