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

ABSTRACT

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-CAGB sustained VT have not been deeply investigated. Hence, the aim of our paper was to identify which perioperative variables predict post-CABG VT occurrence. One hundred fifty-two consectivity 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 university 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 CABG[s] [% of patients teceiving three or more CABG[s] 76.9% vs. 38.8%, p=0.018]. VT patients were found to developed intra-or 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 CABG[s] and use of IABP were found to be independent correlates for VT. 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