Non-invasive Stereotactic Body Radiation Therapy for Refractory Ventricular Arrhythmias: Venturing into the Unknown.

Stereotactic body radiation therapy (SBRT) is a promising new method for non-invasive management of life-threatening ventricular arrhythmias. Numerous case reports and case series have provided encouraging short-term results suggesting good efficacy and safety, but randomized data and long-term outcomes are not yet available. The primary hypothesis as to the mechanism of action for SBRT relates to the development of cardiac fibrosis in arrhythmogenic myocardial substrate; however, limited animal model data offer conflicting insights into this theory. The use of SBRT for patients with refractory ventricular arrhythmias is rapidly increasing, but ongoing translational science work and randomized clinical trials will be critical to address many outstanding questions regarding this novel therapy

Acquired Long QT Syndrome after Acute Myocardial Infarction: A Rare but Potentially Fatal Entity.

Acquired long QT syndrome is typically caused by medications, electrolyte disturbances, bradycardia, or catastrophic central nervous system events. We report a case of myocardial infarction-related acquired long QT syndrome in a 58-year-old woman that had no clear cause and progressed to torsades de pointes requiring treatment with isoproterenol and magnesium. Despite negative results of DNA testing against a known panel of genetic mutations and polymorphisms associated with long QT syndrome, the patient's family history of fatal cardiac disease suggests a predisposing genetic component. This report serves to remind clinicians of this potentially fatal ventricular arrhythmia after myocardial infarction

Rotor Stability Separates Sustained Ventricular Fibrillation From Self-Terminating Episodes in Humans

ObjectivesThis study mapped human ventricular fibrillation (VF) to define mechanistic differences between episodes requiring defibrillation versus those that spontaneously terminate.BackgroundVF is a leading cause of mortality; yet, episodes may also self-terminate. We hypothesized that the initial maintenance of human VF is dependent upon the formation and stability of VF rotors.MethodsWe enrolled 26 consecutive patients (age 64 ± 10 years, n = 13 with left ventricular dysfunction) during ablation procedures for ventricular arrhythmias, using 64-electrode basket catheters in both ventricles to map VF prior to prompt defibrillation per the institutional review board–approved protocol. A total of 52 inductions were attempted, and 36 VF episodes were observed. Phase analysis was applied to identify biventricular rotors in the first 10 s or until VF terminated, whichever came first (11.4 ± 2.9 s to defibrillator charging).ResultsRotors were present in 16 of 19 patients with VF and in all patients with sustained VF. Sustained, but not self-limiting VF, was characterized by greater rotor stability: 1) rotors were present in 68 ± 17% of cycles in sustained VF versus 11 ± 18% of cycles in self-limiting VF (p < 0.001); and 2) maximum continuous rotations were greater in sustained (17 ± 11, range 7 to 48) versus self-limiting VF (1.1 ± 1.4, range 0 to 4, p < 0.001). Additionally, biventricular rotor locations in sustained VF were conserved across multiple inductions (7 of 7 patients, p = 0.025).ConclusionsIn patients with and without structural heart disease, the formation of stable rotors identifies individuals whose VF requires defibrillation from those in whom VF spontaneously self-terminates. Future work should define the mechanisms that stabilize rotors and evaluate whether rotor modulation may reduce subsequent VF risk

Ischemia-Induced Ventricular Proarrhythmia and Cardiovascular Autonomic Dysreflexia After Cardioneuroablation

BackgroundCardioneuroablation (CNA) is an attractive treatment for vasovagal syncope. Its long-term efficacy and safety remain unknown. ObjectiveTo develop a chronic porcine model of CNA to examine ventricular tachyarrhythmia (VT/VF) susceptibility and cardiac autonomic function after CNA.MethodsA percutaneous CNA model was developed by ablation of left- and right-sided ganglionated plexi (GP)(n=5), confirmed by histology. Reproducible bilateral vagal denervation was confirmed following CNA by extracardiac vagal nerve stimulation (ECVNS) and histology. Chronic studies included 16 pigs randomized to CNA (n=8) and sham ablation (n=8). After 6 weeks, animals underwent hemodynamic studies, assessment of cardiac sympathetic and parasympathetic function using sympathetic chain stimulation (SCS) and direct VNS respectively, and proarrhythmic potential following left anterior descending coronary artery (LAD) ligation.ResultsAfter CNA, ECVNS responses remained abolished for 6 weeks despite ganglia remaining in ablated GPs. In the CNA group, direct VNS resulted in paradoxical increases in blood pressure, but not in sham animals (CNA group vs. sham: 8.36±7.0% vs. -4.83±8.7%, respectively, p=0.009). Left SCS (8Hz) induced significant QTc prolongation in the CNA group vs. sham (11.23±4.0% vs. 1.49±4.0%, respectively, p&lt;0.001). VT/VF after LAD ligation was more prevalent and occurred earlier in the CNA group vs. control (61.44±73.7sec vs. 245.11±104.0 sec, respectively, p=0.002).ConclusionsCardiac vagal denervation is maintained long-term after CNA in a porcine model. However, chronic CNA was associated with cardiovascular dysreflexia, diminished cardioprotective effects of cardiac vagal tone, and increased VT/VF susceptibility in ischemia. These potential long-term negative impacts of CNA suggest the need for rigorous clinical studies on CNA

Rotors exhibit greater surface ECG variation during ventricular fibrillation than focal sources due to wavebreak, secondary rotors, and meander.

Ventricular fibrillation is a common life-threatening arrhythmia. The ECG of VF appears chaotic but may allow identification of sustaining mechanisms to guide therapy.We hypothesized that rotors and focal sources manifest distinct features on the ECG, and computational modeling may identify mechanisms of such features.VF induction was attempted in 31 patients referred for ventricular arrhythmia ablation. Simultaneous surface ECG and intracardiac electrograms were recorded using biventricular basket catheters. Endocardial phase maps were used to mechanistically classify each VF cycle as rotor or focally driven. ECGs were analyzed from patients demonstrating both mechanisms in the primary analysis and from all patients with induced VF in the secondary analysis. The ECG voltage variation during each mechanism was compared. Biventricular computer simulations of VF driven by focal sources or rotors were created and resulting ECGs of each VF mechanism were compared.Rotor-based VF exhibited greater voltage variation than focal source-based VF in both the primary analysis (n = 8, 110 ± 24% vs. 55 ± 32%, P = 0.02) and the secondary analysis (n = 18, 103 ± 30% vs. 67 ± 34%, P = 0.009). Computational VF simulations also revealed greater voltage variation in rotors compared to focal sources (110 ± 19% vs. 33 ± 16%, P = 0.001), and demonstrated that this variation was due to wavebreak, secondary rotor initiation, and rotor meander.Clinical and computational studies reveal that quantitative criteria of ECG voltage variation differ significantly between VF-sustaining rotors and focal sources, and provide insight into the mechanisms of such variation. Future studies should prospectively evaluate if these criteria can separate clinical VF mechanisms and guide therapy