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Stable coronary artery disease

are there therapeutic benefits of heart rate lowering?

Tanna, Monique S.a; Messerli, Franz H.b; Bangalore, Sripalc

doi: 10.1097/HJH.0000000000002041
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A physiologically lower heart rate, such as that seen in athletes, has been associated with better survival in epidemiological studies. In patients with coronary artery disease, heart rate is considered an independent risk factor for adverse outcomes. Higher heart rate increases cardiac work load and oxygen demand and reduces coronary perfusion by decreasing the amount of time spent in diastole, which in patients with obstructive coronary artery disease can trigger angina and myocardial infarction. Whether pharmacological reduction in heart rate by using a beta-blocker or ivabradine improves prognosis has been debated. In this review, we explore the effect of pharmacological heart rate lowering with a beta-blocker or ivabradine on cardiovascular outcomes in patients with cardiovascular disease and address the question as to whether pharmacological heart rate reduction is ready for prime time in the management of patients with coronary artery disease. Although physiologically lower heart rates are associated with improved survival, the effect of pharmacological heart rate reduction with beta-blockers (in patients without heart failure or postmyocardial infarction) or ivabradine on improvement in survival is weak at best.

aDepartment of Medicine, Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA

bDepartment of Cardiology, University of Bern Medical School, Bern, Switzerland

cDivision of Cardiology, New York University School of Medicine, New York, New York, USA

Correspondence to Sripal Bangalore, Professor of Medicine, Leon H. Charney Division of Cardiology, New York University School of Medicine, 530 First Avenue, SKI 9R/109, New York, NY 10016, USA. Tel: +1 212 263 3540; fax: +1 212 263 3663; e-mail: sripalbangalore@gmail.com

Abbreviations: ACE, angiotensin-converting enzyme; CAD, coronary artery disease; MI, myocardial infarction

Received 12 August, 2018

Revised 11 December, 2018

Accepted 14 December, 2018

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