Key result
Elevated cTnI links to ~100% higher 30-day mortality in patients with ventricular tachyarrhythmias.
Why the study?
Limited data are available regarding the prognostic role of cardiac troponin I levels in the setting of ventricular tachyarrhythmias.
Does elevated cardiac troponin I on admission predict increased 30-day all-cause mortality in patients presenting with ventricular tachyarrhythmias?
Cohort (n=1,104)
No
Does elevated cardiac troponin I on admission predict increased 30-day all-cause mortality in patients presenting with ventricular tachyarrhythmias?
Hazard Ratio: 2.004 (95% CI 1.603–2.505)
Absolute Event Rate: 40% vs 22%
p-value: p=0.001
Elevated cTNI on admission serves as a strong, independent short-term prognostic marker for all-cause mortality in patients with ventricular tachyarrhythmias.
May stratify short-term mortality risk in ventricular tachyarrhythmias; leaves open whether troponin should guide management.
Besides the diagnostic role in acute myocardial infarction, cardiac troponin I levels (cTNI) may be increased in various other clinical conditions, including heart failure, valvular heart disease and sepsis. However, limited data are available regarding the prognostic role of cTNI in the setting of ventricular tachyarrhythmias. Therefore, the present study sought to assess the prognostic impact of cTNI in patients with ventricular tachyarrhythmias (i.e., ventricular tachycardia (VT) and fibrillation (VF)) on admission. A large retrospective registry was used, including all consecutive patients presenting with ventricular tachyarrhythmias from 2002 to 2015. The prognostic impact of elevated cTNI levels was investigated for 30-day all-cause mortality (i.e., primary endpoint) using Kaplan–Meier, receiver operating characteristic (ROC), multivariable Cox regression analyses and propensity score matching. From a total of 1104 patients with ventricular tachyarrhythmias and available cTNI levels on admission, 46% were admitted with VT and 54% with VF. At 30 days, high cTNI was associated with the primary endpoint (40% vs. 22%; log rank p = 0.001; HR = 2.004; 95% CI 1.603–2.505; p = 0.001), which was still evident after multivariable adjustment and propensity score matching (30% vs. 18%; log rank p = 0.003; HR = 1.729; 95% CI 1.184–2.525; p = 0.005). Significant discrimination of the primary endpoint was especially evident in VT patients (area under the curve (AUC) 0.734; 95% CI 0.645–0.823; p = 0.001). In contrast, secondary endpoints, including all-cause mortality at 30 months and a composite arrhythmic endpoint, were not affected by cTNI levels. The risk of cardiac rehospitalization was lower in patients with high cTNI, which was no longer observed after propensity score matching. In conclusion, high cTNI levels were associated with increased risk of all-cause mortality at 30 days in patients presenting with ventricular tachyarrhythmias.
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Akın et al. (2022) conducted a cohort in Ventricular tachyarrhythmias (ventricular tachycardia and ventricular fibrillation) (n=1,104). Elevated cardiac troponin I (cTNI) vs. Low cTNI levels (below or equal to assay-specific median) was evaluated on 30-day all-cause mortality (HR 2.004, 95% CI 1.603-2.505, p=0.001). Elevated cardiac troponin I levels on admission were associated with a significantly increased risk of 30-day all-cause mortality (HR 2.004) compared to low cTNI in patients presenting with ventricular tachyarrhythmias.
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