Ulleryd Marcus A, Prahl Ulrica, Börsbo Johannes, Schmidt Caroline, Nilsson Staffan, Bergström Göran, Johansson Maria E
Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Department of Molecular and Clinical Medicine, Wallenberg Laboratory for Cardiovascular and Metabolic Research, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
PLoS One. 2017 Apr 4;12(4):e0174974. doi: 10.1371/journal.pone.0174974. eCollection 2017.
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.
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.
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.
We demonstrate that autonomic dysfunction is associated with atherosclerosis and that inflammation could play an important role in mediating this relationship.
自主神经功能障碍是心血管疾病（CVD）的一个危险因素，然而，将自主神经功能障碍与心血管疾病联系起来的确切机制尚不清楚。在本研究中，我们假设自主神经功能障碍会增加炎症反应，进而加速动脉粥样硬化。本研究的目的是调查自主神经张力、炎症与动脉粥样硬化之间的关联。
对124名接受颈动脉粥样硬化检查的男性进行自主神经功能（心率变异性；HRV和压力反射敏感性；BRS）、炎症标志物（白细胞计数；WBCC和C反应蛋白；CRP）以及颈动脉粥样硬化程度的检查。通过多元线性回归研究自主神经功能、炎症参数与颈动脉斑块面积之间的直接或间接关联。
与无CVD病史的受试者相比，患有CVD的男性受试者颈动脉斑块面积更大、WBCC更高且BRS降低。此外，BRS与颈动脉斑块面积呈负相关（r = -0.21，p = 0.018），与炎症参数WBCC和CRP也呈负相关（分别为r = -0.29，p = 0.001和r = -0.23，p = 0.009），而仅HRV与WBCC呈负相关（r = -0.22，p = 0.014）。为了研究炎症是否能在自主神经功能与颈动脉粥样硬化之间建立联系，我们相应地调整了关联。在调整WBCC和CRP后，BRS与颈动脉斑块面积之间的负相关减弱且不再显著，而WBCC和CRP均与颈动脉斑块面积保持显著相关，表明低度炎症可能将BRS与动脉粥样硬化联系起来。此外，在调整年龄、抗高血压治疗和心血管危险因素后，BRS与WBCC和CRP均独立呈负相关，HRV与WBCC独立呈负相关。调整后，WBCC是唯一与颈动脉斑块面积独立相关的炎症标志物。
我们证明自主神经功能障碍与动脉粥样硬化有关，并且炎症可能在介导这种关系中起重要作用。
