Evaluation of myocardial injury following repeated internal atrial shocks by monitoring serum cardiac troponin I levels

Citation
G. Boriani et al., Evaluation of myocardial injury following repeated internal atrial shocks by monitoring serum cardiac troponin I levels, CHEST, 118(2), 2000, pp. 342-347
Citations number
46
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CHEST
ISSN journal
00123692 → ACNP
Volume
118
Issue
2
Year of publication
2000
Pages
342 - 347
Database
ISI
SICI code
0012-3692(200008)118:2<342:EOMIFR>2.0.ZU;2-J
Abstract
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 fi brillation (AF) of different etiologies underwent CV with delivery of synch ronized biphasic shocks (3.0/3.0 ms) between two catheters positioned in th e 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 ne cessary). In 23 patients, AF was reinduced after baseline CV, and CV was re peated. Myocardial injury was monitored by measuring cardiac troponin I (cT nI) 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, less than or equal to 0.6 ng/mL). A mean (+/- SD) of 6.9 +/- 3.4 shocks per patient were delivered (range, 2 to 17). Shocks delivered i n 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, less th an or equal to 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 s uggested 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), in dicating a necrotic damage. Patients with no cTnI elevation, with mild cTnI elevation, or with cTnI levels greater than or equal to 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 de livered. No clinical complications were observed. Conclusions: Following internal CV with the delivery of repeated shocks, mi nor elevations of cTnI serum levels could be detected in a significant prop ortion of patients, and this suggests subtle asymptomatic minor myocardial injury. The elevations of cTnI levels do not appear to be related to the nu mber of shocks or to the amount of energy delivered.