Why the study?
Whether 12-lead ECG can determine biological age and if the gap between chronological age and ECG-predicted biological age reflects differences in prognosis were unclear.
Does a positive gap between ECG-predicted biological age and chronological age predict all-cause mortality in patients without structural heart disease?
Does a positive gap between ECG-predicted biological age and chronological age predict all-cause mortality in patients without structural heart disease?
A positive gap between 12-lead ECG-predicted biological age and chronological age is associated with an increased risk of all-cause mortality in patients without structural heart disease.
Background: The 12-lead electrocardiogram (ECG) is affected by not only the cardiovascular but also the non-cardiovascular status. Whether ECG can be the determinant of biological age (BA) and the gap between chronological age (CA) and ECG-predicted BA reflect differences in prognosis are unclear. Methods: In the Shinken Database 2010 – 2017 ( n = 19170), 12-lead ECG was analyzed in 13005 patients excluding those with structural heart disease or having pacing beats, atrial or ventricular tachyarrhythmia, and indeterminate axis (R axis > 180˚) on index ECG. The prediction model of BA was developed by principal component analysis with 438 ECG parameters. The gap between ECG-predicted BA and CA was calculated (AgeDiff = ECG-predicted BA − CA). Results: The ECG-predicted BA was significantly correlated with CA (r = 0.967). Patients with a positively wide AgeDiff had a higher incidence of all-cause mortality compared to those with a narrow AgeDiff or those with negative AgeDiff. The risk of AgeDiff > 0 for all-cause mortality compared with AgeDiff ≤ 0 was 1.78 (95%CI: 1.00 − 3.16), which increased according to the aging and became the highest in patients with CA of 71 − 80 years. Conclusion: Our data suggested that 12-lead ECG can be a tool to estimate BA. The gap between ECG-predicted BA and CA allowed estimation of increased risk of all-cause mortality in patients without structural heart disease.
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Hirota et al. (2020) studied this question.
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