Türker Duyuler Pinar, Duyuler Serkan, Demir Mevlüt, Uçar Elalmiş Özgül, Güray Ümit, İleri Mehmet
aDepartment of Cardiology, Ankara Numune Training and Research Hospital bDepartment of Cardiology, Acibadem Ankara Hospital, Ankara, Turkey.
Blood Press Monit. 2017 Dec;22(6):333-338. doi: 10.1097/MBP.0000000000000300.
Exaggerated blood pressure response to exercise is a risk factor for the development of future hypertension. In this study, we aimed to investigate the association between homocysteine, epicardial fat thickness, nonalcoholic hepatic steatosis, and exaggerated blood pressure response to exercise.
We included 44 normotensive and 40 patients with exaggerated blood pressure response to exercise who have normal resting blood pressure and without a previous diagnosis of hypertension. All patients underwent treadmill exercise test and clinical, ultrasonographic, and echocardiographic evaluation. Exaggerated blood pressure response to exercise is defined as peak exercise systolic blood pressure of at least 210 mmHg in men and at least 190 mmHg in women. Homocysteine and other biochemical parameters were determined with standardized automated laboratory tests.
Mean age of all participants is 47.9±8.5 years, and 36 of 84 participants were female. The frequency of diabetes mellitus in both groups was similar (P=0.250). Homeostasis model assessment index-insulin resistance had a statistically insignificant trend to be higher in a patient with exercise hypertension (P=0.058). The nonalcoholic fatty liver was more frequent in patients with exercise hypertension (13.6 vs. 47.5%, P=0.002). Epicardial fat thickness was increased in patients with exercise hypertension (5.5±1.5 vs. 7.3±1.1 mm; P=0.001). However, homocysteine levels did not significantly differ between normotensive and exercise hypertensive patients [12.3 μmol/l (5.7-16.9 μmol/l) vs. 13 μmol/l (5.9-28.3 μmol/l); P=0.883].
In our study, homocysteine levels were not associated with exaggerated blood pressure response to exercise; however, fatty liver and epicardial fat thickness as visceral adiposity-related cardiometabolic risk factors were significantly related with exaggerated blood pressure response to exercise in patients without a previous diagnosis of hypertension.
运动时血压反应过度是未来发生高血压的一个危险因素。在本研究中，我们旨在调查同型半胱氨酸、心外膜脂肪厚度、非酒精性肝脂肪变性与运动时血压反应过度之间的关联。
我们纳入了44名血压正常者以及40名运动时血压反应过度的患者，这些患者静息血压正常且既往无高血压诊断史。所有患者均接受了跑步机运动试验以及临床、超声和超声心动图评估。运动时血压反应过度定义为男性运动高峰收缩压至少为210 mmHg，女性至少为190 mmHg。同型半胱氨酸和其他生化参数通过标准化自动实验室检测来确定。
所有参与者的平均年龄为47.9±8.5岁，84名参与者中有36名女性。两组糖尿病的发生率相似（P = 0.250）。稳态模型评估指数-胰岛素抵抗在运动性高血压患者中虽有升高趋势，但无统计学意义（P = 0.058）。运动性高血压患者中非酒精性脂肪肝更为常见（13.6% 对47.5%，P = 0.002）。运动性高血压患者的心外膜脂肪厚度增加（5.5±1.5对7.3±1.1 mm；P = 0.001）。然而，血压正常者与运动性高血压患者的同型半胱氨酸水平无显著差异[12.3 μmol/L（5.7 - 16.9 μmol/L）对13 μmol/L（5.9 - 28.3 μmol/L）；P = 0.883]。
在我们的研究中，同型半胱氨酸水平与运动时血压反应过度无关；然而，作为内脏肥胖相关心脏代谢危险因素的脂肪肝和心外膜脂肪厚度与既往无高血压诊断史患者的运动时血压反应过度显著相关。
