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Notes: Background: QT dispersion (QTd) has been found to correlate to the amount of viable myocardium in patients with Q-wave myocardial infarction and well-preserved LV function. However, this relationship is unknown in patients with severe left ventricular dysfunction.Methods: Thirty-four patients with prior large myocardial infarction and severe left ventricular dysfunction underwent Tc-99m sestamibi single photon emission cardiac tomography (SPECT) and F-18 fluorodeoxyglucose (FDG) SPECT. Viability was defined as a defect relative count density (DCD) of at least 20% greater on FDG SPECT. QTd, corrected QT dispersion (QTcd), and QT coefficient of variation (cv) in patients with viable myocardium was compared to those without viable mvocardium in the infarct area.Results: Thirteen patients were excluded from analysis for poor FDG images or inadequate ECG tracings. Of the remaining patients, 10 (48%) were found to have viability on FDG SPECT. QTd, QTcd, and QTcv in patients with viability were: 58 ± 22 ms, 61 ± 23 ms, and 4.81 ± 1.76%, respectively, which did not differ significantly from those in patients without viability (QTd = 56 ± 14 ms, QTcd = 70 ± 16 ms and Qtcv = 5.06 ± 1.20% (P = NS]). Moreover, neither FDG defect size, nor LVEF correlated with QTd.Conclusions: This study indicates no relationship between QTd and viability in patients with myocardial infarction and severe left ventricular dysfunction. A.N.E. 2002;7(1):53–59

Notes: Ablation and Coagulation Activation. Introduction: Although thromboembolism is an uncommon complication of radiofrequency (RF) ablation, some preliminary reports have suggested that RF ablation results in activation of the coagulation system, possibly increasing this risk. We hypothesized that the insertion of intravenous catheters and their prolonged intravenous placement rather than RF ablation activates the coagulation cascade. Methods and Results: Thirty-seven patients, group 1 (n = 21) during RF ablation, and group 2 (n = 16) during routine electrophysiologic studies (EPS), were studied prospectively. Blood was drawn for coagulation and fibrinolytic studies following insertion of venous sheaths (TO), following catheter placement (T1), and 1 hour after completion of RF ablation or EPS {T2). Conversion of prothrombin to thrombin was measured using thrombin-antithrombin complex (TAT) and prothrombin activation peptide (F1+2). and fibrinolytic activity was assessed using D-dlmer concentration. Levels of D-dimer increased in group 1 from 823.52 ± 323.52 ng/mL at TO to 1,314.28 ± 297.63 ng/mL at T2 (P= 0.005), and in group 2 from 658.15 ± 161.70 ng/mL at T0 to 1625 641.45 ng/mL at T2 (P=±0.064). TAT levels increased from to 27.74 ± 5.6 μg/L at T0 to 52.99 ± 5.93 μg/L at T2 in group 1 (P= 0.09), and from 19.79 ± 5.14 μg/L at T0 to 73.5 ± 24.15 μg/L at T2 in group 2 (P= 0.05). F1+2 concentration increased from 1.52 ± 0.30 nmol/L at T0 to 3.06 ± 0.41 nmol/L at T2 in group 1 (P= 0.004), and from 1.32 ± 0.30 nmol/L at T0 to 3.11 ± 0.46 nmol/L at T2 in group 2 (P= 0.087). There was no significant difference in the concentration of the three coagulation variables between group 1 and group 2 at any given time point. No correlation was demonstrable between concentration of D-dimers, TAT, or F1+2 and variables of RF delivery such as cumulative energy, number of RF energy applications, or number of impedance rises. However, a significant positive correlation (r = 0.65, P 〈 0.01) was noted between the duration of the RF ablation procedure and the concentration of D-dimers. Conclusion: We conclude that activation of the coagulation cascade in RF ablation procedures is not related to the delivery of RF energy, but is related to the placement of intravascular catheters and to the duration of the ablation procedure.