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Valsartan in the treatment of heart failure or left ventricular dysfunction after myocardial infarction.

Bissessor N, White H - Vasc Health Risk Manag (2007)

Bottom Line: This causes myocardial remodeling which eventually leads to left ventricular hypertrophy, dilation and dysfunction.Angiotensin receptor blockers (ARBs) specifically inhibit the AT1 receptor.We also discuss pharmacokinetics, dosing, side effects, and usage in the elderly.

View Article: PubMed Central - PubMed

Affiliation: Green Lane Cardiovascular Research Unit,Auckland City Hospital, Auckland, New Zealand.

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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Related in: MedlinePlus

The renin angiotensin aldosterone system. Reproduced with permission from McMurray JJ, Pfeffer MA, Swedberg K, et al. 2004. Which inhibitor of the renin-angiotensin system should be used in chronic heart failure and acute myocardial infarction? Circulation, 110:3281–8. Copyright © 2004. Massachusetts Medical Society. All rights reserved.
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fig1: The renin angiotensin aldosterone system. Reproduced with permission from McMurray JJ, Pfeffer MA, Swedberg K, et al. 2004. Which inhibitor of the renin-angiotensin system should be used in chronic heart failure and acute myocardial infarction? Circulation, 110:3281–8. Copyright © 2004. Massachusetts Medical Society. All rights reserved.

Mentions: The RAAS is responsible for maintaining the integrity of the cardiovascular system (see Figure 1). The ACE catalyzes the conversion of angiotensin I to angiotensin II. Homeostasis of sodium and the extracellular fluid volume as well as vasoconstriction occur through direct action of angiotensin II on the AT1 (angiotensin I) receptor. In addition the ACE is also responsible for the degradation of bradykinin which is a potent vasodilator (Goodfriend et al 1996). Stimulation of the AT2 receptor has also been shown to induce vasodilation and natriuresis (Goodfriend et al 1996). This effect is in contrast to stimulation of the AT1 receptor which causes vasoconstriction and sodium retention. In heart failure a vicious cycle prevails in which the RAAS activity is increased. This results in increased angiotensin II that perpetuates vasoconstriction, left ventricular hypertrophy, endothelial dysfunction, and myocardial remodeling (see Table 1). Aldosterone and catecholamine increases also maintain hemodynamics.


Valsartan in the treatment of heart failure or left ventricular dysfunction after myocardial infarction.

Bissessor N, White H - Vasc Health Risk Manag (2007)

The renin angiotensin aldosterone system. Reproduced with permission from McMurray JJ, Pfeffer MA, Swedberg K, et al. 2004. Which inhibitor of the renin-angiotensin system should be used in chronic heart failure and acute myocardial infarction? Circulation, 110:3281–8. Copyright © 2004. Massachusetts Medical Society. All rights reserved.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2291334&req=5

fig1: The renin angiotensin aldosterone system. Reproduced with permission from McMurray JJ, Pfeffer MA, Swedberg K, et al. 2004. Which inhibitor of the renin-angiotensin system should be used in chronic heart failure and acute myocardial infarction? Circulation, 110:3281–8. Copyright © 2004. Massachusetts Medical Society. All rights reserved.
Mentions: The RAAS is responsible for maintaining the integrity of the cardiovascular system (see Figure 1). The ACE catalyzes the conversion of angiotensin I to angiotensin II. Homeostasis of sodium and the extracellular fluid volume as well as vasoconstriction occur through direct action of angiotensin II on the AT1 (angiotensin I) receptor. In addition the ACE is also responsible for the degradation of bradykinin which is a potent vasodilator (Goodfriend et al 1996). Stimulation of the AT2 receptor has also been shown to induce vasodilation and natriuresis (Goodfriend et al 1996). This effect is in contrast to stimulation of the AT1 receptor which causes vasoconstriction and sodium retention. In heart failure a vicious cycle prevails in which the RAAS activity is increased. This results in increased angiotensin II that perpetuates vasoconstriction, left ventricular hypertrophy, endothelial dysfunction, and myocardial remodeling (see Table 1). Aldosterone and catecholamine increases also maintain hemodynamics.

Bottom Line: This causes myocardial remodeling which eventually leads to left ventricular hypertrophy, dilation and dysfunction.Angiotensin receptor blockers (ARBs) specifically inhibit the AT1 receptor.We also discuss pharmacokinetics, dosing, side effects, and usage in the elderly.

View Article: PubMed Central - PubMed

Affiliation: Green Lane Cardiovascular Research Unit,Auckland City Hospital, Auckland, New Zealand.

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.

Show MeSH
Related in: MedlinePlus