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Association of heart rate with microalbuminuria in cardiovascular risk patients: data from I-SEARCH

Böhm, Michaela; Reil, Jan-Christiana; Danchin, Nicolasb; Thoenes, Martinc,d; Bramlage, Peterd; Volpe, Massimoe

doi: 10.1097/HJH.0b013e3282f05c8a
Original papers: Epidemiology

Background Microalbuminuria (MAU) is an indicator of impaired renal function and a relevant risk predictor for cardiovascular events. An increased heart rate is closely correlated with increased cardiovascular mortality. The International Survey Evaluating Microalbuminuria Routinely by Cardiologists in Patients with Hypertension (I-SEARCH) investigated 21 050 patients with hypertension and risk factors for cardiovascular disease. In patients in sinus rhythm (n = 18 900) the relationship between increased heart rate and the prevalence of MAU was analysed.

Methods and results The study was performed in 26 countries worldwide from September 2005 to March 2006. Heart rate, blood pressure, urine albumin and serum creatinine were measured as key parameters. With increasing heart rate (> 80 bpm to < 120 bpm) the proportion of patients with MAU increased from 63 to 69% (P < 0.0001). The odds ratio (OR) for MAU increased with increasing heart rate [heart rate 80–100 bpm compared with 60 bpm: OR, 1.47; 95% confidence interval (CI), 1.29–1.68; P < 0.0001; and heart rate 100–120 bpm compared with 60 bpm: OR, 1.56; 95% CI, 1.22–1.99; P = 0.0004]. The prevalence of MAU was similar whether or not patients were receiving beta-blockers; but MAU was significantly reduced in physically active patients compared with sedentary patients (OR, 0.78; 95% CI, 0.73–0.84; P < 0.0001).

Summary These results show that heart rate is an independent predictor for the prevalence of MAU in hypertensive patients with cardiovascular risk factors. In contrast to beta-blocker therapy, physical activity markedly decreased MAU with increasing heart rates. Further controlled and prospective studies are needed to show that lowered heart rates in combination with MAU can significantly reduce kidney damage, as well as cardiovascular events.

aKlinik für Innere Medizin III (Cardiology, Angiology and Intensive Care Medicine), University of the Saarland, Homburg Saar, Germany

bDepartment of Cardiology, Hôpital Européen Georges Pompidou, Paris

cSanofi-Aventis, Paris, France

dInstitute of Clinical Pharmacology, Technical University of Dresden, Germany

eUniversity of Roma ‘La Sapienza’, S.Andrea Hospital, Roma, and IRCCS Neuromed, Pozzilli, Italy

Received 7 May, 2007

Revised 9 July, 2007

Accepted 20 July, 2007

Correspondence to Michael Böhm, MD, Universitätsklinikum des Saarlandes, Innere Medizin III, Kardiologie, Angiologie und Internistische Intensivmedizin, Kirrberger Straße, 66424 Homburg, Germany Tel: +49 6841 16 23372; fax: +49 6841 16 23369; e-mail:

© 2008 Lippincott Williams & Wilkins, Inc.