Primary hypertension ACE inhibitors versus angiotensin receptor blockers
Angiotensin converting enzyme inhibitors ( ACE inhibitors ) and angiotensin receptor blockers ( ARBs; sartans ) are widely prescribed for primary hypertension ( systolic blood pressure greater than 140 mmHg or diastolic blood pressure greater than 90 mmHg ). However, while ACE inhibitors have been shown to reduce mortality and morbidity in placebo-controlled trials, sartans have not.
Therefore, a comparison of the efficacies of these two drug classes in primary hypertension for preventing total mortality and cardiovascular events is important.
The effects of ACE inhibitors and sartans on total mortality and cardiovascular events, and their rates of withdrawals due to adverse effects ( WDAEs ), in people with primary hypertension were compared.
Researchers included randomized controlled trials enrolling people with uncontrolled or controlled primary hypertension with or without other risk factors, and comparing an ACE inhibitor and an sartan in a head-to-head manner, for a duration of at least one year.
Nine studies with 11,007 participants were included. Of the included studies, five reported data on total mortality, three reported data on total cardiovascular events, and four reported data on cardiovascular mortality.
No study separately reported cardiovascular morbidity. In contrast, eight studies contributed data on WDAE.
Included studies were of good to moderate quality.
There was no evidence of a difference between ACE inhibitors and sartans for total mortality ( risk ratio, RR 0.98; 95% confidence interval 0.88 to 1.10 ), total cardiovascular events ( RR 1.07; 95% CI 0.96 to 1.19 ), or cardiovascular mortality ( RR 0.98; 95% CI 0.85 to 1.13 ).
Conversely, a high level of evidence indicated a slightly lower incidence of WDAE for sartans as compared with ACE inhibitors ( RR 0.83; 95% CI 0.74 to 0.93; absolute risk reduction [ ARR ] 1.8%, number needed to treat for an additional beneficial outcome [ NNTB ] 55 over 4.1 years ), mainly attributable to a higher incidence of dry cough with ACE inhibitors.
The quality of the evidence for mortality and cardiovascular outcomes was limited by possible publication bias, in that several studies were initially eligible for inclusion in this review, but had no extractable data available for the hypertension subgroup. To this end, the evidence for total mortality was judged to be moderate, while the evidence for total cardiovascular events was judged to be low by the GRADE approach.
In conclusion, the analyses found no evidence of a difference in total mortality or cardiovascular outcomes for angiotensin receptor blockers as compared with ACE inhibitors, while angiotensin receptor blockers caused slightly fewer WDAEs than ACE inhibitors.
Although ACE inhibitors have shown efficacy in these outcomes over placebo, the results cannot be used to extrapolate the same conclusion for angiotensin receptor blockers directly, which have not been studied in placebo-controlled trials for hypertension. Thus, the substitution of an angiotensin receptor blocker for an ACE inhibitor, while supported by evidence on grounds of tolerability, must be made in consideration of the weaker evidence for the efficacy of angiotensin receptor blockers regarding mortality and morbidity outcomes compared with ACE inhibitors.
Additionally, data mostly derives from participants with existing clinical sequelae of hypertension, and it would be useful to have data from asymptomatic people to increase the generalizability of this review.
Unpublished subgroup data of hypertensive participants in existing trials comparing ACE inhibitors and angiotensin receptor blockers needs to be made available for this purpose.
Li EC et al, Cochrane Database Syst Rev 2014;8:CD009096
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