Key result
Acute post-MI sustained VT is linked to an ~8-fold higher mortality risk.
Why the study?
Sustained ventricular tachycardia during the acute phase of myocardial infarction is rare with poor short-term prognosis, but its clinical characteristics and therapeutic implications are not well defined.
Case-Control (n=154)
Odds Ratio: 19.64 (95% CI 5.3–73)
Absolute Event Rate: 65% vs 11%
p-value: p=<0.0001
BACKGROUND: Sustained ventricular tachycardia (VT) complicating the acute phase of myocardial infarction (AMI) is a quite rare event but with short-term unfavorable prognosis. The clinical characteristics as well as the therapeutic implications have not yet been well defined. HYPOTHESIS: This paper attempts to prove that VT may be considered a marker of inadequate myocardial perfusion after thrombolysis. METHODS: To assess the clinic-electroangiographic characteristics and prognosis of patients with VT occurring within the first 4 days of an AMI, a case-control study was carried out in 23 patients from a total of 1,100 patients (1.9%) hospitalized with AMI between March 1993 and July 1997. These patients were compared with a control group of 131 patients hospitalized consecutively. A statistical analysis was made using the chi-square test, t-test, and logistic regression. RESULTS: There were no differences among groups with regard to age, gender, and area of necrosis. Average time for the onset of VT was 26 h (range 0-92 h). Sixteen patients underwent coronary angiography: 4 patients had left main coronary artery disease, 2 had single-vessel disease, 8 had lesions in two vessels, and 2 had triple-vessel disease. Univariate analysis showed that patients with VT had a higher incidence of creatine phosphokinase (CPK)-MB peak > 300 UI/l (61 vs. 30%; p<0.001), more frequent occurrence of previous AMI (48 vs. 17%; p<0.001), and acute intraventricular conduction disorders (26 vs. 4%; p<0.001). Furthermore, these patients suffered ischemia previous to VT more frequently (65 vs. 11%; p<0.0001), and had a greater mortality rate than that in the control group (35 vs. 4%; p<0.0001). In the multivariant analysis, the variables related to the occurrence of VT were CPK-MB peak > 300 IU/l (OR 5.9; 95% CI 1.6-21), acute intraventricular conduction disorders (OR 9.02; 95% CI 1.7-48), and ischemia immediately prior to VT (odds ratio [OR] 19.64; 95% confidence interval [CI] 5.3-73). CONCLUSIONS: Ventricular tachycardia may be considered a marker of inadequate myocardial perfusion after thrombolysis; therefore, a more aggressive revascularization treatment in these patients would be advisable. The profile of patients with AMI, hospitalized in the coronary care unit, who will likely suffer from VT is previous AMI, CPK-MB peak > 300, acute intraventricular conduction disorders, Killip > I, and ischemia previous to VT.
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Fiol et al. (2002) conducted a case-control in Acute myocardial infarction (n=154). Sustained ventricular tachycardia vs. No sustained ventricular tachycardia was evaluated on Ischemia immediately prior to VT (OR 19.64, 95% CI 5.3-73, p=<0.0001). Sustained ventricular tachycardia during the acute phase of myocardial infarction was strongly associated with prior ischemia (OR 19.64; 95% CI 5.3-73) and higher mortality (35% vs 4%).
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