Heart rate and cardiovascular risk

The tonic influence of both divisions of the autonomic nervous system on the intrinsic activity of the sinus node represents resting heart rate. Changes in heart rate, usually involving a reciprocal action of vagal and sympathetic activity, are the final response of a number of neural pathways aimed at maintaining stability and/or providing adaptation of the circulatory and cardiorespiratory systems. Resting tachycardia is due to an increase in sympathetic activity not adequately counterbalanced by vagal modulation. Increased sympathetic activity negatively affects metabolic, hemodynamic and electrophysiological properties of the heart by favoring the development of arterial hypertension and atherosclerotic lesions and by precipitating cardiovascular events. Epidemiological evidence in the general population has been provided showing an increased risk of all-cause and coronary heart disease mortality as resting heart rate increases. Heart rate remained significantly predictive of increased mortality after adjusting for traditional risk factors, including arterial hypertension. The linear relationship between reduction in heart rate and improved survival observed in the overall beta-blocker studies, strongly supports the adverse effects of increased heart rate among patients with known heart disease. The use of the simple measurement of resting heart rate as a risk predictor for cardiovascular disease in subjects without known heart disease may be limited by the lack of normal values, which could take into account the individual differences in intrinsic heart rate. Although several studies suggest that the analysis of heart rate variability might be a better risk predictor than simple heart rate, definitive evidence has not yet been provided.