From the Department of Cardiovascular Medicine, Graduate School of Biomedical and Health Sciences (T.M., J.S., N.F., N.I., S.M., Y.I., A.I., M.K., T.M., N.O., S.K., S.M., H.H., T.H., Y.K.) and Department of Cardiovascular Regeneration and Medicine, Research Institute for Radiation Biology and Medicine (Y.A., F.B.M.Y., K.N., Y.H.), Hiroshima University, Japan; Department of Gastroenterology and Metabolism, Biomedical Sciences, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan (K.C.); Division of Regeneration and Medicine, Hiroshima University Hospital, Japan (K.N., A.N., Y.H.); Department of Rehabilitation, Faculty of General Rehabilitation, Hiroshima International University, Japan (C.G.); Department of Cardiology, Tokyo Medical University, Japan (H.T., A.Y., T.K.); Division of Biomedical Engineering, National Defense Medical College Research Institute, Tokorozawa, Japan (B.T.); Cardiovascular Medicine, University of Leicester, United Kingdom (T.S.); Cardiovascular Division, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan (T.I.); Department of Clinical Pharmacology and Therapeutics, University of the Ryukyu School of Medicine, Okinawa, Japan (S.U.); Clinical Research Support Center, Faculty of Medicine, The University of Tokyo, Japan (T.Y.); Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Japan (T.F.); Division of Cardiovascular Medicine, Jichi Medical University School of Medicine, Tochigi, Japan (K.K.); Department of Cardiovascular Medicine, Dokkyo Medical University, Mibu, Japan (T.I.); Division of Cardiology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan (S.K.); Department of Neurology, Hematology, Metabolism, Endocrinology, and Diabetology, Yamagata University School of Medicine, Japan (K.W.); Department of Internal Medicine and Cardiology, Osaka City University Graduate School of Medicine, Japan (Y.T.); Department of Medical Education and Population-Based Medicine, Postgraduate School of Medicine, Wakayama Medical University, Japan (T.H.); Department of Cardiovascular Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, Japan (M.S.); Department of General Medicine, Shimane University Faculty of Medicine, Izumo, Japan (Y.I.); Department of Cardiovascular and Renal Medicine, Saga University, Japan (K.N.); Department of Cardiovascular Medicine, Nagasaki University Graduate School of Biomedical Sciences, Japan (K.M.); The Third Department of Internal Medicine, University of the Ryukyus, Okinawa, Japan (Y.O.); Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan (T.F.); Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Japan (H.I.); and Faculty of Fukuoka Medical Technology, Teikyo University, Japan (H.I.).
Hypertension. 2017 Oct;70(4):790-797. doi: 10.1161/HYPERTENSIONAHA.117.09612. Epub 2017 Aug 14.
Hypertension is associated with endothelial dysfunction. Blood pressure significantly correlates with endothelial function in antihypertensive drug-naive subjects. The purpose of this study was to determine whether treatment status affects the relationship between blood pressure and endothelial function. We measured flow-mediated vasodilation (FMD) in 2297 subjects, including 1822 antihypertensive drug-naive subjects and 475 treated hypertensive patients. FMD significantly decreased in relation to increase in systolic blood pressure (8.2±3.1% in subjects with systolic blood pressure of <120 mm Hg, 7.5±2.8% for 120-129 mm Hg, 7.1±2.8% for 130-139 mm Hg, and 6.7±2.6% for ≥140 mm Hg; <0.001). Systolic blood pressure was independently associated with FMD in untreated subjects. In contrast, there was no significant relationship between systolic blood pressure and FMD in treated hypertensive patients (4.6±3.1% in treated hypertensives with systolic blood pressure of <120 mm Hg, 4.8±2.7% for 120-129 mm Hg, 4.9±2.8% for 130-139 mm Hg, and 4.5±2.3% for ≥140 mm Hg; =0.77). Propensity score matching analysis revealed that the prevalence of endothelial dysfunction defined as FMD of less than the division point for the lowest tertile, and the middle tertile of FMD was significantly higher in treated hypertensive patients than in untreated subjects in all systolic blood pressure categories. Endothelial function assessed by FMD was impaired regardless of the level of blood pressure achieved by antihypertensive drug treatment in hypertensive patients.
高血压与血管内皮功能障碍有关。在未经抗高血压药物治疗的受试者中，血压与内皮功能显著相关。本研究旨在确定治疗状态是否会影响血压与内皮功能之间的关系。我们测量了 2297 名受试者的血流介导的血管扩张（FMD），包括 1822 名未经抗高血压药物治疗的受试者和 475 名接受治疗的高血压患者。随着收缩压的升高，FMD 显著下降（收缩压<120mmHg 的受试者为 8.2±3.1%，120-129mmHg 的为 7.5±2.8%，130-139mmHg 的为 7.1±2.8%，≥140mmHg 的为 6.7±2.6%；<0.001）。未治疗的受试者中，收缩压与 FMD 独立相关。相比之下，接受治疗的高血压患者中，收缩压与 FMD 之间没有显著关系（收缩压<120mmHg 的接受治疗的高血压患者为 4.6±3.1%，120-129mmHg 的为 4.8±2.7%，130-139mmHg 的为 4.9±2.8%，≥140mmHg 的为 4.5±2.3%；=0.77）。倾向评分匹配分析显示，在所有收缩压类别中，定义为最低三分位和中三分位 FMD 低于分界点的内皮功能障碍的患病率，以及 FMD 中间三分位的患病率，在接受治疗的高血压患者中均显著高于未治疗的受试者。在接受抗高血压药物治疗的高血压患者中，无论血压水平如何，FMD 评估的内皮功能均受损。
