Stroke Prevention Research Unit, University of Oxford, Oxford, UK.
Stroke. 2012 Oct;43(10):2631-6. doi: 10.1161/STROKEAHA.112.655837. Epub 2012 Aug 23.
Arterial stiffening reduces damping of the arterial waveform and hence increases pulsatility of cerebral blood flow, potentially damaging small vessels. In the absence of previous studies in patients with recent transient ischemic attack or stroke, we determined the associations between leukoaraiosis and aortic and middle cerebral artery stiffness and pulsatility.
Patients were recruited from the Oxford Vascular Study within 6 weeks of a transient ischemic attack or minor stroke. Leukoaraiosis was categorized on MRI by 2 independent observers with the Fazekas and age-related white matter change scales. Middle cerebral artery (MCA) stiffness (transit time) and pulsatility (Gosling's index: MCA-PI) were measured with transcranial ultrasound and aortic pulse wave velocity and aortic systolic, diastolic, and pulse pressure with applanation tonometry (Sphygmocor).
In 100 patients, MCA-PI was significantly greater in patients with leukoaraiosis (0.91 versus 0.73, P<0.0001). Severity of leukoaraiosis was associated with MCA-PI and aortic pulse wave velocity (Fazekas: χ(2)=0.39, MCA-PI P=0.01, aortic pulse wave velocity P=0.06; age-related white matter change: χ(2)=0.38, MCA-PI P=0.015; aortic pulse wave velocity P=0.026) for periventricular and deep white matter lesions independent of aortic systolic blood pressure, diastolic blood pressure, and pulse pressure and MCA transit time with MCA-PI independent of age. In a multivariate model (r(2)=0.68, P<0.0001), MCA-PI was independently associated with aortic pulse wave velocity (P=0.016) and aortic pulse pressure (P<0.0001) and inversely associated with aortic diastolic blood pressure (P<0.0001) and MCA transit time (P=0.001).
MCA pulsatility was the strongest physiological correlate of leukoaraiosis, independent of age, and was dependent on aortic diastolic blood pressure and pulse pressure and aortic and MCA stiffness, supporting the hypothesis that large artery stiffening results in increased arterial pulsatility with transmission to the cerebral small vessels resulting in leukoaraiosis.
动脉僵硬度降低了动脉波形的阻尼，从而增加了脑血流的搏动性，可能会损害小血管。由于之前没有研究过近期短暂性脑缺血发作或中风患者，我们确定了脑白质疏松症与主动脉和大脑中动脉僵硬度和搏动性之间的关联。
患者在短暂性脑缺血发作或小中风后 6 周内从牛津血管研究中招募。通过 2 位独立观察者使用 Fazekas 和年龄相关性白质改变量表对 MRI 上的脑白质疏松症进行分类。使用经颅超声测量大脑中动脉（MCA）僵硬度（通过时间）和搏动性（Gosling 指数：MCA-PI），使用平板血压计测量主动脉脉搏波速度和主动脉收缩压、舒张压和脉搏压。
在 100 名患者中，脑白质疏松症患者的 MCA-PI 显著更高（0.91 比 0.73，P<0.0001）。脑白质疏松症的严重程度与 MCA-PI 和主动脉脉搏波速度相关（Fazekas：χ(2)=0.39，MCA-PI P=0.01，主动脉脉搏波速度 P=0.06；年龄相关性白质改变：χ(2)=0.38，MCA-PI P=0.015；主动脉脉搏波速度 P=0.026），与主动脉收缩压、舒张压和脉搏压独立相关，MCA 僵硬度与 MCA-PI 独立相关，与年龄无关。在多元模型中（r(2)=0.68，P<0.0001），MCA-PI 与主动脉脉搏波速度独立相关（P=0.016）和主动脉脉搏压（P<0.0001）负相关，与主动脉舒张压（P<0.0001）和 MCA 通过时间（P=0.001）相关。
MCA 搏动性是脑白质疏松症最强的生理相关性，独立于年龄，并取决于主动脉舒张压和脉搏压以及主动脉和 MCA 僵硬度，支持大动脉僵硬度导致动脉搏动性增加，从而导致脑小血管发生脑白质疏松症的假说。
