Ventricular Tachycardia Publications (35327)
Ventricular Tachycardia Publications
Secondary prevention includes placement after a high-risk event including sustained ventricular tachycardia or resuscitated cardiac arrest. Although liberal device implantation may be appealing even in patients having marginal indications, studies have shown high rates of adverse effects including inappropriate device discharges and the need for re-intervention because of hardware malfunction. The indications for placement of an implantable cardioverter-defibrillator, whether for primary or secondary prevention of sudden cardiac death, vary based on cardiac pathology. This review will assist the provider in understanding the risks and benefits of device implantation in order to enhance the shared decision-making capacity of patients, families, and providers.
He postulated that such a device "when adapted for clinical use, might be implanted temporarily or permanently in selected patients particularly prone to develop ventricular fibrillation and thus provide them with some degree of protection from sudden coronary death". In 1980 he reported on the first human implants of an "electronic device designed to monitor cardiac electrical activity, to recognise ventricular fibrillation and ventricular tachyarrhythmias … and then to deliver corrective defibrillatory discharges". Through innovations in circuitry, battery, and capacitor technologies, the current implantable cardioverter-defibrillator is 10 times smaller and exponentially more sophisticated than that first iteration. This article will review the inner workings of the implantable cardioverter-defibrillator and outline several features that make it the wonder in technology that it has become.
Owing to the relatively high prevalence of asymptomatic Wolff-Parkinson-White pattern and availability of catheter ablation, there has been a need to identify risk among asymptomatic patients. Recent guidelines recommend invasive evaluation for such patients where pre-excitation clearly does not disappear during exercise testing. This strategy has a high negative predictive value only. The accuracy of this approach is under continued investigation, especially in light of other considerations: Patients having intermittent pre-excitation, once thought to be at minimal risk may not be, and the role of isoproterenol in risk assessment.
Up to half of cases remain genetically elusive. The condition is presently incurable, but one basic intervention, the universal administration of β-blockers, has improved survival. In the past, implantable cardioverter-defibrillators (ICDs) were frequently implanted, especially in those with a history of cardiac arrest. Treatment limitations include under-dosing and poor compliance with β-blockers, and potentially lethal ICD-related electrical storm. Newer therapies include flecainide and sympathetic ganglionectomy. Limited data have suggested that genotype may predict phenotype in catecholaminergic polymorphic ventricular tachycardia, including a higher risk of life-threatening cardiac events in subjects with variants in the C-terminus of ryanodine receptor-2 (RyR2). At present, international efforts are underway to better understand this condition through large prospective registries. The recent publication of gene therapy in an animal model of the recessive form of the disease highlights the importance of improving our understanding of the genetic underpinnings of the disease.
Although the complex interactions of a specific genotype, modifying cofactors, and risk are only now being explored, scientific evidence based on clinical experience now suggests that in many instances such restrictive guidelines are unwarranted. In particular, patients with this condition who are compliant with β-blocker therapy and who have never had symptoms during exertion are now enjoying the benefits of athletic activity.
Clinical variables, VT recurrence, and mortality were analyzed by NYHA IV status using Kaplan-Meier analysis and Cox proportional hazard models. There were significant differences between NYHA IV (n=111) and NYHA II and III (n=1254) patients: NYHA IV had lower left ventricular ejection fraction; more had diabetes mellitus, kidney disease, cardiac resynchronization implantable cardioverter-defibrillator, and VT storm despite greater antiarrhythmic drug use (P<0.01). NYHA IV subjects required more hemodynamic support, were inducible for more and slower VTs, and were less likely to undergo final programmed stimulation. There was no significant difference in acute complications. In-hospital deaths, recurrent VT, and 1-year mortality were higher in the NYHA IV group, in the context of greater baseline comorbidities. Importantly, NYHA IV patients without recurrent VT had similar survival compared with NYHA II and III patients with recurrent VT (68% versus 73%). Early VT recurrence (≤30 days) was significantly associated with mortality, especially in NYHA IV patients.
Despite greater baseline comorbidities, VT radiofrequency ablation can be safely performed among NYHA IV patients. Early VT recurrence is significantly associated with subsequent mortality regardless of NYHA status. Elimination of recurrent VT in NYHA IV patients may reduce mortality to a level comparable to NYHA II and III with arrhythmia recurrence.
Thirty-four patients receive both endocardial and epicardial mapping. Abnormal endocardial substrates and epicardial substrates were characterized. Three groups were defined according to the epicardial and endocardial scar gradient (<10%: transmural, 10-20%: intermediate, >20%: horizontal, as groups 1, 2, and 3, respectively). Sinus rhythm electrograms underwent a Hilbert-Huang spectral analysis and were displayed as 3D Simultaneous Amplitude Frequency Electrogram Transformation (SAFE-T) maps, which represented the arrhythmogenic potentials. The baseline characteristics were similar between the three groups. Group 3 patients had a higher incidence of fatal ventricular arrhythmias requiring defibrillation and cardiac arrest during the initial presentation despite having fewer premature ventricular complexes. A larger area of arrhythmogenic potentials in the epicardium was observed in patients with horizontal scar. The epicardial-endocardial scar gradient was independently associated with the occurrence of fatal ventricular arrhythmias after a multivariate adjustment. The total, ventricular tachycardia, and VF recurrent rates were higher in Group 3 during 38 ± 21 months of follow-up.
For ARVC, the epicardial substrate that extended in the horizontal plane rather than transmurally provided the arrhythmogenic substrate for a fatal ventricular arrhythmia circuit.
Here, we study the most severe CPVT-associated RyR2 mutation (K4750Q) known to date. We define the molecular and cellular dysfunction generated by this mutation and detail how it alters RyR2 function, using Ca(2+) imaging, ryanodine binding, and single-channel recordings. HEK293 cells and cardiac HL-1 cells expressing RyR2-K4750Q show greatly enhanced spontaneous Ca(2+) oscillations. An endoplasmic reticulum-targeted Ca(2+) sensor, R-CEPIA1er, revealed that RyR2-K4750Q mediates excessive diastolic Ca(2+) leak, which dramatically reduces luminal [Ca(2+)]. We further show that the K4750Q mutation causes three RyR2 defects: hypersensitization to activation by cytosolic Ca(2+), loss of cytosolic Ca(2+)/Mg(2+)-mediated inactivation, and hypersensitization to luminal Ca(2+) activation. These defects combine to kinetically stabilize RyR2-K4750Q openings, thus explaining the extensive diastolic Ca(2+) leak from the sarcoplasmic reticulum, frequent Ca(2+) waves, and severe CPVT phenotype. As the multiple concurrent defects are induced by a single point mutation, the K4750 residue likely resides at a critical structural point at which cytosolic and luminal RyR2 control input converge.