[Show abstract][Hide abstract] ABSTRACT: Magnesium and Arrhythmias. Introduction: Magnesium deficiency has been implicated in the pathogenesis of sudden death, but the investigation of arrhythmic mechanisms has been hindered by difficulties in measuring cellular tissue magnesium stores.Methods and Results: To see if magnesium deficiency is associated with a propensity toward triggered arrhythmias, we measured tissue magnesium levels and QT interval dispersion (as an index of repolarization dispersion) in 40 patients with arrhythmic complaints. Magnesium was measured in sublingual epithelium using X-ray dispersive analysis. QT interval dispersion was assessed on 12-lead surface F-XCs in all patients, and programmed stimulation was performed in 28. The sublingual epithelial magnesium level ([Mg]i), but the not the serum level, correlated Inversely with QT interval dispersion in 40 patients (r = 0.58, P < 0.0.5); in 12 patients undergoing repeat testing on therapy, the change in magnesium also correlated inversely with the change in QT dispersion (r = 0.61, P < 0.05). Patients with left ventricular ejection fractions > 40% had significantly higher tissue magnesium and lower QT dispersion (34.5 ± 0.5 mEq/L, 81 ± 8 msec) than those with left ventricular ejection fractious < 40% (32.7 ± 0.5 mEq/L, P < 0.01, and 114 ± 9 msec, P < 0.05). There was no difference in either [Mg]i, or QT dispersion in the 16 patients with inducible monomorphic ventricular tachycardia versus the 12 noninducible patients.Conclusion: Reduced tissue magnesium stores may represent a significant risk factor for arrhythmias associated with abnormal repolarization, particularly in patients with poor left ventricular systolic function, but may not represent a risk for excitable gap arrhythmias associated with a fixed anatomic substrate (e.g., monomorphic ventricular tachycardia).
[Show abstract][Hide abstract] ABSTRACT: Introduction: There are currently no studies systematically evaluating pulmonary vein (PV) stenosis following catheter ablation of atrial fibrillation (AF) using the anatomic PV ablation approach.Methods and Results: Forty-one patients with AF underwent anatomic PV ablation under the guidance of a three-dimensional electroanatomic mapping system. Gadolinium-enhanced magnetic resonance (MR) imaging was performed in all patients prior to and 8–10 weeks after ablation procedures for screening of PV stenosis. A PV stenosis was defined as a detectable (≥3 mm) narrowing in PV diameter. The severity of stenosis was categorized as mild (<50% stenosis), moderate (50–70%), or severe (>70%). A total 157 PVs were analyzed. A detectable PV narrowing was observed in 60 of 157 PVs (38%). The severity of stenosis was mild in 54 PVs (34%), moderate in five PVs (3.2%), and severe in one PV (0.6%). All mild PV stenoses displayed a concentric pattern. Moderate or severe PV stenosis was only observed in patients with an individual encircling lesion set. Multivariable analysis identified individual encircling lesion set and larger PV size as the independent predictors of detectable PV narrowing. All patients with PV stenosis were asymptomatic and none required treatment.Conclusions: The results of this study demonstrate that detectable PV narrowing occurs in 38% of PVs following anatomic PV ablation. Moderate or severe PV stenosis occurs in 3.8% of PVs. The high incidence of mild stenosis likely reflects reverse remodeling rather than pathological PV stenosis. The probability of moderate or severe PV stenosis appears to be related to creation of individual encircling rather than encircling in pairs lesion.