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The Lancet, Volume 358, Issue 9297, Pages 1995 - 1996, 8 December 2001
doi:10.1016/S0140-6736(01)06984-7Cite or Link Using DOI

The lowering of blood pressure after stroke

Authors' reply
Sir—Our metaregression model1 includes primary and secondary prevention trials. Indeed, from 20% to 45% of the patients randomised in the STOP2, INSIGHT, ALLHAT, and NICS trials had previous cardiovascular complications. HOPE, PART2, and SCAT included patients with atherosclerotic complications. In MIDAS, participants had intima-media thickening of 1·3—3·5 mm, albeit in the absence of ultrasonographic signs of plaque instability, such as mineralisation or haemorrhage.2
The HSCS, PATS, and PROGRESS trials were mounted with the specific goal to study stroke recurrence. The pathophysiological mechanisms leading to cardiovascular events and the actions of the drugs used to prevent these complications are not different in high-risk normotensive patients or in hypertensive patients, with or without clinically overt cardiovascular disease. By contrast with the proposition of Fournier and colleagues, we believe that there is a continuum between primary and secondary prevention, and that, as in clinical practice, there is little reason to dichotomise prevention.
In our metaregression models, odds ratios were correlated with achieved differences in systolic pressure between treatment groups. For fatal combined with non-fatal events, the relation was curvilinear. A substantial part of the benefit of blood-pressure-lowering treatment was already achieved by small 5 mm Hg differences in systolic pressure. The variance explained by the systolic blood pressure differences ranged from 53% to 71%, of which one-fifth to two-fifths in a significant way were attributable to the curvilinear term in the model.1 Our results cannot be directly compared with those reported by Rodgers and colleagues. Indeed, they expressed the risk of stroke relative to the overall risk in the patients enrolled in the UK Transient Ischaemic Attack trial. The relative risks were plotted by quartiles of the blood pressure distribution at entry, corrected for regression dilution bias.3
In the CAPPP patients assigned captopril, risk of stroke was only 25% higher than in those receiving diuretics, βblockers, or both. The ALLHAT, CAPPP, and HOPE investigators have attributed part of the observed risks and benefits in their trials to ancillary properties of the tested drugs. However, none of these trials was designed to elucidate the mechanisms of cardiovascular protection. We showed that blood pressure differences could explain most, if not all, of the outcome results. We believe that speculations about the ancillary properties of blood-pressure-lowering medicines are counterproductive and detract from the main message that these trials convey. All antihypertensive drugs have similar long-term efficacy and safety. What matters is that blood pressure is controlled.


1 Staessen JA, Wang JG, Thijs L. Cardiovascular protection and blood pressure reduction:a meta-analysis.. Lancet 2001; 358: 1305-1315. Summary | Full Text | PDF(137KB) | CrossRef | PubMed
2 Borhani NO, Mercuri M, Borhani PA, et al. Final outcome results of the multicenter isradipine diuretic atherosclerosis study (MIDAS): a randomized controlled trial.. JAMA 1996; 276: 785-791. CrossRef | PubMed
3 MacMahon S, Peto R, Cutler J, et al. Blood pressure, stroke, and coronary heart disease, part 1: prolonged differences in blood pressure:prospective observational studies corrected for the regression dilution bias.. Lancet 1990; 335: 765-774. Summary | CrossRef | PubMed
a Studiecoördinatiecentrum, Hypertensie en Cardiovasculaire Revalidatie Eenheid, Departement Moleculair en Cardiovasculair Onderzoek, Katholieke Universiteit Leuven, Leuven, Belgium
Corresponding Author Information Studiecoördinatiecentrum, Hypertensie en Cardiovasculaire Revalidatie Eenheid, Departement Moleculair en Cardiovasculair Onderzoek, Katholieke Universiteit Leuven, Leuven, Belgium
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