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脑血管老化:通过毛细血管将脉搏波脑病的概念扩展至脑静脉。

Cerebral vascular aging: extending the concept of pulse wave encephalopathy through capillaries to the cerebral veins.

作者信息

Henry-Feugeas Marie Cecile, Koskas Pierre

机构信息

Henri Huchard, Paris cedex, France.

出版信息

Curr Aging Sci. 2012 Jul;5(2):157-67. doi: 10.2174/1874609811205020157.

DOI:10.2174/1874609811205020157
PMID:22894741
Abstract

The recent concept of pulse wave encephalopathy helps understanding the cerebral venous remodeling in aging. This so-called periventricular venous collagenosis is an expected mechanical consequence of the age-related changes in arterial pulsations and the mechanical fatigue of vascular smooth muscles. Unlike arteriolar mechanical stress, venular mechanical stress depends on both the blood pulse wave amplitude and the mechanical properties of the environment tissue. Thereby, there is a preferential periventricular location of venous collagenosis and a mechanistic link between venous collagenosis and foci of white matter rarefaction or leukoaraiosis. The recent concept of pulse wave encephalopathy also helps understanding the widening of retinal venules, the "mirror" of cerebral venules, in various manifestations of pulse wave encephalopathy, including progressive leukoara�osis, lacunar and hemorrhagic "pulse wave" strokes, and dementia. Indeed, the age-related chronic increase in arterial pulsations explains subsequent arteriolar myogenic "fatigue", marked attenuation in the arteriolar myogenic tone and abnormal penetration of the insufficiently dampened arterial pulse wave into the venules. Thus, retinal venular widening, a biomarker of advanced pulse wave encephalopathy, is also increasingly recognized as a biomarker for high cardiovascular risk. All these data support a shift in the concept of chronic cerebrovascular disease, from the classical model which is restricted to steno-occlusive cerebrovascular diseases to an enlarged model which would include the pulse wave encephalopathy concept. Thereby, preventing damage to the cerebral microvasculature by an undampened arterial pulse wave will become a logical target for the prevention and treatment of late-onset cognitive decline.

摘要

脉搏波脑病的最新概念有助于理解衰老过程中的脑静脉重塑。这种所谓的脑室周围静脉胶原化是动脉搏动的年龄相关变化以及血管平滑肌机械疲劳的预期机械后果。与小动脉机械应力不同,小静脉机械应力既取决于血液脉搏波幅度,也取决于周围组织的机械特性。因此,静脉胶原化在脑室周围有优先定位,并且静脉胶原化与白质稀疏或脑白质疏松灶之间存在机制联系。脉搏波脑病的最新概念还有助于理解视网膜小静脉(脑小静脉的“镜子”)在脉搏波脑病的各种表现形式中的扩张,包括进行性脑白质疏松、腔隙性和出血性“脉搏波”中风以及痴呆。实际上,与年龄相关的动脉搏动慢性增加解释了随后小动脉肌源性“疲劳”、小动脉肌源性张力显著减弱以及未充分衰减的动脉脉搏波异常渗入小静脉。因此,视网膜小静脉扩张作为晚期脉搏波脑病的生物标志物,也越来越被认为是高心血管风险的生物标志物。所有这些数据支持了慢性脑血管疾病概念的转变,从局限于狭窄闭塞性脑血管疾病的经典模型转变为包括脉搏波脑病概念的扩大模型。由此,通过未衰减的动脉脉搏波预防对脑微血管的损伤将成为预防和治疗迟发性认知衰退的合理目标。

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