Heart Rate Modulation in Cardiovascular Disease
Summary
Heart rate modulation occupies a central role in the management and understanding of cardiovascular disease. Physiologically, the sinoatrial node generates electrical impulses through a delicate interplay between ion channels—including the hyperpolarisation-activated “funny” current—and autonomic inputs. In pathological states such as heart failure, ischaemic heart disease and hypertension, elevated resting heart rate is both a marker and mediator of adverse outcomes, reflecting sympathetic overactivity and impaired vagal tone. Pharmacological strategies to reduce heart rate encompass beta-adrenergic antagonists, non-dihydropyridine calcium-channel blockers and selective If channel inhibitors. By lowering myocardial oxygen demand, prolonging diastolic filling and attenuating maladaptive remodelling, these therapies improve symptoms, enhance left ventricular performance and, in selected populations, confer survival benefit. Emerging insights into intracellular signalling pathways—such as PI3K/AKT/mTOR, autophagy regulation and neurohormonal feedback loops—have deepened our appreciation of heart rate as not merely a hemodynamic variable but also a driver of cellular homeostasis. Translational advances continue to refine patient selection for rate-modulating interventions and to identify molecular targets that may amplify the protective effects of established agents.
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Heart Rate Modulation in Cardiovascular Disease publication trend
The graph below shows the total number of articles in heart rate modulation in cardiovascular disease across all publications each year (not limited to Nature Index journals).
Technical terms
Sinoatrial node: The heart’s primary pacemaker, where spontaneous depolarisation initiates each cardiac cycle.
Funny current (I(f)): A hyperpolarisation-activated, non-selective cation current that contributes to the diastolic depolarisation phase in pacemaker cells.
Ivabradine: A selective inhibitor of the I(f) current that reduces heart rate without affecting myocardial contractility or conduction.
Autophagy: A regulated process of intracellular degradation that maintains cardiomyocyte homeostasis and organelle quality control.
Ejection fraction: The percentage of blood volume ejected from the left ventricle during systole, used to gauge cardiac pump function.
Heart failure with reduced ejection fraction (HFrEF): A syndrome characterised by impaired left ventricular contractile function, often with elevated resting heart rate and neurohormonal activation.
References
- HCN Channels and Heart Rate. Molecules (2012).
- Therapeutic Use and Molecular Aspects of Ivabradine in Cardiac Remodeling: A Review. International Journal of Molecular Sciences (2023).
- Ivabradine protects rats against myocardial infarction through reinforcing autophagy via inhibiting PI3K/AKT/mTOR/p70S6K pathway. Bioengineered (2021).
- Association of pulse rate with outcomes in heart failure with reduced ejection fraction: a retrospective cohort study. BMC Cardiovascular Disorders (2020).
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