Heart rate variability and cardiovascular diseases: A Mendelian randomization study

Yan Zhao1, Hangtian Yu1, Angwei Gong1

  • 1Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

Insights

This study found that higher peak-valley respiratory sinus arrhythmia or high-frequency power (pvRSA/HF) is genetically linked to an increased risk of cardiac arrest. This genetic evidence clarifies a potential causal relationship in cardiovascular disease events.

Area of Science:

  • Cardiology
  • Genetics
  • Epidemiology

Background:

  • The link between heart rate variability (HRV) and cardiovascular diseases (CVD) remains unclear, with inconsistent findings in existing research.
  • Mendelian randomization studies offer a method to investigate potential causal relationships using genetic variants.

Purpose of the Study:

  • To explore the causal relationship between heart rate variability and cardiovascular diseases and associated events.
  • To utilize Mendelian randomization to assess the genetic influence of HRV on CVD outcomes.

Main Methods:

  • Selected instrumental variables for HRV: standard deviation of NN intervals (SDNN), root mean square of successive differences (RMSSD), and peak-valley respiratory sinus arrhythmia/high-frequency power (pvRSA/HF).
  • Utilized publicly available genome-wide association study data for exposures and outcomes, including various CVDs and related events.
  • Employed inverse variance weighted (IVW) for primary causal estimation, with MR-Egger, Cochran's Q test, and leave-one-out analyses to assess heterogeneity and pleiotropy.

Main Results:

  • Genetically predicted pvRSA/HF showed a significant association with an increased risk of cardiac arrest (OR 2.02, 95% CI 1.25-3.28, p=0.004).
  • The association remained robust, with no significant heterogeneity or pleiotropy detected.
  • Leave-one-out analysis confirmed the reliability of the findings.

Conclusions:

  • This Mendelian randomization study provides strong genetic evidence for a causal relationship between pvRSA/HF and cardiac arrest.
  • The findings contribute to understanding the role of autonomic function, specifically parasympathetic activity reflected by pvRSA/HF, in cardiac arrest etiology.
Abstract

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