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Impact of telmisartan on cardiovascular outcome in hypertensive patients at high risk: a Telmisartan Randomised AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease subanalysis

Foulquier, Sébastiena; Böhm, Michaelb; Schmieder, Rolandc; Sleight, Peterd; Teo, Koone; Yusuf, Salime; Schumacher, Helmutf; Unger, Thomasa

doi: 10.1097/HJH.0000000000000154
ORIGINAL PAPERS: Therapeutic aspects

Background: In the Telmisartan Randomised AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease, all patients were at high cardiovascular risk, and a substantial proportion were hypertensive. We performed a post-hoc analysis to explore the hypothesis that telmisartan has a differential action in hypertensive vs. nonhypertensive patients.

Methods: The primary four-fold endpoint (composite of cardiovascular death, myocardial infarction (MI), stroke, or hospitalization for heart failure), the secondary three-fold endpoint (cardiovascular death, MI, and stroke), the individual components, new onset of left ventricular hypertrophy (LVH), and new onset of albuminuria were analyzed.

Results: There was no evidence for a significantly differential treatment effect of telmisartan in hypertensive and nonhypertensive patients for any endpoints, although the occurrence of the secondary three-fold endpoint was significantly lower in the telmisartan group (13.0%) compared with placebo (15.0%, P < 0.05) only in hypertensive patients. Moreover, data from this post-hoc analysis suggest that MI may be less frequent in hypertensive patients treated with telmisartan (3.8 vs. 5.1%; P < 0.05). Telmisartan may also reduce new onset of LVH (nonhypertensive patients P < 0.05; hypertensive patients P < 0.001) in both subgroups, and new onset of microalbuminuria and macroalbuminuria in hypertensive patients (P < 0.001 and P < 0.01, respectively).

The effect of telmisartan in hypertensive and nonhypertensive patients at high cardiovascular risk was not different. This post-hoc analysis suggests that MI may be further reduced by telmisartan in hypertensive patients. Further investigations are needed to study the hypotheses raised by this explanatory analysis.

aCARIM, School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands

bKlinik für Innere Medizin III, University Clinic of the Saarland, Homburg/Saar

cDepartment of Nephrology and Hypertension, University of Erlangen-Nürnberg, Erlangen, Germany

dCardiovascular Medicine, John Radcliffe Hospital, Oxford, UK

ePopulation Health Research Institute, McMaster University, Hamilton, Ontario, Canada

fBoehringer Ingelheim Pharma GmbH & Co KG, Ingelheim am Rhein, Germany

Correspondence to Professor Thomas Unger, MD, PhD, CARIM – School for Cardiovascular Diseases, Maastricht University – PO Box 616, 6200 MD, Maastricht, The Netherlands. Tel: +31 43 388 1652; fax: +31 43 367 0916; e-mail: t.unger@maastrichtuniversity.nl

Abbreviations: ACE, angiotensin converting enzyme; ARB, AT1 receptor blocker; ASA, acetylsalicylic acid; CAD, coronary artery disease; CCB, calcium channel blocker; LVH, left ventricular hypertrophy; MI, myocardial infarction; TIA, transient ischemic attack; UACR, urinary albumin–creatinine ratio

Received 24 October, 2013

Revised 28 January, 2014

Accepted 28 January, 2014

© 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins