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In sinus rhythm, we have characterized endocardial and epicardial atrial activation and voltage, and provide an analysis and understanding of the genesis of the P wave complex in humans.

CSH is associated with a significantly increased risk of infection requiring hospitalization within 1 year following cardiac implantable electronic device surgery. Strategies aimed at reducing hematomas may decrease the long-term risk of infection. (Bridge or Continue Coumadin for Device Surgery Randomized Controlled Trial [BRUISE CONTROL]; NCT00800137).

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This report describes the clinical, laboratory, and electrophysiologic features of 52 patients with ventricular tachycardia (VT) who had no clinical evidence of heart disease. The mean age of patients was 36 years, cardiovascular collapse occurred in 18 patients (35%), and exerciserelated symptoms were present in 24 of 49 patients (49%). There were 20 patients with sustained monomorphic VT, 11 with incessant VT, and 21 with nonsustained VT. Abnormalities were present in 14 of 38 patients (37%) during echocardiography and in 21 of 47 patients (45%) who underwent cardiac catheterization. During baseline evaluation while patients were not receiving antiarrhythmic drugs, ambulatory monitoring and exercise testing showed an 88% and 57% incidence, respectively, of nonsustained or sustained monomorphic VT, whereas 31 of 50 patients (62%) had inducible VT (requiring an infusion of isoproterenol in 11 patients) during programmed electrical stimulation. The clinical VT (when a 12-lead electrocardiogram was available for analysis) had a left bundle branch block (LBBB) configuration in 20 of 33 patients (61%) and a right axis deviation in 17 of 33 patients (51%). The VT occurring during exercise testing and programmed electrical stimulation had the same configuration as the clinical VT in 22 of 22 patients. Three patients have received an antitachycardia pacemaker, and one patient underwent endocardial resection. Forty-eight patients (92%) were treated medically. One patient died of cancer; the remaining 47 patients were alive at a mean follow-up of 96 months after initial symptoms and 46 months after programmed electrical stimulation. We conclude that in patients without clinical evidence of heart disease, VT may be incessant, sustained, or nonsustained and that VT originates from the right ventricular outflow tract in more than 501% of patients. Although cardiac abnormalities may be found in more than 30% of patients, the exact significance of these abnormalities is unclear because of the absence of progressive changes and the excellent prognosis of this group of patients. (Circulation 1989:79:990-999) "What seems to be important is the general myocardial integrity in young subjects who are capable of tolerating the most frequent paroxysms."Froment et all V entricular tachycardia (VT) occurring in subjects without evidence of clinical heart disease was described more than 60 years ago. Gallavardin's2 initial observations, later followed by those of Parkinson and Papp,3 led Froment et all in 1953 to classify VT into four groups, of which two groups had apparently normal hearts: On one hand, "ventricular extrasystoles with parox-

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Background-Atrial fibrillation (AF) is the most common sustained arrhythmia observed in otherwise healthy individuals.Most lone AF cases are nonfamilial, leading to the assumption that a primary genetic origin is unlikely. In this study, we provide data supporting a novel paradigm that atrial tissue-specific genetic defects may be associated with sporadic cases of lone AF. Methods and Results-We sequenced the entire coding region of the connexin 43 (Cx43) gene (GJA1) from atrial tissue and lymphocytes of 10 unrelated subjects with nonfamilial, lone AF who had undergone surgical pulmonary vein isolation. In the atrial tissue of 1 patient, we identified a novel frameshift mutation caused by a single nucleotide deletion (c.932delC) that predicted 36 aberrant amino acids followed by a premature stop codon, leading to truncation of the C-terminal domain of Cx43. The mutation was absent from the lymphocyte DNA of the patient, indicating genetic mosaicism. Protein trafficking studies demonstrated intracellular retention of the mutant protein and a dominantnegative effect on gap junction formation of both wild-type Cx43 and Cx40. Electrophysiological studies revealed no electrical coupling of cells expressing the mutant protein alone and significant reductions in coupling when coexpressed with wild-type connexins. Conclusions-This study reports atrial tissue genetic mosaicism of a novel loss-of-function Cx43 mutation associated with lone AF. These findings implicate somatic genetic defects of Cx43 as a potential cause of AF and support the paradigm that sporadic, nonfamilial cases of lone AF may arise from genetic mosaicism that creates heterogeneous coupling patterns, predisposing the tissue to reentrant arrhythmias. (Circulation. 2010;122:236-244.)