Editor—The editorial by Verma and Strauss does not accord with the BMJ's usual impartial evidence based approach.1 Evidence that angiotensin receptor blockers increase myocardial infarction is scant, and I remain puzzled about what exactly patients should be told—that the BMJ published an incorrect analysis?
Regarding angiotensin receptor blockers and myocardial infarction in hypertension, the data from the valsartan antihypertensive long term use evaluation (VALUE) trial, quoted by Verma and Strauss, can be added to a prior meta-analysis by the Blood Pressure Trialists.2 The incidence of coronary heart disease and myocardial infarction is 804/16061 (5%) in the treated groups and 763/15948 (4.78%) in the controls (odds ratio 1.046), a non-significant increase of myocardial infarction of 4.6% v controls, whereas lisinopril increased combined cardiovascular disease by 10%.3
Regarding candesartan and heart failure, in the predefined group of patients with low left ventricular ejection fractions (< 40%), candesartan reduced all cause mortality by 12% (P = 0.018), and the composite end point including myocardial infarction by 16% (P < 0.001).4
Regarding diabetic nephropathy, they misquote the meta-analysis of Strippoli et al, which specifically concludes that because there are very few head to head comparisons of angiotensin receptor blockers with angiotensin converting enzyme (ACE) inhibitors, their relative survival effects remain unknown.5 Clearly, both these types of agents are of substantial clinical value. New data show potentially additive renoprotection, implying potentially different fundamental mechanisms. ACE inhibitors first changed cardiovascular treatments, and now angiotensin receptor blockers need to be fully tested in direct comparative studies.
Competing interests: LHO has given paid lectures and received travel funds from manufacturers of both angiotensin converting enzyme inhibitors and angiotensin receptor blockers.
References
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