Resting Heart Rate as a Cardiovascular Risk Factor in Hypertensive Patients: An Update.

Abstract

A large body of evidence has shown that resting heart rate (RHR) holds important prognostic information in several clinical conditions. In the majority of the general population studies, a graded association between RHR and mortality from all causes, cardiovascular (CV) disease, ischemic heart disease, and stroke has been observed. These associations appeared even stronger and more consistent in hypertensive patients. Studies performed with 24-hour ambulatory recording have shown that an elevated nighttime heart rate may confer an additional risk on top of office RHR. The mechanisms by which tachycardia alone or in association with sympathetic overactivity induces CV damage are well understood. Fast RHR is a strong predictor of future hypertension, metabolic disturbances, obesity, and diabetes. Several experimental lines of research point to high RHR as a main risk factor for the development of atherosclerosis, large artery stiffness, and CV disease. Elevated RHR is a common feature in patients with hypertension. Thus, there is a large segment of the hypertensive population that would benefit from a treatment able to decrease RHR. Improvement of unhealthy lifestyle should be the first goal in the management of the hypertensive patient with elevated RHR. Most clinical guidelines now recommend the use of combination therapies even in the initial treatment of hypertension. Although no results of clinical trials specifically designed to investigate the effect of RHR lowering in human beings without CV diseases are available, in hypertensive patients with high RHR a combination therapy including a cardiac slowing drug at optimized dose seems a sensible strategy. Tachycardia can be considered both as a marker of sympathetic overactivity and as a risk factor for cardiovascular events. In this sketch, the main cardiovascular and metabolic effects of increased sympathetic tone underlying high heart rate are shown. The link between tachycardia and cardiovascular events can be explained also by the direct hemodynamic action of heart rate on the arteries and the left ventricular (LV) wall.