INTRODUCTION: Electrical shocks delivered for atrial cardioversion (CV) may cause myocardial damage. The aim of this study was to assess the extent of myocardial injury caused by repeated intracardiac shocks delivered for low-energy internal atrial CV. METHODS AND RESULTS: Thirty-five patients with chronic persistent atrial fibrillation (AF) of different etiologies underwent CV with delivery of synchronized biphasic shocks (3.0/3.0 ms) between two catheters positioned in the right atrium and the coronary sinus. Shocks were delivered according to a step-up protocol (50 V, 180 V, then steps of 40 to 56 V up to 500 V, if necessary). In 23 patients, AF was reinduced after baseline CV, and CV was repeated. Myocardial injury was monitored by measuring cardiac troponin I (cTnI) serum concentrations in blood samples taken at baseline and at 2, 4, 8, 12, and 24 h after the procedure, by means of an immunoenzymologic assay (normal values, < or =0.6 ng/mL). A mean (+/- SD) of 6.9 +/- 3.4 shocks per patient were delivered (range, 2 to 17). Shocks delivered in each patient had a maximal energy of 7.3 +/- 4.0 J (range, 1.7 to 15.7). In 20 patients (57%), no evidence of myocardial injury (cTnI level, < or = 0.6 ng/mL) was found. In 13 patients (37%), mildly elevated cTnI levels (range, 0.7 to 1.4 ng/mL) in samples taken 4 to 12 h after CV suggested minor myocardial injury. In two patients (6%), higher cTnI levels were found in samples taken 4 to 8 h after CV (peak, 1.7 and 2.4 ng/mL), indicating a necrotic damage. Patients with no cTnI elevation, with mild cTnI elevation, or with cTnI levels >or =1.5 ng/mL did not differ significantly with respect to the total number of shocks delivered, the mean amount of energy delivered, and the cumulative amount of energy delivered. No clinical complications were observed. CONCLUSIONS: Following internal CV with the delivery of repeated shocks, minor elevations of cTnI serum levels could be detected in a significant proportion of patients, and this suggests subtle asymptomatic minor myocardial injury. The elevations of cTnI levels do not appear to be related to the number of shocks or to the amount of energy delivered.
INTRODUCTION: Electrical shocks delivered for atrial cardioversion (CV) may cause myocardial damage. The aim of this study was to assess the extent of myocardial injury caused by repeated intracardiac shocks delivered for low-energy internal atrial CV. METHODS AND RESULTS: Thirty-five patients with chronic persistent atrial fibrillation (AF) of different etiologies underwent CV with delivery of synchronized biphasic shocks (3.0/3.0 ms) between two catheters positioned in the right atrium and the coronary sinus. Shocks were delivered according to a step-up protocol (50 V, 180 V, then steps of 40 to 56 V up to 500 V, if necessary). In 23 patients, AF was reinduced after baseline CV, and CV was repeated. Myocardial injury was monitored by measuring cardiac troponin I (cTnI) serum concentrations in blood samples taken at baseline and at 2, 4, 8, 12, and 24 h after the procedure, by means of an immunoenzymologic assay (normal values, < or =0.6 ng/mL). A mean (+/- SD) of 6.9 +/- 3.4 shocks per patient were delivered (range, 2 to 17). Shocks delivered in each patient had a maximal energy of 7.3 +/- 4.0 J (range, 1.7 to 15.7). In 20 patients (57%), no evidence of myocardial injury (cTnI level, < or = 0.6 ng/mL) was found. In 13 patients (37%), mildly elevated cTnI levels (range, 0.7 to 1.4 ng/mL) in samples taken 4 to 12 h after CV suggested minor myocardial injury. In two patients (6%), higher cTnI levels were found in samples taken 4 to 8 h after CV (peak, 1.7 and 2.4 ng/mL), indicating a necrotic damage. Patients with no cTnI elevation, with mild cTnI elevation, or with cTnI levels >or =1.5 ng/mL did not differ significantly with respect to the total number of shocks delivered, the mean amount of energy delivered, and the cumulative amount of energy delivered. No clinical complications were observed. CONCLUSIONS: Following internal CV with the delivery of repeated shocks, minor elevations of cTnI serum levels could be detected in a significant proportion of patients, and this suggests subtle asymptomatic minor myocardial injury. The elevations of cTnI levels do not appear to be related to the number of shocks or to the amount of energy delivered.