Key result
One standard deviation unit increase in heart rate was associated with a 1.82 mmHg elevation of diastolic blood pressure, suggesting a causal relationship between cardiac autonomic function and DBP.
Why the study?
It is unclear how cardiac autonomic function, as indicated by HR, HRV, HR increase during exercise, and HR recovery after exercise, is related to blood pressure.
Do genetically predicted cardiac autonomic function traits causally affect blood pressure in the general population?
Observational (n=757,601)
Yes
Do genetically predicted cardiac autonomic function traits causally affect blood pressure in the general population?
Effect estimate: 1.82 mmHg (95% CI 1.50-2.14)
p-value: p=2.17e-28
Observational and Mendelian randomization analyses suggest that a larger relative contribution of the sympathetic versus parasympathetic nervous system to cardiac function may causally elevate diastolic blood pressure.
Supports causal inference for autonomic traits on DBP; leaves open therapeutic implications pending interventional studies.
Background: It is unclear how cardiac autonomic function, as indicated by heart rate (HR), heart rate variability (HRV), HR increase during exercise, and HR recovery after exercise, is related to blood pressure (BP). We aimed to examine the observational and genetic evidence for a potential causal effect of these HR(V) traits on BP. Methods: We performed multivariable adjusted linear regression using Lifelines and UK Biobank cohorts to investigate the relationship between HR(V) traits and BP. Linkage disequilibrium score regression was conducted to examine genetic correlations. We used two-sample Mendelian randomization (2SMR) to examine potential causal relations between HR(V) traits and BP. Results: Observational analyses showed negative associations of all HR(V) traits with BP, except for HR, which was positively associated. Genetic correlations were directionally consistent with the observational associations, but most significant genetic correlations between HR(V) traits and BP were limited to diastolic blood pressure (DBP). 2SMR analyses suggested a potentially causal relationship between HR(V) traits and DBP but not systolic blood pressure (SBP). No reverse effect of BP on HR(V) traits was found. One standard deviation (SD) unit increase in HR was associated with a 1.82 mmHg elevation of DBP. In contrast, one ln(ms) unit increase of the root mean square of the successive differences (RMSSD) and corrected RMSSD (RMSSDc), decreased DBP by 1.79 and 1.83 mmHg, respectively. For HR increase and HR recovery at 50 s, every additional SD increase was associated with a lower DBP by 2.05 and 1.47 mmHg, respectively. Results of secondary analyses with pulse pressure as outcome were inconsistent between observational and 2SMR analyses, as well as between HR(V) traits, and therefore inconclusive. Conclusion: Both observational and genetic evidence show strong associations between indices of cardiac autonomic function and DBP, suggesting that a larger relative contribution of the sympathetic versus the parasympathetic nervous system to cardiac function may cause elevated DBP.
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Chen et al. (2023) conducted an observational in Blood pressure (n=757,601). Heart rate (HR) was evaluated on Diastolic blood pressure (DBP) (1.82 mmHg, 95% CI 1.50-2.14, p=2.17e-28). One standard deviation unit increase in heart rate was associated with a 1.82 mmHg elevation of diastolic blood pressure, suggesting a causal relationship between cardiac autonomic function and DBP.
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