The impact of dose of the angiotensin-receptor blocker valsartan on the post-myocardial infarction ventricular remodeling: study protocol for a randomized controlled trial

Valsartan in post-MI remodeling (VALID) is a randomized, open-label, single-blinded multicenter study designed to compare the efficacy of different clinical dose of valsartan on the post-MI ventricular remodeling. This study also aims to assess neurohormone change and clinical parameters of patients during the post-infarct period. A total of 1116 patients with left ventricular dysfunction following the first episode of acute ST-elevation MI are to be enrolled and randomized to a maximal tolerable dose (up to 320 mg/day) or usual dose (80 mg/day) of valsartan for 12 months in 2:1 ratio. Echocardiographic analysis for quantifying post-MI ventricular remodeling is to be conducted in central core laboratory. Clinical assessment and laboratory test are performed at fixed times.VALID is a multicenter collaborative study to evaluate the impact of dose of valsartan on the post-MI ventricular remodeling. The results of the study provide information about optimal dosing of the drug in the management of patients after MI. The results will be available by 2012.NCT01340326Progressive enlargement of the heart chamber and deterioration of contractile function after myocardial infarction (MI), termed post-MI ventricular remodeling, is associated with development of heart failure and poor prognosis [1-3]. The magnitude of post-MI remodeling is influenced by several determinants, most notably infarct size [4], but also by ventricular wall stress [5], patency of infarct-related artery [6], and a number of neurohormonal factors [7]. Thus, the consequence of post-MI remodeling varies among patients with acute MI even in the era of reperfusion therapy [8]. Modification of neurohormonal acitivities, particularly the rennin-angiotensin-aldosterone system (RAAS), can significantly influence the process of ventricular remodeling after acute MI. Suppression of angiotensin activity either by inhibition of angiotensin-converting enzyme (ACE) [9-11] or by blockade of angiotensin II receptor [12]