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Published on: April 8, 2013
Valsartan in the treatment of heart failure or left ventricular dysfunction after myocardial infarction
Naylin Bissessor1, Harvey White
1Green Lane Cardiovascular Research Unit,Auckland City Hospital, Auckland, New Zealand.
Insights
Valsartan, an angiotensin receptor blocker, proved as effective as ACE inhibitors for post-myocardial infarction patients. Combination therapy offered no added benefit and increased adverse effects.
Area of Science:
- Cardiology
- Pharmacology
Background:
- The renin-angiotensin-aldosterone system (RAAS) regulates cardiovascular integrity.
- Angiotensin II effects, mediated by AT1 receptors, cause vasoconstriction and myocyte growth, leading to cardiac remodeling.
- Acute myocardial infarction (AMI) management aims to prevent left ventricular dysfunction.
Purpose of the Study:
- To evaluate the efficacy of angiotensin receptor blockers (ARBs) versus ACE inhibitors in post-AMI patients.
- To determine if combination therapy with an ARB and ACE inhibitor offers superior outcomes.
- To review valsartan's role in managing left ventricular dysfunction post-AMI.
Main Methods:
- The VALIANT trial compared valsartan (ARB) with captopril (ACE inhibitor) in high-risk post-AMI patients.
- Patients had left ventricular dysfunction or heart failure.
- Outcomes included cardiovascular morbidity and mortality.
Main Results:
- Valsartan demonstrated equal efficacy and non-inferiority to captopril.
- Combination therapy provided no incremental benefit over monotherapy.
- Combination therapy resulted in a higher incidence of adverse effects.
Conclusions:
- Valsartan is a viable alternative to ACE inhibitors for high-risk post-AMI patients.
- ARB monotherapy is effective, and combination therapy offers no additional advantage.
- Valsartan's pharmacokinetics, dosing, and safety profile are important considerations.
Abstract:
The physiological role of the renin angiotensin aldosterone system (RAAS) is to maintain the integrity of the cardiovascular system. The effect of angiotensin II is mediated via the angiotensin type I receptor (AT1 ) resulting in vasoconstriction, sodium retention and myocyte growth changes. This causes myocardial remodeling which eventually leads to left ventricular hypertrophy, dilation and dysfunction. Inhibition of the RAAS with angiotensin converting enzyme (ACE) inhibitors after acute myocardial infarction has been shown to reduce cardiovascular morbidity and mortality. Angiotensin receptor blockers (ARBs) specifically inhibit the AT1 receptor. It has not been known until the performance of the VALIANT (valsartan in acute myocardial infarction trial) whether blockade of the angiotensin receptor with an ARB or combination of an ACE inhibitor and ARB leads to similar outcomes as an ACE inhibitor. The VALIANT trial demonstrated equal efficacy and non-inferiority of the ARB valsartan 160 mg bid compared with captopril 50 mg tds, when administered to high risk patients with left ventricular dysfunction or heart failure in the immediate post myocardial infarction period. The combination therapy showed no incremental benefit over ACE inhibition or an ARB alone and resulted in increased adverse effects. This review examines the role of valsartan in left ventricular dysfunction post myocardial infarction. We also discuss pharmacokinetics, dosing, side effects, and usage in the elderly.
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