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  4. Cardiac Innervation and Sudden Cardiac Death

Cardiac Innervation and Sudden Cardiac Death

Circ Res, 2015 · DOI: 10.1161/CIRCRESAHA.116.304679 · Published: June 5, 2015

Cardiovascular SciencePhysiology

Simple Explanation

The heart's function is intricately controlled by its nerve supply, which sends and receives signals influencing heart rate, strength, and rhythm. This nerve system maintains a delicate balance between stimulating (sympathetic) and calming (parasympathetic) effects, crucial for short-term and long-term heart health. Understanding how these nerves control the heart at a cellular level could lead to new treatments for preventing sudden cardiac death and other dangerous arrhythmias.

Study Duration
Not specified
Participants
Not specified
Evidence Level
Review

Key Findings

  • 1
    Cardiac injury leads to abnormal signaling in the nervous system, resulting in excessive sympathetic activity and potentially fatal arrhythmias.
  • 2
    Semaphorin 3A (sema3A) is crucial for proper sympathetic nerve development in the heart; abnormalities can lead to increased susceptibility to arrhythmias and sudden death.
  • 3
    Nerve growth factor (NGF) plays a critical role in nerve sprouting and sensory innervation. Dysregulation of NGF contributes to neuropathy, silent ischemia, and lethal arrhythmias.

Research Summary

The autonomic nervous system intricately modulates nearly all physiological functions of the heart. Cardiac autonomic dysregulation is central to the development and progression of most cardiovascular diseases. Neuromodulation strategies show promise of sustaining cardiac function while maintaining electrical stability.

Practical Implications

Neuraxial Therapies

Development of neuraxial therapies for preventing SCD and other arrhythmias.

Autonomic Regulation Therapy (ART)

Mechanism based autonomic regulation therapy holds promise to treat both arrhythmias and HF.

Risk Stratification

Value of autonomic indices to identify patients at risk for sudden death.

Study Limitations

  • 1
    Specific mechanisms underlying the relationship between the ANS and AF have yet to be fully elucidated
  • 2
    Current ART therapies are delivered in the open-loop configuration (no feedback) and with the cardiac nervous system considered a ‘black box’.
  • 3
    More precise studies on reliable and efficient methods of gene therapy and optimal dosage or route of administration are required for further clinical trials with recombinant human NGF

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