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The heart rate hypothesis: ready to be tested
  1. A S Hall1,
  2. S Palmer2
  1. 1
    British Heart Foundation Heart Research Centre at Leeds, University of Leeds, Leeds, UK
  2. 2
    Centre for Health Economics, University of York, York, UK
  1. Professor of Clinical Cardiology, Alistair S Hall, G Floor, Jubilee Wing, Leeds General Infirmary, Leeds, LS2 3EX, UK; A.S.Hall{at}


There is increasing evidence that increased heart rate may be an independent risk factor for cardiovascular morbidity and mortality both in patients with ischaemic heart disease and in the general population. Elevated heart rate in coronary artery disease is a major determinant of oxygen consumption and appears to evoke most episodes of ischaemia. Increased resting heart rate may also contribute to the development of atherosclerosis, facilitate plaque destabilisation and initiate arrhythmias, leading to acute coronary events and sudden death. Reducing heart rate is a central aim in the treatment of stable angina pectoris; this therapeutic approach may have an essential role in lowering the incidence of cardiovascular morbidity and mortality in patients with pre-existing ischaemic heart disease. However, this heart rate hypothesis has not thus far been proven. Evidence suggests that the use of heart rate-lowering drugs may have a beneficial effect; however, most treatments for angina have additional negative inotropic effects on the heart. This hypothesis can now be tested following the recent development of selective heart rate drugs.

  • heart rate
  • If channel inhibitors
  • ivabradine
  • angina pectoris
  • heart rate hypothesis

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  • Competing interests: Professor Hall has received research grants from Astra-Zeneca, Servier UK, and Sanofi-Aventis UK; has received honoraria from Astra-Zeneca and Servier UK; and has been paid consultant fees by Servier UK.