Heart rhythm : the official journal of the Heart Rhythm Society
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The initial experience with left atrial esophageal fistula (LAEF) secondary to atrial fibrillation (AF) ablation procedures revealed a near-universal mortality. A comprehensive description of the principles of LAEF repair in the modern era and its resulting impact on morbidity and mortality are lacking in the literature. ⋯ While improved relative to initial reports, mortality associated with LAEF remains high after corrective intervention. Primary esophageal repair with the placement of tissue between the repaired esophagus and the left atrium may result in lower morbidity and mortality.
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Calsequestrin-associated catecholaminergic polymorphic ventricular tachycardia (CPVT2) can cause sudden death in young individuals in response to stress. Beta-blockers are the mainstay medical treatment for patients with CPVT2. However, they do not prevent syncope and sudden death in all patients. Flecainide was reported to reduce exercise-induced ventricular arrhythmias (EIVA) in patients with ryanodine receptor-associated CPVT. The role of flecainide in CPVT2 is not known. ⋯ Flecainide can completely prevent ventricular arrhythmia during exercise and partially prevent recurrent ICD shocks in high-risk patients with CPVT2.
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Idiopathic ventricular arrhythmias (VAs) can be rarely ablated from the noncoronary cusp (NCC) of the aorta. ⋯ NCC VAs were very rare (7%) and occurred in significantly younger patients than those among the other aortic root VAs. In a limited set of six patients, the ECG and electrophysiologic characteristics of NCC VAs were similar to those of RCC VAs but were characterized by narrower QRS duration, smaller III/II ratio, earlier ventricular activation in the HB region, and A/V ratio >1 at the successful ablation site.
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The transient receptor potential melastatin 4 (TRPM4) channel is expressed in the sinoatrial node, but its physiologic roles in this tissue with cardiac pacemaker properties remain unknown. This Ca(2+)-activated nonselective cation channel (NSCCa) induces cell depolarization at negative potentials. It is implicated in burst generation in neurons and participates in induction of ectopic beating in cardiac ventricular preparations submitted to hypoxia/reoxygenation. Accordingly, TRPM4 may participate in action potential (AP) triggering in the sinoatrial node. ⋯ These data showed that TRPM4 modulates beating rate. Pacemaker activity in the sinoatrial node results from the slow diastolic depolarization slope due to the "funny" current, Na/Ca exchange, and a Ca(2+)-activated nonselective cation current, which can be attributable in part to TRPM4 that may act against bradycardia.