White-Coat Hypertension: A True Cardiovascular Risk?: Commentary on "The impact of white-coat hypertension on cardiac mechanics".
White-Coat Hypertension: A True Cardiovascular Risk?: Commentary on "The impact of white-coat hypertension on cardiac mechanics".
复制标题
白大衣高血压：真正的心血管风险？：“白大衣高血压对心脏力学的影响”的评论。
DOI：
10.1111/jch.12823
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Mani,Arya
中科院分区：
文献类型：
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作者：
Mani,Arya
白大衣高血压（WCH）是一种在医疗环境中血压（BP）升高的情况，显然是焦虑的结果。这是一种常见的现象，约有三分之一的患者在门诊出现血压升高。一般认为，WCH导致血压正常的患者收缩压升高不超过15 mm Hg和/或舒张压升高不超过7 mm Hg，并在随后的医疗服务提供者访视中恢复至基线值。典型的患者通常是不吸烟的老年女性。目前，没有可靠的预后数据可用于WCH，因为患者通常是在办公室血压升高的基础上进行治疗，并且缺乏大型前瞻性随机试验。在文章“白大衣高血压对心脏力学的影响”中，Tadic及其同事1研究了WCH和持续性动脉高血压（SHT）对右心室（RV）和左心室（LV）重塑的影响。采用改进的二维应变散斑跟踪法测定左、右心室的多层纵向应变。总体而言，研究者重复了先前关于高血压对LV和RV变形影响的研究结果。他们还得出结论，与血压正常的患者相比，WCH患者右心室的变形变化始于右心室内膜下，因为它们在右心室内膜下而不是心肌和心外膜下层较低。有趣的是，尽管保留了RV结构，这些变化仍然发生。然而，这项研究有几个局限性。主要的限制是研究人群的规模较小。此外，WCH患者和对照组之间的应变参数差异并不显著，然而，这些发现仍然很有趣，因为它们：（1）提供了对心脏病理学事件顺序的深入了解，（2）可能暗示WCH需要降压治疗，特别是如果未来的研究表明这些内膜下结构异常可以进展到心肌，导致舒张和潜在的收缩功能障碍。其他几项研究表明，与血压正常的患者相比，WCH患者的心血管（CV）风险增加。
White-coat hypertension (WCH) is a condition in which blood pressure (BP) rises in the medical setting, apparently as a result of anxiety. It is a common phenomenon, with about one third of all patients presenting with elevated BP in outpatient clinics. It is generally assumed that WCH causes no more than a 15 mm Hg increase in systolic and/or a 7 mm Hg increase in diastolic BP in otherwise normotensive patients and returns to baseline values in subsequent visits to a medical provider. A typical patient is generally a nonsmoking, higher-aged woman. Currently, there are no reliable prognostic data available for WCH, as patients are often treated on the basis of elevated office BP and large prospective randomized trials are lacking. In the article “The Impact of White-Coat Hypertension on Cardiac Mechanics,” Tadic and colleagues1 examine the effect of WCH and sustained arterial hypertension (SHT) on right ventricular (RV) and left ventricular (LV) remodeling. Multilayer longitudinal strain was determined by modified two-dimensional strain speckle tracking for the left and right ventricle. Overall, the investigators reproduced previous findings on the effects of hypertension on LV and RV deformation. They also concluded that deformational changes start in RV subendocardium as they were lower in subendocardial but not myocardial and subepicardial layers of the right ventricle in patients with WCH compared with normotensives. Interestingly, these changes happened despite preserved RV structure. The study has several limitations, however. The major limitation is the small size of the study population. Furthermore, the differences between patients with WCH and controls for the strain parameters were not substantial.Nonetheless, these findings remain interesting because they:(1) provide insight into the sequences of events in cardiac pathology, and (2) may implicate the need for antihypertensive therapy in WCH, particularly if future studies show that these structural abnormalities of subendocardium can advance to myocardium and result in diastolic and potentially systolic dysfunction. Several other studies have shown an increased cardiovascular (CV) risk in WCH compared with normotensive patients.