Role of invasive electrophysiologic testing in the management of life-threatening ventricular arrhythmias

1988 ◽  
Vol 62 (14) ◽  
pp. I13-I17 ◽  
Author(s):  
Christopher R.C. Wyndham
Physiology ◽  
1997 ◽  
Vol 12 (4) ◽  
pp. 152-157 ◽  
Author(s):  
MC Sanguinetti ◽  
MT Keating

Cardiac action potentials are long because the magnitude of some potassium currents is reduced at depolarized potentials. The slow onset of repolarization is initiated by the opening of delayed rectifier potassium channels. A decrease in function of these channels resulting from gene mutations or pharmacological block increases risk of life-threatening ventricular arrhythmias.


Author(s):  
Brenda Gerull ◽  
Andreas Brodehl

Abstract Purpose of Review Arrhythmogenic cardiomyopathy (ACM) is a genetic disease characterized by life-threatening ventricular arrhythmias and sudden cardiac death (SCD) in apparently healthy young adults. Mutations in genes encoding for cellular junctions can be found in about half of the patients. However, disease onset and severity, risk of arrhythmias, and outcome are highly variable and drug-targeted treatment is currently unavailable. Recent Findings This review focuses on advances in clinical risk stratification, genetic etiology, and pathophysiological concepts. The desmosome is the central part of the disease, but other intercalated disc and associated structural proteins not only broaden the genetic spectrum but also provide novel molecular and cellular insights into the pathogenesis of ACM. Signaling pathways and the role of inflammation will be discussed and targets for novel therapeutic approaches outlined. Summary Genetic discoveries and experimental-driven preclinical research contributed significantly to the understanding of ACM towards mutation- and pathway-specific personalized medicine.


2007 ◽  
Vol 28 (14) ◽  
pp. 1746-1749 ◽  
Author(s):  
Jeffrey S. Healey ◽  
Al P. Hallstrom ◽  
Karl-Heinz Kuck ◽  
Girish Nair ◽  
Eleanor P. Schron ◽  
...  

1987 ◽  
Vol 59 (8) ◽  
pp. 817-823 ◽  
Author(s):  
Roger L. Click ◽  
Bernard J. Gersh ◽  
Declan D. Sugrue ◽  
David R. Holmes ◽  
Douglas L. Wood ◽  
...  

2021 ◽  
Vol 23 (5) ◽  
Author(s):  
Ronpichai Chokesuwattanaskul ◽  
Koonlawee Nademanee

Abstract Purpose of Review To discuss the role of catheter ablation in treating life-threatening ventricular arrhythmias associated with Brugada syndrome (BrS), by presenting recent findings of BrS arrhythmogenic substrate, mechanisms underlying ventricular arrhythmias, and how they can be treated with catheter ablation. Recent Findings Almost three decades ago when the clinical entity of Brugada syndrome (BrS) was described in patients who had abnormal coved-type ST elevation in the right precordial EKG leads in patients who had no apparent structural heart disease but died suddenly from ventricular fibrillation. Since its description, the syndrome has galvanized explosive research in this field over the past decades, driving major progress toward better understanding of BrS, gaining knowledge of the genetic pathophysiology and risk stratification of BrS, and creating significant advances in therapeutic modalities. One of such advances is the ability for electrophysiologists to map and identify the arrhythmogenic substrate sites of BrS, which serve as good target sites for catheter ablation. Subsequently, several studies have shown that catheter ablation of these substrates normalizes the Brugada ECG pattern and is very effective in eliminating these substrates and preventing recurrent VF episodes. Summary Catheter ablation has become an important addition for treatment of symptomatic BrS patients with recurrent VT/VF episodes.


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