Can a High Resting Heart Rate Increase Your Risk of Heart Failure?
Is a fast heartbeat a hidden danger? Learn how high heart rate can increase your risk of heart failure and how to manage it for a healthier heart.
DR T S DIDWAL MD
4/23/20245 min read
According to a review in the . Updates in Hypertension and Cardiovascular Protection Heart failure (HF) is worsened by chronic overactivity of the sympathetic nervous system (SNS), which initially tries to help a failing heart. This SNS overdrive backfires, damaging the heart and worsening blood flow.Both systolic and diastolic HF (weak or stiff heart muscle) experience SNS issues. Beta-blockers can improve outcomes in systolic HF by lowering heart rate, but their role in diastolic HF is less clear.Finding the optimal heart rate target for HF patients remains a challenge.
Key Points
Neurohormonal Model: Heart failure (HF) is linked to prolonged activation of the body's hormonal systems, particularly the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS). Initially, SNS activation acts as a compensatory mechanism in response to heart injury, aiming to maintain blood pressure and circulation by increasing heart rate, enhancing electrical conduction within the heart, and strengthening heart muscle contraction.
Double-edged sword: While initially helpful, chronic SNS overactivity becomes detrimental. The heart becomes less responsive to the SNS signals, leading to diminished effectiveness. Constant stimulation can damage the heart muscle itself. Additionally, SNS activation triggers blood vessel narrowing, increasing blood pressure and workload on the heart. It also activates RAAS, further constricting vessels and worsening fluid buildup. This cycle contributes to organ damage, a hallmark of congestive HF.
SNS Beyond HFrEF: Sympathetic overactivity isn't exclusive to systolic HF (HFrEF), where pumping power weakens. It's also present in diastolic HF (HFpEF) with a stiff but relatively normally pumping heart muscle. Factors like inflammation, other health conditions, and genetics can further increase SNS activity in both types of HF.
Beta-Blockers and Heart Rate Management: Given the detrimental effects of chronic SNS overactivity, managing heart rate becomes crucial. Beta-blockers, which block stress hormones from binding to heart cells, have proven benefits in HFrEF patients. Studies have shown specific beta-blockers like bisoprolol, carvedilol, metoprolol succinate CR/XL, or nebivolol can significantly improve outcomes.
Uncertain Role in HFpEF: The effectiveness of beta-blockers in HFpEF remains less clear. The SHIFT study offered some hope, demonstrating that adding ivabradine (an I(f) inhibitor) to standard beta-blocker therapy improved prognosis in HFpEF patients with a high baseline heart rate (≥75 bpm).
The Challenge of Optimal Heart Rate: Current guidelines lack specific recommendations on the ideal heart rate target for HF patients. Further research is needed to understand how low we should aim for heart rate and how individual patient characteristics influence this target. Tailoring heart rate management will be crucial for optimizing treatment.
Future Directions: Researchers are exploring alternative approaches to modulate SNS activity, including drugs targeting specific aspects of the SNS pathway and neuromodulation techniques like vagus nerve stimulation, which aim to activate the body's relaxation response.
The Heart of the Matter: Sympathetic Tone and Heart Failure
Heart failure (HF) is a debilitating condition where the heart struggles to pump blood effectively throughout the body. While the causes are diverse, a key player in its development and progression is the sympathetic nervous system (SNS). This intricate dance between the heart and the SNS is a crucial aspect of understanding and managing HF.
The Neurohormonal Model: A Double-Edged Sword
The widely accepted neurohormonal model proposes that HF arises due to a prolonged activation of the body's hormonal systems, particularly the SNS and the renin-angiotensin-aldosterone system (RAAS). Following an initial heart injury, the SNS kicks in as a compensatory mechanism.
Imagine your heart as a failing pump. The SNS, acting like a metaphorical firefighter, aims to maintain blood pressure and circulation by:
Increasing heart rate (HR): This gets more blood pumping with each beat.
Enhancing atrioventricular (AV) conductance: This ensures efficient passage of blood from the upper to lower chambers of the heart.
Heightening myocardial contractility: This strengthens the heart muscle's squeezing power.
In systolic HF (HFrEF), where the heart's pumping power weakens, this SNS activation initially provides some support. However, there's a catch.
The Downside of Overdrive: When SNS Becomes Detrimental
Chronic SNS overactivity turns from a helpful firefighter into a destructive force. Here's why:
Reduced responsiveness: The heart becomes less receptive to the SNS signals over time, leading to a diminished effect.
Myocardial damage: Constant stimulation can damage the heart muscle itself.
Vasoconstriction: The SNS triggers narrowing of blood vessels, increasing blood pressure and workload on the heart.
RAAS activation: This further constricts blood vessels and promotes salt and water retention, worsening fluid buildup in the body.
This vicious cycle ultimately contributes to peripheral organ dysfunction and damage, a hallmark of congestive HF.
Beyond HFrEF: SNS and the Spectrum of Heart Failure
Interestingly, SNS overactivity isn't exclusive to HFrEF. It's also present in diastolic HF (HFpEF), where the heart muscle is stiff but pumping strength remains relatively normal. Additionally, factors like inflammation, coexisting conditions, and genetics can further increase SNS activity.
Tailoring Treatment: Beta-Blockers and Beyond
Given the detrimental effects of chronic SNS overactivity, managing heart rate becomes a crucial therapeutic target. Beta-blockers, which work by blocking the action of stress hormones on heart cells, have proven their benefits in HFrEF patients. Studies have shown that beta-blockers like bisoprolol, carvedilol, metoprolol succinate CR/XL, or nebivolol can significantly improve outcomes in HFrEF.
However, the picture gets murkier in HFpEF. While beta-blockers are often used, their effectiveness remains less clear. The SHIFT study offered some hope, demonstrating that adding ivabradine (an I(f) inhibitor that specifically targets heart rate) to standard beta-blocker therapy improved prognosis in HFpEF patients with a high baseline heart rate (≥75 bpm).
The Challenge and the Future
The big question remains: how low should we aim for heart rate in HF patients? Current guidelines lack specific recommendations, highlighting the need for further research. Understanding individual patient characteristics and tailoring heart rate management strategies will be crucial for optimizing treatment.
Beyond Beta-Blockers: Exploring New Avenues
Researchers are actively exploring alternative approaches to modulating SNS activity in HF. These include drugs targeting specific aspects of the SNS pathway and neuromodulation techniques like vagus nerve stimulation, which aims to activate the body's relaxation response.
Conclusion: A Symphony of Systems
Heart failure is a complex interplay between the heart, the nervous system, and hormonal systems. Understanding the intricate relationship between the sympathetic nervous system and heart failure is paramount for developing better treatment strategies. By effectively managing SNS activity and personalizing heart rate control, we can strive to improve the lives of those living with this challenging condition.
Journal Reference
Palatini, P. (2023, January 1). High Heart Rate: A Predictor of Heart Failure in Healthy Subjects and a Risk Factor for Adverse Outcome in Patients with Heart Failure. Updates in Hypertension and Cardiovascular Protection. https://doi.org/10.1007/978-3-031-39315-0_5
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