Clinical relevance of brachial pulse pressure as a measure of cerebrovascular disease risk.
Clinical relevance of brachial pulse pressure as a measure of cerebrovascular disease risk.
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肱动脉脉压作为脑血管疾病风险衡量指标的临床相关性。
DOI：
10.1111/jch.13582
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发表时间：
2019
期刊：
影响因子：
--
通讯作者：
Perdomo,SophyJ
中科院分区：
文献类型：
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作者：
Perdomo,SophyJ
脉压（PP），收缩压和舒张压之间的差异，是动脉僵硬度的量度。1较高的PP与心血管发病率和死亡率增加2以及脑血管疾病结局（如中风、阿尔茨海默病和认知能力下降）相关。3-5此外，较高的PP与脑血管病理学相关，如白色物质高信号（WMH）。6-9 WMH是死亡、中风、痴呆、抑郁和丧失活动能力风险增加的临床有意义的标志物。10鉴于WMH的临床相关性，重要的是要阐明潜在的机制。为此，假设PP通过将增加的脉动流传输到大脑中而导致WMH。1，7-9，11，12心脏收缩产生的脉动流不能被较硬的动脉很好地缓冲（由PP增加指示），因此，脉动流渗透到大脑的深层结构中，损害微血管系统和周围组织（WMH）。1，7-9，11，12许多研究已经证明了PP、脉动流和WMH之间的关联。例如，较高的主动脉和颈动脉PP与大脑中动脉中较高的脑脉动流和较大的WMH相关。8，9此外，肱动脉PP（bPP; 3年期间）增加与颈内动脉中较高的脉动流和较大的WMH相关。11总之，这些数据支持以下假设：较高的PP将增加的脉动流传输到大脑，随后导致WMH。除了WMH，bPP似乎也在中风和阿尔茨海默病中发挥作用。一项系统性综述和荟萃分析得出结论，bPP升高10 mm Hg与卒中风险增加独立相关。3 bPP还与卒中后的临床结局相关，如30天死亡率、复发性卒中和神经功能恶化。3此外，较高的bPP与阿尔茨海默病和痴呆4的风险增加以及tau磷酸化（阿尔茨海默病生物标志物）增加相关。此外，研究发现，bPP增加可以预测11年后整体认知、记忆和注意力的下降。5 bPP与脑血管病风险相关，bPP可作为脑血管病的临床筛查工具。颈动脉-股动脉脉搏波速度是动脉硬度的黄金标准，14主要用于研究，临床医生或普通人群不易获得。相反，bPP可以在任何常规临床访视时测量，并且与颈动脉-股动脉脉搏波速度和中心PP（cPP）密切相关，使其成为主动脉僵硬度的有效且可获得的指标。1，2此外，与cPP相比，bPP与脑脉动流的相关性更强，1表明bPP可以更准确地表示脑血管健康风险。由于bPP是简单地从血压计算，这提供了一个独特的机会，使用bPP作为一个代理的脑血管疾病的风险在常规医生检查。最后，bPP可以很容易地随着时间的推移进行监测，使其成为跟踪脑血管疾病风险（“大脑健康状况不佳”）的有吸引力的评估工具。因此，进一步的研究是必要的应用bPP作为一个代理的脑血管疾病的风险。
Pulse pressure (PP), the difference between systolic blood pressure and diastolic blood pressure, is a measure of arterial stiffness. 1 Higher PP is associated with increased cardiovascular morbidity and mortality2 and with cerebrovascular disease outcomes such as stroke, Alzheimer's disease, and cognitive decline. 3-5 Furthermore, higher PP is associated with cerebrovascular pathology such as white matter hyperintensities (WMH). 6-9 WMH are clinically meaningful markers of increased risk of death, stroke, dementia, depression, and loss of mobility. 10 Given the clinical relevance of WMH, it is important to elucidate the underlying mechanisms. To this end, PP is hypothesized to result in WMH via its transmission of increased pulsatile flow into the brain. 1, 7-9, 11, 12 The pulsatile flow created by cardiac contractions is not buffered well by stiffer arteries (indicated by increased PP), and thus, pulsatile flow penetrates into the deep structures of the brain, damaging the microvasculature and surrounding tissue (WMH). 1, 7-9, 11, 12 A number of studies have demonstrated associations between PP, pulsatile flow, and WMH. For instance, higher aortic and carotid PP are associated with higher cerebral pulsatile flow in the middle cerebral artery and greater WMH. 8, 9 Moreover, increased brachial PP (bPP; over a 3-year period) is associated with higher pulsatile flow in the internal carotid artery and greater WMH. 11 Taken together, these data support the hypothesis that higher PP transmits increased pulsatile flow to the brain, which subsequently results in WMH. In addition to WMH, bPP also appears to play a role in stroke and Alzheimer's disease. A systematic review and meta-analysis concluded that a 10 mm Hg increase in bPP is independently associated with an increased risk in stroke. 3 bPP is also associated with clinical outcomes following stroke, such as 30-day mortality, recurrent stroke, and neurologic deterioration. 3 Moreover, a higher bPP is associated with an increased risk of Alzheimer's disease and dementia4 and with increased tau phosphorylation (Alzheimer's disease biomarker). 13 Furthermore, increased bPP has been found to predict declines in overall cognition, memory, and concentration 11 years later. 5Given the association of higher bPP with cerebrovascular disease risk, bPP could serve as a valuable clinical screening tool for cerebrovascular health. Carotid-femoral pulse wave velocity, the gold standard for arterial stiffness, 14 is primarily used for research and not readily accessible to clinicians or the general population. bPP, conversely, can be measured at any routine clinical visit and is strongly correlated with carotid-femoral pulse wave velocity and central PP (cPP), making it a valid and accessible indicator of aortic stiffness. 1, 2 Additionally, bPP is more strongly correlated with cerebral pulsatile flow compared to cPP, 1 suggesting that bPP may provide a more accurate representation of cerebrovascular health risk. Since bPP is simply calculated from blood pressure, this offers a unique opportunity to use bPP as a proxy for cerebrovascular disease risk at routine physician examinations. Finally, bPP can easily be monitored over time, making it an attractive assessment tool to track cerebrovascular disease risk (“poor brain health”). Thus, further research is warranted on the application of bPP as a proxy for cerebrovascular disease risk.