Hypertension in thoracic transplant recipients

Abstract

There are many mechanisms underlying the hypertension which occurs after thoracic transplantation. Previous disease, effects of cyclosporin, tacrolimus and steroid immunosuppression and cardiac denervation are major contributory factors. Abnormal sodium and water balance is an important common mediating factor. A new approach is clearly needed for classifying the severity of hypertension in these patients taking into account day-night variation and total blood pressure

New-Onset Cardiovascular Risk Factors in Lung Transplant Recipients

“…Previously reported pre-operative characteristics of patients with manifest hypertension after organ transplantation include pre-transplant hypertension, age and male gender. 7,16 In this study we could not confirm these factors, but the discrepancy may be partially explained by our study design wherein we sought to identify new-onset hypertension, and thus patients with pre-existing hypertension were excluded. In other studies, older male patients probably have a higher prevalence of hypertension both before and after transplantation, which may obscure the importance of other factors.…”

Blunted Vascular Response to Endothelin-A Receptor Blockade in Cyclosporine-Treated Lung Transplant Recipients

“…The prevalence is highest for heart transplant recipients, with approximately 70% developing hypertension 1 year after transplantation, whereas lung, kidney, and liver transplant recipients have a lower prevalence, around 50%. 1,3,19 The higher prevalence for heart transplant recipients has been blamed on heart denervation and a higher prevalence of preexisting vascular disease before transplantation. 3,19 In the present investigation, we decided to include only lung transplant recipients without manifest hypertension because this group has a low incidence of pretransplantation vascular dysfunction 19,20 and we wanted to discriminate between the vascular effects of chronic CsA treatment and hypertension per se.…”

Angiotensin converting enzyme insertion/deletion polymorphism does not influence postcardiac transplantation hypertension onset or progression

“…1 Hypertension also has a contributory role in the development of other posttransplantation morbidities (eg, chronic renal dysfunction, left ventricular dysfunction, and graft coronary artery disease). 13 The etiology of posttransplantation hypertension is multifactorial. Early postoperative volume overload, peripheral vasoconstriction (secondary to long-standing reduced cardiac output), and denervation of the transplanted organ (loss of vagal tone and baroceptor reflex) are significant factors.…”