Department of Internal Medicine, Faculty of Medicine, Comenius University, Bratislava, Slovak Republic.
Physiol Res. 2021 Apr 30;70(2):183-191. doi: 10.33549/physiolres.934467. Epub 2021 Mar 8.
The relationship between baroreflex sensitivity (BRS) and inflammatory vascular biomarker Lipoprotein associated phospholipase A2 (Lp-PLA2) in subjects with high normal blood pressure (HNBP, prehypertensives) with a positive family history of hypertension (FHH+) and hypertension history free control subjects (FHH-) was evaluated. A total of 24 HNBP participants (age 39.5 ± 2.5 years, 18 male/ 6 female) were studied. 14 HNBP subjects FHH+ were compared to 10 HNBP participants FHH-, being of similar age and body mass index. BRS (ms/mmHg) was determined by the sequence and spectral methods (five-minute non-invasive beat-to-beat recording of blood pressure and RR interval, controlled breathing at a frequency of 0.33 Hz). Venous blood was analyzed for Lp-PLA2 biomarker of vascular inflammation and atherothrombotic activity. A significant negative correlation between spontaneous BRS obtained by both methods and systolic blood pressure (BP) was present (BRS spect r = -0.54, P<0.001, BRS seq r = -0.59, P<0.001). BRS obtained by sequence and spectral methods were reduced in HNBP FHH+ compared to the group of HNBP FHH- (P = 0.0317 BRS seq, P = 0.0395 BRS spect). Lp-PLA2 was significantly higher in HNBP FHH+ compared to FHH- controls (P<0.05). Lp-PLA2 was negatively correlated with BRS obtained by sequence method (r = -0.798, R2 = 0.636, P<0.001) in the HNBP FHH+ subjects. These findings demonstrate that reduced baroreflex sensitivity, as a marker of autonomic dysfunction, is associated with vascular inflammation, predominantly in otherwise healthy participants with a positive family history of hypertension who could predispose to increased risk of hypertension. We conclude that our transversal study suggests that a lowbaroreflex sensitivity could be an early sign of autonomic dysfunction even in the prehypertensive period, and to corroborate these findings, a longitudinal study is needed.
在具有高血压阳性家族史(FHH+)和无高血压病史的正常血压(HNBP,高血压前期)的受试者中,评估了压力反射敏感性(BRS)与炎症性血管生物标志物脂蛋白相关磷脂酶 A2(Lp-PLA2)之间的关系。共研究了 24 名 HNBP 参与者(年龄 39.5±2.5 岁,18 名男性/6 名女性)。将 14 名具有 FHH+的 HNBP 受试者与 10 名具有 FHH-的 HNBP 参与者进行了比较,两组年龄和体重指数相似。BRS(ms/mmHg)通过序列和光谱方法(非侵入性血压和 RR 间隔五分钟逐拍记录,受控呼吸频率为 0.33 Hz)确定。分析静脉血中的 Lp-PLA2 血管炎症和动脉血栓形成活性的生物标志物。两种方法获得的自发 BRS 与收缩压(BP)之间存在显著负相关(BRS spect r =-0.54,P<0.001,BRS seq r =-0.59,P<0.001)。与 HNBP FHH-组相比,HNBP FHH+中的序列和光谱方法获得的 BRS 降低(P=0.0317 BRS seq,P=0.0395 BRS spect)。与 HNBP FHH-对照组相比,HNBP FHH+中的 Lp-PLA2 显着升高(P<0.05)。在 HNBP FHH+受试者中,Lp-PLA2 与序列方法获得的 BRS 呈负相关(r=-0.798,R2=0.636,P<0.001)。这些发现表明,作为自主神经功能障碍的标志物,压力反射敏感性降低与血管炎症有关,主要与具有高血压阳性家族史的健康参与者有关,这可能导致高血压风险增加。我们得出结论,我们的横断面研究表明,即使在高血压前期,低压力反射敏感性也可能是自主神经功能障碍的早期迹象,需要进行纵向研究来证实这些发现。