The pathological changes in CAVS are much more than a simple age related
“wear and tear”. There is some resemblance of CAVS with atherosclerosis, but
important differences have also been authenticated. Both conditions share a number of
risk factors, however
The mechanisms leading to the microscopically observable changes in CAVS include
many molecules and pathways. There is a considerable “cross talk” between these
mechanisms which makes their description difficult.
The unravelling of these pathways requires a description in layers.
The outer layer consists of the risk factors of which the most common are
lipid disorders and hypertension.
The middle layer consists of the molecules and mediators involved. Some of
these molecules are inflammatory, others are the result of mechanical or
oxidative stress, still others play a role in the remodelling of the ECM.
The inner layer consists of the mechanisms, which are inflammation,
calcification or ossification, angiogenesis, remodelling of the ECM and
programmed cell death.
The unravelling of these processes in CAVS is an ongoing process and is still not
completely understood. This understanding might have some consequences in terms of
prevention or slowing down of the process.
Keywords: Angiotensin, apoptosis, atheromatosis, autophagy, calcification,
Heyde’s syndrome, inflammation, lipid infiltration, mechanical stress, neoangiogenesis,
osteoblastic differentiation, oxidative stress, vitamin K antagonists.
