Glucocorticoid-remediable aldosteronism in a young adult with a family history of Conn's syndrome.

Glucocorticoid-remediable aldosteronism is a hereditary form of primary hyperaldosteronism and the most common monogenic cause of hypertension. We present the case of a 24-year-old man with a family history of Conn's syndrome. Yet, in the index patient, classical characteristics of mineralocorticoid excess could be reversed by exogenous glucocorticoids.

Cytomegalovirus infection in heart transplant recipients is associated with impaired endothelial function.

Background: Cardiac allograft vasculopathy (CAV) is initiated by allograft endothelial injury. We hypothesized that a major mechanism by which cytomegalovirus (CMV) could contribute to CAV is by dysregulation of the endothelial vasomotor response.

Methods: Coronary endothelial vasomotor function was determined in 183 consecutive patients (24+/-33 months after transplantation), and was correlated with recipient and donor CMV serological status before transplantation and with documented CMV infection episodes (CMVpp65Ag+).

Beneficial effects of quinaprilat on coronary vasomotor function, endothelial oxidative stress, and endothelin activation after human heart transplantation.

Background: We evaluated the potential of angiotensin-converting enzyme inhibition (ACEI) to modulate resting coronary vasomotor tone and endothelial dysfunction, and to decrease vascular oxidative stress and endothelin (ET)-1 activity in human heart transplant recipients.

Methods: Coronary vasomotor responses and transcardiac metabolism of glutathione, oxidized glutathione, and ET-1 were determined before and after quinaprilat infusion in 32 heart transplant recipients. Furthermore, the potential effects of ACEI on endothelial oxidative stress, ET-1 activity, and nitrosoglutathione formation were investigated using endothelial cell cultures.

Vasodilator response to nifedipine in human coronary arteries with endothelial dysfunction.

The purpose of the current study was to evaluate nifedipine-induced epicardial and microvascular response in human coronary arteries with and without endothelial dysfunction and intimal thickening. The investigation was performed in 70 patients 5 +/- 5 months after heart transplantation. Coronary vasomotor function was determined with intracoronary acetylcholine adenosine, and nifedipine, respectively.