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Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which...
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Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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Arrhythmia or dysrhythmia refers to an abnormal heart rhythm caused by a defect in the heart's conduction system. It can cause the heart to beat irregularly, too quickly, or too slowly, leading to symptoms like chest pain, shortness of breath, and fainting. Factors such as stress, caffeine, alcohol, nicotine, cocaine, certain drugs, congenital defects, diseases, and electrolyte abnormalities can trigger arrhythmias.
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Trigger Type and Breakthrough Cardiac Events in Inherited Arrhythmia Syndromes After Left Cardiac Sympathetic

Vanessa Karlinski Vizentin1, Iuri Ferreira Felix2, Sahej Bains3

  • 1Windland Smith Rice Sudden Death Genomics Laboratory, Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota, USA. Electronic address: https://twitter.com/VizentinVanessa.

JACC. Clinical Electrophysiology
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PubMed
Summary

Left cardiac sympathetic denervation (LCSD) is more effective for patients with genetic heart conditions whose symptoms are triggered by adrenergic factors. Patients with non-adrenergic triggers experienced more breakthrough cardiac events after LCSD.

Keywords:
adrenergiccatecholaminergic polymorphic ventricular tachycardialeft cardiac sympathetic denervationlong QT syndrome

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Area of Science:

  • Cardiology
  • Genetics
  • Electrophysiology

Background:

  • Left cardiac sympathetic denervation (LCSD) is a proven therapy for genetic heart diseases like long QT syndrome (LQTS) and catecholaminergic polymorphic ventricular tachycardia (CPVT).
  • The study investigates if LCSD's effectiveness varies based on whether symptoms are triggered by adrenergic (AD) or non-adrenergic (non-AD) factors before the procedure.

Purpose of the Study:

  • To determine the association between AD and non-AD triggered events and the risk of breakthrough cardiac events (BCEs) following LCSD.
  • To evaluate the impact of pre-LCSD symptom triggers on therapeutic outcomes in patients with LQTS and CPVT.

Main Methods:

  • Retrospective review of patients with LQTS or CPVT who underwent LCSD since 2005.
  • Abstraction of electronic medical records to identify cardiac event (CE) trigger types (AD vs. non-AD) before and after LCSD.
  • Definition of CEs and BCEs included syncope, seizures, appropriate defibrillator therapies, and sudden cardiac arrest/death.

Main Results:

  • Among 154 patients (LQTS: 105, CPVT: 49), 32% experienced BCEs post-LCSD.
  • Patients with non-AD triggered CEs had significantly higher BCE rates (54%) compared to those with AD-triggered CEs (19%; P < 0.0001).
  • LQT1 patients with AD triggers showed the fewest BCEs (OR: 0.24, P < 0.0001); no BCEs occurred in LQT2, LQT3, or LQT Minor patients with AD triggers.

Conclusions:

  • Pre-LCSD symptom triggers are a significant determinant of LCSD's therapeutic efficacy.
  • Patients with AD-triggered symptoms experience a greater reduction in disease-mediated BCEs, irrespective of their specific genotype.
  • LCSD offers substantial benefit, particularly for patients with AD-triggered genetic arrhythmias.