Clinical predictors of in-hospital sustained ventricular tachyarrhythmias following coronary artery bypass grafting

Background Sustained ventricular tachyarrhythmias (VT) such as monomorphic or polymorphic ventricular tachycardia and ventricular fibrillation represent the most dreadful arrhythmic events that can complicate the postoperative course of coronary artery bypass grafting (CABG). The perioperative factors that are potentially associated with the onset of post-CABG sustained VT have not been deeply investigated. Hence, the aim of our paper was to identify which perioperative variables might predict post-CABG VT occurrence. Methods and Results One hundred fifty-two consecutive patients who underwent CABG surgery at our institution between September and December 1997 comprised the study population. Post-CABG VT occurred in 13 (8.5%) out of 152 patients (6 cases of monomorphic ventricular tachycardia and 7 cases of ventricular fibrillation). Using univariate analysis, VT patients were compared with those who remained in sinus rhythm (SR). VT patients were significantly younger (54.8 ± 6.6 vs. 60.1 ± 8.8, p=0.038), had more severe coronary artery disease (CAD) (No. of diseased vessels 2.92 ± 0.3 vs 2.45 ± 0.7, p=0.023), had a higher incidence of three-vessel CAD (91.7% vs 57.3%, p=0.043), and received a greater number of CABGs (% of patients receiving three or more CABGs 76.9% vs. 38.8%, p=0.018). VT patients were found to developed intra- or post-operative myocardial infarction more frequently (total CK > 1000 76.9% vs. 38%, p= 0.016; and MB-CK > normal range 72.7% vs 30.7%, p= 0.014), had a higher incidence of electrolyte derangement (84.6% vs 45.6%, p=0.017) and more severe hemodynamic impairment (need of IABP 23% vs 2.9%, p=0.009). At multivariate analysis, total CK > 1000, postoperative electrolyte imbalance, the need of three or more CABGs and use of IABP were found to be independent correlates for VT. Conclusions Post-CABG VT seem to be related to the pre-existence of severe underlying coronary artery disease and to triggering factors such as acute ischemia, electrolyte disorders, and a sudden hemodynamic impairment that might precipitate the onset of VT.