Resting Heart Rate as a Cardiovascular Risk Factor in Hypertensive Patients: An Update
1Department of Medicine, University of Padova, Padua, Italy.
Insights
Resting heart rate (RHR) is a key indicator of cardiovascular risk, especially in hypertensive patients. Lowering RHR through lifestyle changes and medication may reduce mortality and cardiovascular events.
Area of Science:
- Cardiology
- Hypertension Research
- Preventive Medicine
Background:
- Resting heart rate (RHR) provides significant prognostic information across various clinical conditions.
- A strong association exists between elevated RHR and all-cause, cardiovascular disease, ischemic heart disease, and stroke mortality.
- This association is particularly pronounced in hypertensive patients, with elevated nighttime heart rate adding further risk.
Purpose of the Study:
- To explore the prognostic value of RHR in general and hypertensive populations.
- To understand the mechanisms linking elevated RHR to cardiovascular damage and metabolic disturbances.
- To evaluate potential therapeutic strategies for lowering RHR in hypertensive individuals.
Main Methods:
- Review of existing evidence on RHR and mortality in general and hypertensive populations.
- Analysis of studies utilizing 24-hour ambulatory heart rate monitoring.
- Examination of experimental research on the pathophysiological links between RHR, sympathetic activity, and cardiovascular disease.
Main Results:
- Elevated RHR is a consistent predictor of increased mortality and cardiovascular events.
- High RHR is linked to hypertension, metabolic syndrome, obesity, diabetes, atherosclerosis, and arterial stiffness.
- Elevated RHR is prevalent in hypertensive patients, indicating a need for RHR-lowering treatments.
Conclusions:
- Elevated RHR is both a marker of sympathetic overactivity and an independent cardiovascular risk factor.
- Lifestyle modification is the primary strategy for managing elevated RHR in hypertensive patients.
- Combination therapy including cardiac-slowing drugs may be a sensible strategy for hypertensive patients with high RHR.
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.
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