BACKGROUND: The clinical value of T-wave variability (T-var) for ventricular arrhythmia (VA) risk prediction was evaluated. METHODS AND RESULTS: Three 20-min Holter-ECG-based T-var measurements (I1 at baseline, I2 after 6.5 ± 1.6 months and I3 after 13.1 ± 2.0 months) were done in 121 patients. T-var was defined as the amplitude variability of the T-wave with the maximum of T-wave oscillation. The endpoint was a fast, potentially fatal VA (>240 beats/min). During follow-up (20 ± 4 months) 20/121 patients (55% ischemic heart disease, 15% preserved left ventricular ejection fraction [LVEF]) had fast VA terminated by ICD or external shock. Although T-var did not differ between patients with vs. without fast VA at baseline (I1: 10.7 ± 7.3 µV vs. 7.8 ± 4.1 µV, P=0.170), patients with fast VA had higher T-var compared to those without fast VA at 2 subsequent measurements (I2: 14.0 ± 6.5 µV vs. 8.2 ± 3.6 µV, P=0.030; I3: 17.0 ± 5.4 µV vs. 8.8 ± 4.6 µV, P=0.004). The increase in T-var between I1 and I2 was higher in patients with fast VA (∆T-var=7.0 ± 9.3 µV), as compared to patients without (∆T-var=0.4 ± 4.3 µV). After adjustment for LVEF in a multiple logistic regression model, the odds ratio for developing fast VA was 1.1 (P=0.056) for each 1-µV increment in T-var at I1. CONCLUSIONS: T-var is elevated in patients with fast VA, and both elevation of T-var and increase in T-var may complement LVEF in VA risk stratification.
BACKGROUND: The clinical value of T-wave variability (T-var) for ventricular arrhythmia (VA) risk prediction was evaluated. METHODS AND RESULTS: Three 20-min Holter-ECG-based T-var measurements (I1 at baseline, I2 after 6.5 ± 1.6 months and I3 after 13.1 ± 2.0 months) were done in 121 patients. T-var was defined as the amplitude variability of the T-wave with the maximum of T-wave oscillation. The endpoint was a fast, potentially fatal VA (>240 beats/min). During follow-up (20 ± 4 months) 20/121 patients (55% ischemic heart disease, 15% preserved left ventricular ejection fraction [LVEF]) had fast VA terminated by ICD or external shock. Although T-var did not differ between patients with vs. without fast VA at baseline (I1: 10.7 ± 7.3 µV vs. 7.8 ± 4.1 µV, P=0.170), patients with fast VA had higher T-var compared to those without fast VA at 2 subsequent measurements (I2: 14.0 ± 6.5 µV vs. 8.2 ± 3.6 µV, P=0.030; I3: 17.0 ± 5.4 µV vs. 8.8 ± 4.6 µV, P=0.004). The increase in T-var between I1 and I2 was higher in patients with fast VA (∆T-var=7.0 ± 9.3 µV), as compared to patients without (∆T-var=0.4 ± 4.3 µV). After adjustment for LVEF in a multiple logistic regression model, the odds ratio for developing fast VA was 1.1 (P=0.056) for each 1-µV increment in T-var at I1. CONCLUSIONS: T-var is elevated in patients with fast VA, and both elevation of T-var and increase in T-var may complement LVEF in VA risk stratification.
Authors: Achim Leo Burger; Stefan Stojkovic; André Diedrich; Svitlana Demyanets; Johann Wojta; Thomas Pezawas Journal: Clin Biochem Date: 2020-06-04 Impact factor: 3.625