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High heart rate is associated with longevity in many animal species including men.1 It has been shown in various cardiovascular diseases that high resting heart rate is a known marker of cardiovascular outcomes in hypertension,2 atherosclerosis,3 myocardial infarction4 and heart failure.5 ,6 Among the different conditions the threshold from which risk is increased is different. More close correlations at low thresholds (≥70 bpm) to risk have been established in heart failure.5–8 One beat increase of baseline heart rate and five beats increase of resting heart rate is associated with an increase of cardiovascular death and heart failure hospitalisation of 3% and 16%, respectively.6 Therefore, it was tempting to speculate that heart rate reduction reverses risk, in particular in heart failure, where the association of heart rate and risk is very close. Furthermore, the pathophysiology is plausible for heart failure, because the force-frequency relationship is reversed in the failing heart in vitro9 ,10 and in vivo.11 Shortening of diastole reduces oxygen supply to the myocardium. High heart rates are associated with atherosclerosis12 ,13 potentially important in energy starvation of the failing heart.7 ,8 Finally, high heart rates are a reflection of neurohormonal activation and are associated with malignant arrhythmias.14–16 A reduction of events by heart rate reduction only, would qualify heart rate as a target of treatment and risk factor beyond representing just a surrogate or risk marker.
Intervention to reduce heart rate
Evidence for heart rate being indeed one of the crucial pathophysiological steps in progression of left ventricular dysfunction, has already been scrutinised by β blocker trials in heart failure.17–20 There is evidence that β blockers …
Competing interests None.
Provenance and peer review Commissioned; externally peer reviewed.
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