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 leukoaraïosis, 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.