Broad use of RAS inhibitors in patients with coronary artery disease may not be justified
medwireNews: Results of a meta-analysis suggest no benefit of treatment with renin angiotensin system inhibitors (RASi) compared with active controls in patients with stable coronary artery disease (CAD) without heart failure.
These findings “do not support the broad use of RASi for all patients with stable ischemic heart disease as has been recommended by current guidelines,” Sripal Bangalore (New York University School of Medicine, USA) and colleagues write in The BMJ.
The researchers analyzed data from 61,961 participants of 24 randomized trials comparing RASi (ACE inhibitors or angiotensin receptor blockers) with placebo or an active comparator. Of the seven active controlled trials, four included calcium antagonists, one involved a thiazide diuretic, and two used conventional treatment.
When compared with placebo, RASi significantly reduced the risk for all-cause and cardiovascular mortality, with corresponding rate ratios (RR) of 0.84 and 0.74. The authors also observed a significant reduction in the incidence of myocardial infarction (MI), stroke, angina, and heart failure among patients receiving RASi relative to placebo (RR=0.82, 0.79, 0.94, and 0.78, respectively).
However, RASi had no significant effect on the rates of all-cause and cardiovascular mortality, MI, stroke, angina, or heart failure when compared with active controls.
Furthermore, in meta-regression analyses, RASi only reduced the risk for all-cause and cardiovascular mortality relative to placebo in trials with more than 14.10 deaths and 7.65 cardiovascular deaths per 1000 patient–years in the control group, but not in those with lower control event rates, suggesting that “the benefits were only seen in trials with high baseline risk,” say the authors.
The lack of benefit seen in trials with lower baseline risk “could have implications for patients with stable coronary artery disease with aggressive management of risk factors such as hypertension and hypercholesterolemia (with high intensity statins) and consequent lower baseline residual risk,” they add.
Bangalore and colleagues hypothesize that RASi did not provide benefit over the other drugs tested because the trial participants may not have had an activated renin-angiotensin-aldosterone system, or the effects could have been mediated by a reduction in blood pressure. Alternatively, “the benefit might not have been apparent during the short follow-up in these trials,” they suggest.
And the team concludes that: “Evidence does not support a preferred status of RASi over other active controls.”
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