Paolo Cesarano

Effects of AT1 receptor antagonism with candesartan on endothelial function in patients with hypertension and coronary artery disease.

Endothelial dysfunction is a major determinant of atherosclerosis and a negative prognostic factor in patients with coronary artery disease and hypertension. Recovery of endothelial dysfunction has been associated with improved prognosis in these patients. The aim of the present study was to verify whether antagonism of angiotensin II AT1 receptors with an angiotensin receptor blocker, candesartan, improved endothelial function in patients with hypertension, stable coronary artery disease, and endothelial dysfunction. We studied 26 patients who were receiving β‐blockers with optimal blood pressure control, in a randomized, double blind study. Patients were randomized to placebo (n=13) or to candesartan 16 mg/d (n=13) for 2 months. Endothelial function was assessed by ultrasound using hyperemic flow‐mediated dilation of the brachial artery. Mean arterial blood pressure was unchanged in both groups (from 93.3±9.2 to 93.2±17.3 mm Hg in the candesartan group and from 101.3±14.2 to 102.3±13.9 mm Hg in the placebo group; both P=ns). Maximal blood flow was similar between placebo and candesartan groups at baseline and at the end of the study, whereas flow‐mediated dilation significantly increased in the candesartan group (from 5.27%±1.69% to 7.15%±2.67%; P=0.01) but remained unchanged in the placebo group (from 4.49%±1.97% to 5.88%±2.30%; P=ns). AT1 receptor antagonism with candesartan, in addition to β‐blocker therapy, improves endothelial function in high‐risk hypertensive patients.

Rest-redistribution 201-Thallium single photon emission computed tomography predicts myocardial infarction and cardiac death in patients with ischemic left ventricular dysfunction

The prognostic role of rest-redistribution 201-Thallium imaging has not been extensively investigated in patients with left ventricular ischemic dysfunction. Objective The aim of this study was to evaluate the ability of rest-redistribution 201-Thallium single photon emission computed tomography to predict cardiac death and occurrence of acute myocardial infarction in patients with ischemic mild-to-moderate left ventricular dysfunction. Methods One-hundred and twenty-six patients with chronic coronary artery disease and mean left ventricular ejection fraction 39 ± 11% were followed-up for 30 ± 17 months after a rest-redistribution 201-Thallium imaging single photon emission computed tomography. Cardiac death and acute myocardial infarction were considered as major cardiac events. Results During the follow up, 11 (9%) cardiac deaths and 9 (7%) acute myocardial infarctions occurred. The only variable showing significant difference between patients with and without events was the number of severe irreversible defects (1.7 ± 1.9 versus 0.9 ± 1.2, respectively; P = 0.02). By Kaplan–Meier analysis, the presence of three or less, or more than three severe defects was selected as the best cutoff to identify patients with longer event-free survival from cardiac death or acute myocardial infarction (log rank 19.84; P < 0.0001). When only cardiac death was considered as clinical event, the presence of at least two severe defects best separated patients who died from those who survived (log rank 8.68; P = 0.0032). Conclusion Rest-redistribution 201-Thallium single photon emission computed tomography provides prognostic information in coronary patients with mild-to-moderate left ventricular dysfunction. The number of severe irreversible defects per patient is a powerful predictor of prognosis.

Role of Angiotensin-Receptor Blockers in the Prevention of Cardiovascular Risk: Clinical Guidelines

The development and progression of cardiovascular disease can be regarded as a continuum (Fig. 1) [1]. Targeting different points within this continuum is therefore of major importance for reducing cardiovascular morbidity and mortality. Inhibition of the renin-angiotensin-aldosterone system (RAAS) has become a key target in this regard, given that angiotensin II (Ang II) has been implicated as a pathogenic factor at many steps in the development and progression of cardiovascular disease [2, 3].