Idiopathic ventricular arrhythmias (VAs), including premature ventricular contractions (PVCs) and idiopathic ventricular tachycardia (IVT), are common and usually without apparent underlying structural heart disease; treatment with radiofrequency catheter ablation (RFCA) of those of endocardial origin has rapidly increased [ 1 Ouyang F. Fotuhi P. Ho S.Y. et al. Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp: electrocardiographic characterization for guiding catheter ablation. J Am Coll Cardiol. 2002; 39: 500-508 Abstract Full Text Full Text PDF PubMed Scopus (462) Google Scholar , 2 Yoshida N. Inden Y. Uchikawa T. et al. Novel transitional zone index allows more accurate differentiation between idiopathic right ventricular outflow tract and aortic sinus cusp ventricular arrhythmias. Heart Rhythm. 2011; 8: 349-356 Abstract Full Text Full Text PDF PubMed Scopus (89) Google Scholar ], with alternative use of left coronary veins for the estimated 9% of IVT cases of epicardial origin [ 3 Daniels D. Lu Y. Morton J. et al. Idiopathic epicardial left ventricular tachycardia originating remote from the sinus of Valsalva: electrophysiological characteristics, catheter ablation, and identification from the 12-lead electrocardiogram. Circulation. 2006; 113: 1659-1666 Crossref PubMed Scopus (300) Google Scholar , 4 Li Y.C. Lin J.F. Li J. Catheter ablation of idiopathic ventricular arrhythmias originating from left ventricular epicardium adjacent to the transitional area from the great cardiac vein to the anterior interventricular vein. Int J Cardiol. 2013; 167: 2673-2681 Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar , 5 Obel O.A. D'Avila A. Neuzil P. et al. Ablation of left ventricular epicardial outflow tract tachycardia from the distal great cardiac vein. J Am Coll Cardiol. 2006; 48: 1813-1817 Abstract Full Text Full Text PDF PubMed Scopus (108) Google Scholar ]. Based on a 12-patient study [ [4] Li Y.C. Lin J.F. Li J. Catheter ablation of idiopathic ventricular arrhythmias originating from left ventricular epicardium adjacent to the transitional area from the great cardiac vein to the anterior interventricular vein. Int J Cardiol. 2013; 167: 2673-2681 Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar ], we reported in this journal that: 1. differing 12-lead body-surface electrocardiogram (ECG) characteristics of symptomatic PVCs/IVT originating from 3 regions of left coronary veins (distal great vein [DGCV], proximal anterior interventricular vein [PAIV], and extension tributary of EDGV [EDGCV]) help regionalize arrhythmia origin; and 2. RFCA for PVCs/IVT of coronary venous system origin appeared effective. We report here on an expanded study that: 1. recognized distinct ECG characteristics which aid in mapping PVCs/IVT origin to 4, in contrast to the previously reported 3, left ventricular (LV) epicardial regions adjacent to the transitional area from GCV to AIV; 2. defined IDT ≥70 ms and MDI ≥0.54 to differentiate PVCs/IVT of DGCV from those of LV endocardium, aortic sinus of Valsalva (ASOV) or right ventricular outflow tract (RVOT) origin; and 3. confirmed favorable outcomes after successful RFCA for PVCs/IVT within the coronary venous system.

Background Activation of the cholinergic anti-inflammatory pathway, which relies on the α7nAchR (alpha 7 nicotinic acetylcholine receptor), has been shown to decrease proinflammatory cytokines. This relieves inflammatory responses and improves the prognosis of patients with experimental sepsis, endotoxemia, ischemia/reperfusion injury, hemorrhagic shock, pancreatitis, arthritis and other inflammatory syndromes. However, whether the cholinergic anti-inflammatory pathway has an effect on acute viral myocarditis has not been investigated. Here, we studied the effects of the cholinergic anti-inflammatory pathway on acute viral myocarditis. Methodology/Principal Findings In a coxsackievirus B3 murine myocarditis model (Balb/c), nicotine and methyllycaconitine were used to stimulate and block the cholinergic anti-inflammatory pathway, respectively. Relevant signal pathways were studied to compare their effects on myocarditis, survival rate, histopathological changes, ultrastructural changes, and cytokine levels. Nicotine treatments significantly improved survival rate, attenuated myocardial lesions, and downregulated the expression of TNF-α and IL-6. Methyllycaconitine decreased survival rate, aggravated myocardial lesions, and upregulated the expression of TNF-α and IL-6. In addition, levels of the signaling protein phosphorylated STAT3 were higher in the nicotine group and lower in the methyllycaconitine group compared with the untreated myocarditis group. Conclusions/Significance These results show that nicotine protects mice from CVB3-induced viral myocarditis and that methyllycaconitine aggravates viral myocarditis in mice. Because nicotine is a α7nAchR agonist and methyllycaconitine is a α7nAchR antagonist, we conclude that α7nAchR activation increases the phosphorylation of STAT3, reduces the expression of TNF-α and IL-6, and, ultimately, alleviates viral myocarditis. We also conclude that blocking α7nAchR reduces the phosphorylation of STAT3, increases the expression of TNF-α and IL-6, aggravating viral myocarditis.