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Relevance of heart rate as a risk factor in hypertension
1Clinica Medica 4, University of Padova, Italy.
Insights
High resting heart rate is linked to hypertension and increased cardiovascular risk. Lowering heart rate may be a beneficial addition to blood pressure treatment, especially for those with high sympathetic activity.
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
Background:
- Resting heart rate (RHR) correlates with blood pressure and predicts hypertension development.
- Elevated RHR is associated with increased cardiovascular morbidity and mortality.
- RHR acts as both a risk marker and an independent risk factor for cardiovascular events.
Purpose of the Study:
- To explore the role of heart rate in cardiovascular risk.
- To evaluate heart rate reduction as an adjunct antihypertensive therapy goal.
Main Methods:
- Review of existing studies correlating heart rate with blood pressure and cardiovascular outcomes.
- Examination of the physiological mechanisms linking tachycardia to cardiovascular disease.
- Consideration of pharmacological agents for heart rate reduction.
Main Results:
- Sympathetic overactivity contributes to elevated blood pressure, hematocrit, and metabolic issues in tachycardia.
- Experimental data suggests heart rate directly promotes atherosclerosis via arterial wall stress.
- Tachycardia increases the risk of ventricular arrhythmias and sudden cardiac death.
Conclusions:
- Heart rate reduction is a potential therapeutic target in hypertension management, particularly in sympathetic overactive individuals.
- Non-dihydropyridine calcium channel blockers and I1-imidazoline receptor agonists are potential agents.
- Prospective trials are needed to confirm morbidity-mortality benefits of heart rate-lowering therapies.
Abstract:
Numerous studies have shown that resting heart rate is closely correlated with blood pressure and that it is prospectively related to the development of hypertension. Moreover, there is mounting evidence to indicate that a high heart rate is associated with increased cardiovascular morbidity and mortality. In this respect, heart rate can be considered both as a marker of risk and as an independent factor in the induction of risk. Sympathetic overactivity seems to be responsible for the increase in blood pressure and hematocrit, and for the metabolic abnormalities often observed in subjects with tachycardia. Experimental studies in monkeys have shown that heart rate can also exert a direct atherogenic action on the arteries through increased wall stress. Furthermore, tachycardia can favor the occurrence of ventricular arrhythmias and sudden death. Reduction of heart rate appears to be a reasonable additional goal of antihypertensive therapy, especially in subjects with increased sympathetic tone. Nondihydropyridine calcium antagonists and drugs with agonistic properties at the I1-imidazoline receptors of the rostral ventrolateral medulla may be drugs of choice for this purpose, but whether they offer a significant morbidity-mortality advantage must be proven in prospective trials.