Inhibitory effect of valsartan against progression of left ventricular dysfunction after myocardial infarction: T-VENTURE study.
ABSTRACT Angiotensin-converting enzyme inhibitors (ACEI) reduce the mortality in the chronic phase of myocardial infarction (MI), and similar effects of angiotensin receptor blockers (ARB) have been reported. However, these effects of ARB have not yet been established in Japanese patients. A multicenter randomized study was designed for the present study to examine the effect of valsartan as compared to that of ACEI against left ventricular dysfunction after MI.
Patients with acute MI were randomly allocated to either the valsartan group (n=120; mean age 63 +/-1.0) or the ACEI group (n=121; mean age 62.9 +/-1.0) and followed up until 6 months. Left ventriculography was performed during hospital admission and at 6 months. The blood pressure was similar in the 2 groups throughout the study. The incidences of cardiovascular events and target vessel revascularization were similar, although that of adverse events was significantly higher in the ACEI (12.4%) than in the valsartan group (3.3%; P<0.05). There were no differences in left ventricular ejection fraction and left ventricular end-diastolic volume index between the groups.
Valsartan exhibits similar efficacy effective to that of ACEI in preventing left ventricular dysfunction in Japanese patients with acute MI, and is, in addition, better tolerated than ACEI.
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ABSTRACT: The renin-angiotensin-aldosterone system (RAAS) is one of the main regulators of blood pressure, renal hemodynamics, and volume homeostasis in normal physiology, and contributes to the development of renal and cardiovascular (CV) diseases. Therefore, pharmacologic blockade of RAAS constitutes an attractive strategy in preventing the progression of renal and CV diseases. This concept has been supported by clinical trials involving patients with hypertension, diabetic nephropathy, and heart failure, and those after myocardial infarction. The use of angiotensin II receptor blockers (ARBs) in clinical practice has increased over the last decade. Since their introduction in 1995, seven ARBs have been made available, with approved indications for hypertension and some with additional indications beyond blood pressure reduction. Considering that ARBs share a similar mechanism of action and exhibit similar tolerability profiles, it is assumed that a class effect exists and that they can be used interchangeably. However, pharmacologic and dosing differences exist among the various ARBs, and these differences can potentially influence their individual effectiveness. Understanding these differences has important implications when choosing an ARB for any particular condition in an individual patient, such as heart failure, stroke, and CV risk reduction (prevention of myocardial infarction). A review of the literature for existing randomized controlled trials across various ARBs clearly indicates differences within this class of agents. Ongoing clinical trials are evaluating the role of ARBs in the prevention and reduction of CV rates of morbidity and mortality in high-risk patients.Advances in Therapy 05/2010; 27(5):257-84. DOI:10.1007/s12325-010-0028-3 · 2.44 Impact Factor
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ABSTRACT: Angiotensin II receptor blockers (ARBs) inhibit the renin-angiotensin system. As a result, these agents provide beneficial effects in terms of cardiovascular (CV) and renal protection, independent of their blood pressure-lowering effects. Telmisartan and valsartan are the most intensively studied ARBs for the effects on CV outcomes. Randomized clinical trials assessing morbidity and mortality end points have included a range of patient types, including those with hypertension, hypertension with Type 2 diabetes, high CV risk without hypertension, ischemic heart disease, stroke and heart failure. Few head-to-head comparisons between telmisartan and valsartan have been performed. However, some blood pressure-independent properties of these two ARBs can be scrutinized from separate studies in the available literature.Expert Review of Cardiovascular Therapy 08/2012; 10(8):1061-72. DOI:10.1586/erc.12.80
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ABSTRACT: OBJECTIVES: To investigate the protective effects of valsartan against smoking-induced left ventricular dysfunction and explore the potential mechanisms involved. METHODS: Rats were randomly divided into 3 groups: smoking group (exposed to cigarette smoke), valsartan group (exposed to cigarette smoke and treated orally with valsartan), and control group. Transthoracic echocardiography was performed to evaluate left ventricular systolic and diastolic function. Oxidative stress was evaluated by detecting malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the supernatant of left ventricular tissue. Cardiomyocyte apoptotic rate was determined by flow cytometry with Annexin V/PI staining. Serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-a (TNF-α), and monocyte chemotactic protein-1 (MCP-1) were detected to reflect the extent of systemic inflammation. RESULTS: The echocardiographic data indicated that valsartan has protective effects against cigarette smoke-induced left ventricular systolic dysfunction (LVSD). Our findings showed a significant decrease in MDA level and increases in SOD and GSH-Px activities in the valsartan group compared to the smoking group. The apoptotic rate in the valsartan group was significantly lower than in the smoking group. The concentrations of hs-CRP, IL-6, TNF-α and MCP-1 in the valsartan group were significantly lower than in the smoking group. CONCLUSIONS: Our study demonstrates that valsartan has protective effects against smoking-induced LVSD by attenuating oxidative stress, apoptosis, and inflammation.International journal of cardiology 03/2012; DOI:10.1016/j.ijcard.2012.03.068 · 6.18 Impact Factor