Arrhythmogenic right ventricular cardiomyopathy: Electroarchitecture of the substrate

Watanabe, Atsuyuki; Seki, Atsushi; Fishbein, Michael C.; Shivkumar, Kalyanam; Vaseghi, Marmar

doi:10.1016/j.hrcr.2015.09.004

Cited by 3 publications

(2 citation statements)

References 15 publications

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“…Scars contain islands of live myocardium, but border zone regions demonstrated the greatest heterogeneity in ARI, as these regions often contain a complex intertwining of variable amounts of viable myocardium and fibrotic tissue (16,19,39,40). Intermittent VNS significantly reduced ARI dispersion in these regions.…”

Section: Discussionmentioning

confidence: 99%

Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction

Vaseghi¹,

Salavatian²,

Rajendran³

et al. 2017

JCI Insight

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Section: Discussionmentioning

confidence: 99%

Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction

Vaseghi¹,

Salavatian²,

Rajendran³

et al. 2017

JCI Insight

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“…It has been demonstrated both in this infarct model ( 26) and in patients with ischemic and nonischemic cardiomyopathy that scar regions are rarely composed of homogeneous and dense fibrotic tissue (which would not give rise to any electrical signal) and contain many islands of live myocardium (24,26,32,49). These regions of live myocardium or channels within "scar" give rise to fractionated bipolar electrograms, which have been shown to be good targets of catheter ablation in patients with VT (19,32,40).…”

Section: H401mentioning

confidence: 94%

Cardiac sympathetic innervation via middle cervical and stellate ganglia and antiarrhythmic mechanism of bilateral stellectomy

Irie

Yamakawa

Hamon

et al. 2017

American Journal of Physiology-Heart and Circulatory Physiology

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Cardiac sympathetic denervation (CSD) is reported to reduce the burden of ventricular tachyarrhythmias [ventricular tachycardia (VT)/ventricular fibrillation (VF)] in cardiomyopathy patients, but the mechanisms behind this benefit are unknown. In addition, the relative contribution to cardiac innervation of the middle cervical ganglion (MCG), which may contain cardiac neurons and is not removed during this procedure, is unclear. The purpose of this study was to compare sympathetic innervation of the heart via the MCG vs. stellate ganglia, assess effects of bilateral CSD on cardiac function and VT/VF, and determine changes in cardiac sympathetic innervation after CSD to elucidate mechanisms of benefit in 6 normal and 18 infarcted pigs. Electrophysiological and hemodynamic parameters were evaluated at baseline, during bilateral stellate stimulation, and during bilateral MCG stimulation in 6 normal and 12 infarcted animals. Bilateral CSD (removal of bilateral stellates and T ganglia) was then performed and MCG stimulation repeated. In addition, in 18 infarcted animals VT/VF inducibility was assessed before and after CSD. In infarcted hearts, MCG stimulation resulted in greater chronotropic and inotropic response than stellate ganglion stimulation. Bilateral CSD acutely reduced VT/VF inducibility by 50% in infarcted hearts and prolonged global activation recovery interval. CSD mitigated effects of MCG stimulation on dispersion of repolarization and T-peak to T-end interval in infarcted hearts, without causing hemodynamic compromise. These data demonstrate that the MCG provides significant cardiac sympathetic innervation before CSD and adequate sympathetic innervation after CSD, maintaining hemodynamic stability. Bilateral CSD reduces VT/VF inducibility by improving electrical stability in infarcted hearts in the setting of sympathetic activation. Sympathetic activation in myocardial infarction leads to arrhythmias and worsens heart failure. Bilateral cardiac sympathetic denervation reduces ventricular tachycardia/ventricular fibrillation inducibility and mitigates effects of sympathetic activation on dispersion of repolarization and T-peak to T-end interval in infarcted hearts. Hemodynamic stability is maintained, as innervation via the middle cervical ganglion is not interrupted.

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Arrhythmogenic Right Ventricular Cardiomyopathy Diagnosis

Sayed

Pal

Poplawska

et al. 2020

Cardiology in Review

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Arrhythmogenic right ventricular cardiomyopathy, formerly called “arrhythmogenic right ventricular dysplasia,” is an under-recognized clinical entity characterized by ventricular arrhythmias and a characteristic ventricular pathology. Diagnosis is often difficult due to the nonspecific nature of the disease and the broad spectrum of phenotypic variations. Therefore, consensus diagnostic criteria have been developed which combine electrocardiographic, echocardiographic, cardiac magnetic resonance imaging and histologic criteria. In 1994, an international task force first proposed the major and minor diagnostic criteria of arrhythmogenic right ventricular cardiomyopathy based on family history, arrhythmias, electrocardiographic abnormalities, tissue characterization, and structural and functional right ventricular abnormalities. In 2010, the task force criteria were revised to include quantitative abnormalities. These diagnostic modalities and the most recent task force criteria are discussed in this review.

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Arrhythmogenic right ventricular cardiomyopathy: Electroarchitecture of the substrate

Cited by 3 publications

References 15 publications

Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction

Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction

Cardiac sympathetic innervation via middle cervical and stellate ganglia and antiarrhythmic mechanism of bilateral stellectomy

Arrhythmogenic Right Ventricular Cardiomyopathy Diagnosis

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