Author’s reply to RogersBMJ 2012; 344 doi: http://dx.doi.org/10.1136/bmj.e1243 (Published 21 February 2012) Cite this as: BMJ 2012;344:e1243
- Morris J Brown, professor of clinical pharmacology1
The first is the “raw data,” but the second is, in the Oxford view of risk, the more valid way of disentangling the influence of blood pressure from confounders such as age.3 The log-linear relation between cardiovascular risk and blood pressure is proved, for all ages, down to 115/75 mm Hg. It does not automatically follow that the threshold for treatment should be reduced from 140/90 mm Hg.
But it is tragic that the National Institute for Health and Clinical Excellence (NICE) has, without evidence, recommended raising the threshold, with a near certain increase in strokes and myocardial infarction, while proposals (from the Stroke Research Network and British Hypertension Society) to test a lower threshold were rejected by the Health Technology Assessment arm of the NHS as dangerous and impractical. We partly objected to NICE’s unjustified conclusions, but our greater concern was the increasing temptation for guideline and funding committees to skip the obstacles facing high impact high risk research seeking new evidence in favour of derivative meta-analyses and cost effectiveness reviews of existing evidence.4
The threshold question bears also on whether hypertension is “just” the skewed end of normal blood pressure distribution. The failure of large genome-wide association studies to account for more than a few mm Hg of blood pressure contrasts with the excitement of finding single mutations that explain a whole syndrome, such as hypokalaemic hypertension, in 5% of hypertensive patients.5 6 7 It is unlikely that only monogenic syndromes have phenotypes that trip off the autoanalyser. It will be splitting clinicians, not lumping epidemiologists, who recognise new phenotypes.
Cite this as: BMJ 2012;344:e1243
Competing interests: See www.bmj.com/content/344/bmj.d8218.