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Personal-level exposure to environmental temperature is a superior predictor of endothelial-dependent vasodilatation than outdoor-ambient level.
Journal of the American Society of Hypertension Pub Date : 2017-10-11 , DOI: 10.1016/j.jash.2017.09.006
Chinedu Ejike 1 , Lu Wang 2 , Mochuan Liu 2 , Wei Wang 2 , Masako Morishita 3 , Robert L Bard 1 , Wei Huang 4 , Jack Harkema 5 , Sanjay Rajagopalan 6 , Robert D Brook 1
Affiliation  

Environmental temperatures influence cardiovascular physiology. However, the majority of time is spent indoors, making outdoor-ambient temperatures inaccurate estimates of true exposures encountered by most individuals. We evaluated in 50 healthy adults the associations between previous 7-day outdoor-ambient (four occasions) and prior 24-hour personal-level (two occasions) environmental temperature exposures with blood pressure, heart rate variability, sleep parameters, and endothelial-dependent vasodilatation (brachial flow-mediated dilatation [FMD]) using generalized estimating equations. Participants (34 females; age, 32.1 ± 9.6 years) had normal blood pressures (107.8 ± 13.3/70.2 ± 9.4 mm Hg), FMD (7.4 ± 2.8%), as well as sleep and heart rate variability parameters. Mean 7-day outdoor-ambient (4.6 ± 9.7°C) differed from personal-level temperature exposures (22.0 ± 3.0°C). Colder outdoor-ambient temperatures (per -10°C) over the previous 1-6 days (rolling averages) were associated with decreases in FMD: -0.57% (95% confidence interval [CI]: -1.14% to 0.01%, P = .055) to -0.62% (95% CI: -1.07% to -0.18%, P = .006). However, a 10°C decrease in personal-level temperature during the prior 24 hours was associated with a greater decrement in FMD: -2.44% (95% CI: -4.74% to -0.13%, P = .038). Both were also linearly related to FMD during all seasons and without a threshold temperature. Other end points were not significantly related to either temperature level in this study. Short-term exposures to colder environmental temperatures reduced endothelial-dependent vasodilatation, supporting the epidemiologic associations with heightened cardiovascular risk. We show here for the first time that temperature exposures characterized at the personal level may be more robust predictors of endothelial function than outdoor-ambient levels.

中文翻译:

个人水平暴露于环境温度是内皮依赖性血管舒张的优于室外水平的预测指标。

环境温度影响心血管生理。但是,大部分时间都花在室内,使得室外环境温度无法准确估计大多数人所遇到的真实暴露。我们评估了50名健康成年人的前7天户外环境(四次)和之前24小时个人水平(两次)的环境温度暴露与血压,心率变异性,睡眠参数和内皮依赖性的关系血管扩张(肱动脉血流介导的扩张[FMD]),使用广义估计方程。参与者(34名女性;年龄32.1±9.6岁)的血压正常(107.8±13.3 / 70.2±9.4毫米汞柱),FMD(7.4±2.8%)以及睡眠和心率变异性参数。平均7天室外环境(4.6±9。7°C)与个人温度暴露(22.0±3.0°C)不同。前1-6天(滚动平均值)中较冷的室外环境温度(每-10°C)与FMD下降相关:-0.57%(95%置信区间[CI]:-1.14%至0.01%,P = .055)至-0.62%(95%CI:-1.07%至-0.18%,P = .006)。但是,在之前的24小时内,个人水平温度下降10°C会导致FMD下降幅度更大:-2.44%(95%CI:-4.74%降至-0.13%,P = .038)。在所有季节且没有阈值温度的情况下,两者均与FMD呈线性相关。在本研究中,其他终点与任一温度水平均无显着相关。短期暴露于较冷的环境温度可减少内皮依赖性血管舒张,从而支持流行病学与心血管风险的增加。
更新日期:2019-11-01
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