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The association between autonomic dysfunction, inflammation and atherosclerosis in men under investigation for
Marcus A Ulleryd1, Ulrica Prahl2, Johannes Börsbo1
1Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Insights
Autonomic dysfunction is linked to atherosclerosis, with inflammation potentially mediating this connection. Reduced baroreflex sensitivity (BRS) and elevated inflammatory markers like white blood cell count (WBCC) are associated with increased carotid plaque area.
Area of Science:
- Cardiovascular research
- Autonomic nervous system function
- Inflammation and atherosclerosis
Background:
- Autonomic dysfunction is a known cardiovascular disease (CVD) risk factor, but the underlying mechanisms remain unclear.
- This study investigated the hypothesis that autonomic dysfunction promotes inflammation, thereby accelerating atherosclerosis.
- Understanding this link is crucial for developing targeted CVD prevention strategies.
Purpose of the Study:
- To examine the association between autonomic tone, inflammation, and atherosclerosis.
- To determine if inflammation mediates the relationship between autonomic dysfunction and carotid atherosclerosis.
- To identify specific autonomic function and inflammatory markers related to carotid plaque development.
Main Methods:
- 124 men undergoing investigation for carotid atherosclerosis were assessed.
- Autonomic function was measured using heart rate variability (HRV) and baroreflex sensitivity (BRS).
- Inflammatory markers included white blood cell count (WBCC) and C-reactive protein (CRP); carotid plaque area was quantified. Multiple linear regressions analyzed associations.
Main Results:
- Subjects with prevalent CVD had larger carotid plaque area, higher WBCC, and reduced BRS.
- BRS was inversely associated with carotid plaque area and inflammatory markers (WBCC, CRP).
- After adjusting for inflammation, the association between BRS and plaque area diminished, suggesting inflammation as a mediator. WBCC was independently associated with carotid plaque area.
Conclusions:
- Autonomic dysfunction is significantly associated with atherosclerosis.
- Inflammation appears to play a key role in mediating the link between autonomic dysfunction and atherosclerosis.
- Reduced BRS and elevated WBCC are indicators of increased atherosclerosis risk.
Background:
Autonomic dysfunction is a risk factor for cardiovascular disease (CVD), however, the exact mechanism linking autonomic dysfunction to cardiovascular disease is not known. In this study we hypothesized that autonomic dysfunction increases inflammation, which subsequently accelerates atherosclerosis. The aim of the current study was to investigate the association between autonomic tone, inflammation and atherosclerosis.
Methods:
124 men under investigation for carotid atherosclerosis were examined for autonomic function (heart rate variability; HRV and baroreflex sensitivity; BRS), inflammatory markers (white blood cell count; WBCC and C-reactive protein; CRP) and degree of carotid atherosclerosis. The direct or indirect associations between autonomic function, inflammatory parameters and carotid plaque area were investigated with multiple linear regressions.
Results:
Male subjects with prevalent CVD showed larger carotid plaque area, higher WBCC, and reduced BRS compared to subjects with no history of CVD. Further, BRS was inversely associated with carotid plaque area (r = -0.21, p = 0.018) as well as inflammatory parameters WBCC and CRP (r = -0.29, p = 0.001, and r = -0.23, p = 0.009, respectively), whereas HRV only was inversely associated with WBCC (r = -0.22, p = 0.014). To investigate if inflammation could provide a link between autonomic function and carotid atherosclerosis we adjusted the associations accordingly. After adjusting for WBCC and CRP the inverse association between BRS and carotid plaque area was attenuated and did not remain significant, while both WBCC and CRP remained significantly associated with carotid plaque area, indicating that low-grade inflammation can possibly link BRS to atherosclerosis. Also, after adjusting for age, antihypertensive treatment and cardiovascular risk factors, BRS was independently inversely associated with both WBCC and CRP, and HRV independently inversely associated with WBCC. WBCC was the only inflammatory marker independently associated with carotid plaque area after adjustment.
Conclusions:
We demonstrate that autonomic dysfunction is associated with atherosclerosis and that inflammation could play an important role in mediating this relationship.