Captopril Valsartan

Angiotensin II causes vasoconstriction by direct stimulation of ATj receptors on the vascular smooth muscle. It also enhances release of the neurotransmitter norepinephrine from the sympathetic nerve fibers present in the blood vessels. The vasopressor effects of Ag II may be inhibited pharmacologically in order to decrease TPR and treat hypertension. An important class of orally active drugs is the ACE inhibitors, including captopril and enalopril, which prevent formation of Ag II. More recently, angiotensin receptor antagonists have been developed that act at the vascular smooth muscle. These drugs, which include losartin and valsartan, are also orally active. 

Pfeffer MA, McMurray JJ, Velazquez EJ, et al, Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both, N Engl J Med 2003 349 1893-1906. 

The effects of losartan on morbidity/mortality outcomes were not different statistically from those of ACE-inhibitor captopril in a head-to-head comparative trial in the ELITE II Study [36], while the beneficial effects of valsartan was reported in... 

McMurray J, Solomon S, Pieper K, Reed S, Rouleau J, Velazquez E, White H, Howlett J, Swedberg K, Maggioni A, Kober L, Van de Werf F, Califf R, Pfeffer M (2006) The effect of valsartan, captopril, or both on atherosclerotic events after acute myocardial infarction an analysis of the Valsartan in Acute Myocardial Infarction Trial (VALIANT). J Am Coll Cardiol 47 726-733... 

Initial studies indicate that ARBs and ACE inhibitors produce similar hemodynamic effects and that combination therapy improves exercise capacity, ventricular function, quality of life, and neurohormones in heart failure patients. The ELITE II trial was the first to compare the effects of an ARB (losartan) with those of an ACE inhibitor (captopril) on all-cause mortality in patients with NYHA class II-IV heart failure. No significant difference in mortahty between the two groups was observed, although losartan was better tolerated than captopril. The Val-HeFT trial evaluated whether the addition of valsartan to standard background heart failure therapy (which included an ACE inhibitor in 93% and a /3-blocker in 35% of patients) improved survival. The addition of valsartan had no effect on all-cause mortality but produced a 13% reduction in morbidity and mortality (principally due to reductions in heart failure hospitalizations). Subgroup analysis showed that the benefits were greatest in... 

The Valsartan in Acute Myocardial Infarction Trial (VALIANT) compared the effects of valsartan, captopril, and the combination of the two agents in post-MI patients with symptomatic heart failure, left ventricular dysfunction, or both. The primary end point of total mortality occurred in 19.3% of patients receiving valsartan and captopril, 19.5% of captopril-treated patients, and 19.9% of the valsartan-treated group. Thus, in this high-risk post-MI population, valsartan was as effective as captopril in reducing the risk of death, but combination therapy only increased the risk of adverse effects and did not improve survival compared with monotherapy with either agent. 

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