Remote Ischemic Preconditioning on New Onset Post-Cardiac Surgery Atrial Fibrillation: A Single-Centre Prospective Clinical Study

Author Info

Aidonidis Isaac Befani Christina Dipla Konstantina Hatziefthimiou Apostolia Liakos Panagiotis Papadopoulos Eleftherios Simopoulos Vassilios Stamoulis Konstantinos Tsilimingas Nikolaos

Corresponding Author

Aidonidis Isaac
Department of Physiology, of Larissa Medical School, University of Thessaly, Larissa, Greece

A B S T R A C T

Background: Remote ischemic preconditioning (RIPC) has been shown to reduce myocardial ischemiareperfusion injury. However, its efficacy in preventing postoperative atrial fibrillation (POAF) remains unsettled. Methods: A total of 97 eligible patients were prospectively randomized to receive either RIPC or shamRIPC (control) prior to coronary artery bypass graft (CABG) surgery. RIPC was performed by applying 3 alternating cycles of a 5-min upper limb ischemia and reperfusion using a blood-pressure cuff. The primary endpoint was the incidence of POAF. Secondary endpoints included cardiac troponin T (cTnT) and H2O2 serum concentration after revascularization, and P-wave duration (PWD) on a 12-lead electrocardiogram. Results: Twelve out of 49 RIPC patients (24.5%) and 18/48 of control patients (37.5%) developed POAF (p=0.165, χ2-test). H2O2 levels were significantly increased 30 min after revascularization in both groups compared to pre-clamping values (8.8±6 vs 25.5±2 and 8.5±5 vs 39±15.5 µM/L in the RIPC and control group, respectively; P<.001, within-group analysis). However, mean differences of H2O2 levels after reperfusion were lower in RIPC patients than in controls (P<.05). cTnT concentrations though increased between 6 and 12 h after operation in both groups, they began to fall later only in the RIPC group. PWD became shorter in RIPC treated patients but not in controls when measured postoperatively (82±13 vs 75±11 ms, P<.01). Conclusion: RIPC did not significantly reduce the incidence of POAF despite decreases in cTnT/H2O2 levels and PWD, indicating that not the extent of myocardial injury but the injury itself triggers the electrophysiologic mechanisms underlying the development of this arrhythmia.

Article Info

Article Type

Research Article

Publication history

Received: Fri 08, Nov 2019
Accepted: Mon 25, Nov 2019
Published: Sat 14, Dec 2019

Copyright

© 2023 Aidonidis Isaac. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Hosting by Science Repository.
DOI: 10.31487/j.JICOA.2019.04.09