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Ambulatory blood pressure monitoring predicts cardiovascular events in treated hypertensive patients – an Anglo-Scandinavian cardiac outcomes trial substudy

Dolan, Eamona; Stanton, Alice Vb; Thom, Simonc; Caulfield, Markd; Atkins, Neile; McInnes, Gordonf; Collier, Davidd; Dicker, Patrickb; O'Brien, Eoing on behalf of the ASCOT Investigators

doi: 10.1097/HJH.0b013e328322cd62
Original papers: Therapeutic aspects
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Background Results of the Anglo-Scandinavian cardiac outcomes trial-blood pressure lowering arm (ASCOT-BPLA) showed significantly lower rates of coronary and stroke events in individuals allocated an amlodipine–perindopril combination drug regimen than in those allocated an atenolol–thiazide combination drug regimen. The aims of the ambulatory blood pressure (ABP) substudy of ASCOT were to examine the impact of the two blood pressure (BP)- lowering regimens on ambulatory pressures, test to what extent the between-treatment differences in cardiovascular outcome could be attributed to differences in ABP and assess whether ABP provides predictive information additional to that of clinic blood pressure (CBP) in treated hypertensive patients.

Methods and results One thousand, nine hundred and five patients from four ASCOT centres had repeated ABPs performed over a median follow-up period of 5.5 years. As in the whole ASCOT population, CBP values were lower in amlodipine–perindopril-treated patients compared with those treated with atenolol–thiazide [between-regimen difference {95% confidence intervals (CIs)}]: [−1.5 (−2.4 to −0.5)/−1.2 (−1.8 to +0.5) mmHg]. Daytime BP during follow-up was higher in patients treated with amlodipine–perindopril therapy [+1.1 (0.1–2.1)/+1.6 (0.8–2.3) mmHg]; night-time systolic, but not diastolic BP, was lower in patients treated with amlodipine–perindopril therapy [−2.2 (−3.4 to +0.9)/+0.8 (0.0–1.6) mmHg]. The relative risk of a cardiovascular event associated with a 1 SD increment in accumulated mean BP was 1.35 (1.18–1.53) for clinic systolic BP, 1.30 (1.14–1.49) for daytime systolic BP and 1.42 (1.24–1.62) for night-time systolic BP. With adjustment for baseline variables, treatment regimen and clinic systolic BP, the hazard ratios were 1.17 (1.00–1.36) and 1.25 (1.08–1.47) for daytime and night-time systolic BP, respectively. The between-regimen adjusted hazard ratio for cardiovascular events (amlodipine–perindopril therapy versus atenolol–thiazide therapy) was 0.74 (0.55–1.01) and increased to 0.81 (0.60–1.10) after further adjustment for clinic systolic BP. Further, adjustment for night-time systolic BP increased the hazard ratio to 0.85 (0.62–1.16).

Conclusion The amlodipine–perindopril and atenolol–thiazide regimens had different effects on daytime and night-time ABP, which may have contributed to the lower rates of events in patients treated with amlodipine–perindopril therapy. Both CBP and ABP were significantly associated with rates of cardiovascular events. ABP nocturnal pressures provided complimentary and incremental utility over CBP in the prediction of cardiovascular risk in treated hypertensive patients. These data support the use of ABP to assess the effect of antihypertensive treatment in clinical practice.

aCambridge University Hospitals NHS Foundation Trust, Addenbrooke's Hospital, Cambridge, UK

bMolecular and Cellular Therapeutics and RCSI Research Institute, Royal College of Surgeons in Ireland, Dublin, Ireland

cInternational Centre for Circulatory Health, National Heart and Lung Institute at St Mary's Hospital, Imperial College London, Paddington, UK

dDepartment of Clinical Pharmacology, St Bartholomew's Hospital, London, UK

edabl Educational Trust, Dublin, Ireland

fUniversity of Glasgow, Faculty of Medicine, Glasgow, Scotland, UK

gConway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin, Ireland

* A full list of ASCOT investigators may be found in Reference [1].

Received 4 June, 2008

Revised 8 November, 2008

Accepted 14 November, 2008

Correspondence to Professor Eoin O'Brien, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland Tel: +353 1 2803865; fax: +353 1 2803688; e-mail: eobrien@iol.ie

© 2009 Lippincott Williams & Wilkins, Inc.