Key result
Systemic acidosis on admission was a strong independent predictor of sustained ventricular tachycardia and ventricular fibrillation after reperfused STEMI (RR 8.79).
Why the study?
Does systemic acidosis on admission predict the development of malignant ventricular arrhythmias in patients with reperfused STEMI?
Cohort (n=157)
No
Does systemic acidosis on admission predict the development of malignant ventricular arrhythmias in patients with reperfused STEMI?
Relative Risk: 8.79 (95% CI 2.26–34.21)
Absolute Event Rate: 26% vs 4%
p-value: p=0.002
Systemic acidosis on admission is a strong independent predictor of malignant ventricular arrhythmias after reperfusion therapy for STEMI, highlighting a high-risk patient subset.
May identify high-risk reperfused STEMI patients for monitoring; leaves open whether correcting acidosis reduces arrhythmic events.
BACKGROUND: The aim of the present study was to examine the effect of systemic acidosis on the development of malignant ventricular arrhythmias, including sustained ventricular tachycardia and ventricular fibrillation (VT/VF), after reperfused ST-elevation myocardial infarction (STEMI). METHODS AND RESULTS: A total of 157 consecutive patients with a reperfused STEMI were examined. Patients were divided into 2 groups according to the presence or absence of systemic acidosis, defined as arterial blood pH <7.40 on admission. Serum creatine kinase and C-reactive protein (CRP) levels were serially measured. Systemic acidosis was observed in 53 patients (34%). There was no significant difference in coronary risk factors and arrival time from onset between the 2 groups. Estimated glomerular filtration rate (eGFR) on admission was lower in patients with acidosis than in those without (P=0.001). Patients with acidosis had a higher incidence of VT/VF (26% vs 4%, P<0.0001), especially within 48 h after STEMI (23% vs 3%, P=0.0002), than those without. The peripheral white blood cell count on admission was higher in patients with than in those without acidosis. Multivariate analysis showed that systemic acidosis was a strong independent predictor of VT/VF (relative risk =8.79, P=0.002) among variables including prior MI and eGFR <60 ml . min(-1) . 1.73 m(-2). CONCLUSIONS: Systemic acidosis was a significant determinant of VT/VF after reperfused STEMI and was associated with elevated serum CRP level. Systemic acidosis and subsequent inflammation after ischemia reperfusion may play an important role in the development of VT/VF.
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Nagai et al. (2010) conducted a cohort in ST-elevation myocardial infarction (STEMI) (n=157). Systemic acidosis (arterial blood pH <7.40 on admission) vs. Absence of systemic acidosis (arterial blood pH ≥7.40) was evaluated on Development of malignant ventricular arrhythmias, including sustained ventricular tachycardia and ventricular fibrillation (VT/VF) (RR 8.79, 95% CI 2.26-34.21, p=0.002). Systemic acidosis on admission was a strong independent predictor of sustained ventricular tachycardia and ventricular fibrillation after reperfused STEMI (RR 8.79).
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