Abstract
Background: Malignant ventricular arrhythmias, such as sustained ventricular tachycardia and ventricular fibrillation (VT/VF), are fatal complications after acute myocardial infarction (MI) even in the era of reperfusion therapies. We sought to clarify the determinants of VT/VF after reperfused MI. Methods: A total of 528 consecutive acute MI patients, who were treated with primary percutaneous coronary intervention, were divided into 2 groups according to the presence or absence of VT/VF during hospitalization. Serum C-reactive protein (CRP) level and peripheral white blood cell (WBC) count were serially measured for every 24 hours. As a substudy, left ventricular (LV) function and long-term clinical outcome were compared between patients with early (>48 hours after the onset) and late VT/VF (>48 hours). Results: VT/VF was observed in 58 patients (11%). Prior MI and anterior MI are more common in patients with VT/VF than those without. Prevalence of preinfarction angina was less in patients with VT/VF than those without. Peak CRP (14.7±10.1 vs. 8.8±7.1 mg/dl, p< 0.0001), WBC on admission (12833±3513 vs. 10906±4771 /mm 3 , p=0.03) and maximum WBC (14808±5335 vs. 12531±4348 /mm 3 , p=0.009) were higher in patients with VT/VF than those without. Multivariate analysis revealed that prior MI (RR=4.57, p=0.02), absence of preinfarction angina (RR=2.44, p=0.02) and peak serum CRP ≥10 mg/dl (RR=3.37, p=0.003) were independent determinants of VT/VF. Early VT/VF was observed in 49 patients, while late VT/VF in 9 patients. Prevalence of prior MI, preinfarction angina or peak CRP ≥10mg/dl was comparable between early and late VT/VF. LV end-diastolic and end-systolic dimensions are greater in patients with late VT/VF than those with early VT/VF (p< 0.05). Incidence of readmission for heart failure and sudden cardiac death tended to be higher in patients with late VT/VF than those with early VT/VF. Conclusions: VT/VF after reperfused acute MI was associated with prior history of MI, absence of preinfarction angina and increased inflammatory markers. VT/VF occurred in late phase was related to depressed LV function. Lack of ischemic preconditioning, enhanced inflammatory response and subsequent LV remodeling could contribute to the development of VT/VF after MI.
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