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In patients with RV cardiomyopathy and VT, (1) perivalvular electrogram abnormalities represent the commonly identified substrate and source of most VT, (2) LV perivalvular endocardial electrogram abnormalities and VT can occasionally be identified, and (3) aggressive ablative therapy provides long-term VT control.

ICE-diagnosed SEC before transseptal catheterization identifies an increased risk of LA thrombus. Increased intensity of heparin anticoagulation (ACT >300 seconds) during LA ablation for AF may prevent LA thrombus formation especially in patients with SEC.

Background-Although catheter mapping has been used to define the endocardial electrogram characteristics in patients with ventricular tachycardia (VT) and coronary disease, characterization of the electrophysiological substrate in patients with VT and nonischemic cardiomyopathy is limited. Methods and Results-Left ventricular endocardial electroanatomical mapping was performed in 19 patients with nonischemic cardiomyopathy and monomorphic VT with an average of 178Ϯ83 sites per chamber mapped. Abnormal bipolar electrogram was defined as endocardial voltage signal amplitude of Ͻ1.8 mV. The extent and location of abnormal endocardium was estimated by measuring areas of abnormal electrogram recordings from 3D voltage maps. The origin of VT was approximated by identifying sites of entrainment with concealed fusion or early presystolic activity and/or by pace mapping. Abnormal electrograms were recorded over a 41Ϯ28 cm 2 area that represented 20Ϯ12% of total endocardial surface. The majority of patients (14/19 patients) had only a modest area (Ͻ25%) of endocardial abnormality. All patients had abnormal low-voltage endocardial areas located near the ventricular base in the perivalvular region. There were 3Ϯ1 VT morphologies per patient. The majority (88%) of the 57 mapped VTs originated from the ventricular base, corresponding to regions with abnormal endocardial electrograms. Conclusions-Electroanatomical

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Acetylcholine causes endothelium-dependent dilation of normal arteries in most animal species. The effect of acetylcholine on normal human coronary arteries is controversial. Pathologic studies and epicardial echocardiography have shown that diffuse atherosclerosis is often present despite angiographic evidence of discrete coronary artery disease (CAD). Therefore, we postulated that acetylcholine would cause vasoconstriction of coronary arteries that are angiographically normal in patients with CAD. Coronary artery diameter, measured by automated quantification of digitized cineangiograms, was determined before and after the intracoronary infusion of 0.2 mM acetylcholine at 0.8-1.6 ml/min. The diameter of stenotic or irregular segments of six atherosclerotic coronary arteries decreased from 1.80±0.42 mm before acetylcholine to 1.26±0.46 mm after acetylcholine (p=0.0025). Acetylcholine had a significantly diYferent effect on the diameter of two groups of coronary arteries that are angiographically normal. Acetylcholine caused a 0.16±0.09-mm increase in the diameter of 14 normal coronary arteries in patients without CAD, whereas it caused a 0.26+0.12-mm decrease in the diameter of 14 normal coronary arteries in patients with CAD (p <0.01). Thus, the normal response to intracoronary acetylcholine is vasodilation, suggesting that endotheliumderived relaxing factor is released from normal human coronary endothelium. The vasoconstrictive effect of acetylcholine in the angiographically normal coronary arteries of patients with CAD suggests the presence of a diffuse abnormality of endothelial function. (Circulation 1989;79:287-291) T here is growing evidence that acetylcholine and a number of other substances induce vasodilation by stimulating the release of an endothelium-derived relaxing factor (EDRF) from endothelial cells, whereas nitroglycerin and other endothelium-independent vasodilators induce vasodilation through the direct stimulation ofvascular smooth muscle."2,3 Thus, acetylcholine or aggregating platelets cause relaxation of arteries with an intact endothelium but cause contraction of arteries denuded of endothelium.1"2'3 An impairment of endotheliumdependent vasodilation has been observed in rabbits4 and monkeys5'6 that were fed an atherogenic diet. atherosclerosis and restored endothelium-dependent relaxation to normal.6 Conflicting data exist, however, regarding the existence of endothelium-mediated vasodilation in human coronary arteries. Several in vitro studies conclude that acetylcholine and carbachol, both muscarinic agonists, constrict human coronary arteries,7-10 whereas other studies suggest that acetylcholine dilates normal human coronary arteries.1" Similarly, a discrepancy exists regarding the effect of acetylcholine on human coronary arteries in vivo. After the intracoronary infusion of acetylcholine, Horio et al12 observed at least a 25% decrease in the diameter of normal or almost normal coronary arteries in 27 of 70 arteries, whereas Ludmer et al13 reported an 11% increase in the diame...

Ventricular arrhythmias are common in the setting of nonischemic cardiomyopathy. The etiology for the cardiomyopathy is frequently not identified and the label of "idiopathic" is applied. Interstitial fibrosis with conduction system involvement and associated left bundle branch block characterizes the disease process in some patients and the mechanism for monomorphic ventricular tachycardia is commonly bundle branch reentry. However, most patients with nonischemic cardiomyopathy have VT due to myocardial reentry and demonstrate marked myocardial fibrosis and electrogram abnormalities. Although patient specific, the overall distribution of electroanatomic abnormalities appears to be equal on the endocardium and epicardium. The extent of electrogram abnormalities appears to parallel arrhythmia presentation and/or inducibility. Patients with sustained uniform morphology VT have the most extensive endocardial and epicardial electrogram abnormalities. Magnetic electroanatomic voltage mapping provides a powerful tool to characterize the location and extent of the arrhythmia substrate. Basal left ventricular myocardial involvement, as indexed by the location of contiguous electrogram abnormalities, is common in patients with sustained VT and left ventricular cardiomyopathy. The relatively equal distribution of electrogram abnormalities on the endocardium and epicardium, and the results of mapping and ablation attempts, suggest that critical parts of the reentrant circuit may be epicardial. Unique features of the electroanatomic substrate associated with cardiomyopathy due to Chagas' disease, sarcoidosis, and arrhythmogenic right ventricular dysplasia are also discussed.