Objective-Terodiline, an antimuscarinic and calcium antagonist drug, was used to treat detrusor instability but was withdrawn in 1991 after provoking serious ventricular arrhythmias associated with increases in the corrected QT interval (QTc). This research was performed to relate drug induced electrocardiographic changes in asymptomatic recipients to plasma concentrations of the R( +) and S(-) terodiline enantiomers. (443 (33) and 42 (17) ms'12, paired t tests, P < 0-002 and P < 0 01 respectively) in the 12 patients in sinus rhythm. The mean (95% confidence interval) drug induced increases were 48 (23 to 74) Ms112 for QTc and 42 (13 to 70) ms'12 for QTd. These increases correlated with total plasma terodiline (QTc: r = 0-77, P < 0-006, QTd: r = 0*68, P < 0.025) and with plasma concentrations of both terodiline enantiomers.Conclusions-Terodiline increases QTc and QTd in a concentration dependent manner. It is not clear whether this is a stereoselective effect and, if so, which enantiomer is responsible. The results suggest that drug induced torsade de pointes is a type A (concentration dependent) adverse drug reaction. (Br HeartJ7 1995;74:53-56)

The inability to ablate left accessory pathways (APs) from endocardial approaches may suggest an epicardial location. We report on a 43‐year‐old woman presenting with a wide QRS tachycardia with Right Bundle Branch Block (RBBB) morphology, right inferior axis, and the “pattern break” appearance in V2 resembled the outflow tract ventricular tachycardia. An electrophysiology study confirmed an antidromic atrioventricular reentrant tachycardia using an antegrade slow, decrementally conducting AP that was successfully ablated in the great cardiac vein‐anterior interventricular vein junction after failure of endocardial approach.

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Atrial fibrillation (AF) is the most common cardiac arrhythmia globally and increases the risk of mortality and morbidity from stroke, systemic embolism, heart failure (HF), and dementia. [1][2][3] Several studies have demonstrated that AF is mainly associated with advancing age and underlying cardiovascular disease, particularly hypertension and coronary artery disease. Our current understanding of AF is largely based on data from North America and Europe. 4-7 Regional cohort studies have suggested that rheumatic heart disease, diabetes, obesity, and smoking are more important causes of AF than in other regions in the world. 8,9 There are racial and ethnic differences in AF symptom, treatment patterns, and outcomes. 9,10 During the previous four decades, several effective therapies for AF have been developed, 11,12 particularly, the use of direct-acting