Prediction of Sudden Cardiac Death With Ultra-Short-Term Heart Rate Fluctuations.

Background: Conventional measures of heart rate variability (HRV) have shown only modest associations with sudden cardiac death (SCD). Detrended fluctuation analysis (DFA), with novel methodological developments to evaluate the short-term scaling exponent, is a potentially superior method compared to conventional HRV tools.
Objectives: In this study, the authors studied the analysis of the association between DFA and SCD.
Methods: The investigators studied the predictive value of ultra-short-term heart rate fluctuations (1-minute electrocardiogram samples) with DFA at rest and during different stages of physical exertion for incident SCD among 2,794 participants undergoing clinical exercise testing in the prospective FINCAVAS (Finnish Cardiovascular Study). The novel key DFA measure, the short-scale scaling exponent computed with second-order detrending (DFA2 α ₁ ), was the main exposure variable. SCDs were defined by American Heart Association/European Society of Cardiology criteria using death certificates with written accounts of the events.
Results: During a median follow-up of 8.3 years (Q1-Q3: 6.4-10.5), 83 SCDs occurred. DFA2 α ₁ measured at rest (but not in exercise) associated highly significantly with the risk of SCD, with 1-SD lower values associating with a 2.4-fold (Q1-Q3: 2.0-3.0) risk (P < 0.001). The results persisted when adjusting for other major risk factors for SCD, including age, cardiovascular morbidities, cardiorespiratory fitness, heart rate reduction, and left ventricular ejection fraction. Associations between conventional HRV parameters (measured at any stage of exercise or at rest) and SCD were substantially weaker and statistically nonsignificant after adjusting for other risk factors.
Conclusions: Ultra-short-term DFA2 α ₁ , when measured at rest, is a powerful and independent predictor of SCD. The association between DFA2 α ₁ and SCD is modified by physical exertion.
Competing Interests: Funding Support and Author Disclosures FINCAVAS has been financially supported by the Competitive Research Funding of Tampere University Hospital (grants 9M048 and 9N035); the Finnish Cultural Foundation; the Finnish Foundation for Cardiovascular Research (to T.L); the Emil Aaltonen Foundation; the Tampere Tuberculosis Foundation, EU Horizon 2020 (grants 755320 for TAXINOMISIS and 848146 for To Aition); and the Academy of Finland (grant 322098). Additional funding has been also granted by Business Finland, R2B Funding 2022-23 (to E.R). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)