Calcification in arteries is an age-related malfunction of cell behavior, in which cells in blood vessel walls inappropriately take on some of the behaviors of bone cells called osteoblasts. These errant cells deposit calcium structures characteristic of bone tissue into the extracellular matrix, and that is in turn disruptive of tissue properties, particularly to the elasticity needed for constriction and dilation of blood vessels. In effect, blood vessels, and other structures such as heart valves that are subject to calcification, are slowly turning into bone. This causes cardiovascular dysfunctions that, given time, will ultimately prove fatal.
As noted in today's open access review paper, calcification proceeds side by side with the development of atherosclerosis, the formation of fatty deposits in blood vessel walls that narrow and weaken blood vessels. These are two quite distinct processes, however. That they do coincide is most likely because both are influenced strongly by the state of inflammatory signaling, in the body at large, and localized to particular regions of blood vessel walls. Atherosclerosis produces inflamed areas of the blood vessel wall, where lesions form, by virtue of the way in which it derives from and interacts with the malfunction and inflammatory signaling of macrophage cells of the innate immune system. The surrounding vessel is thus more prone to calcification.
Vascular calcification (VC) is one of the characteristics of vascular aging and appears to specifically occur in arteries. It is defined as the deposition of calcium-phosphate complexes in the vessels. Apart from aging, pathological processes like diabetes mellitus, chronic kidney disease, and hereditary disorders might also be the risk factors for arterial calcification. Calcification at different locations in the arterial wall might be associated with different risk factors and outcomes. Intimal calcification is closely related to atherosclerosis and affects the stability of the plaque, while medial calcification, including calcification located in the tunica media and around the internal elastic lamina, is considered to cause arterial stiffening and reduce compliance.
Arterial calcification can take place in various vessels, such as the femoral artery, abdominal aorta, thoracic aorta, coronary artery, carotid artery, and cerebral arteries. Among these, the best-studied are coronary artery calcification (CAC), intracranial artery calcification (IAC), and carotid artery calcification. CAC has been used as a predictor of coronary heart disease and recent studies have shown that CAC can also predict the risk of atherosclerotic cardiovascular disease, including stroke. Similarly, IAC, especially intracranial internal carotid artery calcification (IICAC), and carotid artery calcification are also reported to be closely associated with stroke.
Arterial calcification including IAC, CAC, and carotid calcification can predict the risk of stroke and it also affects treatment response and prognosis of stroke patients. Arterial calcifications and stroke share many risk factors, and in fact, history of ischemic stroke is one of the risk factors for IAC. Arterial calcification might affect plaque stability or cause hemodynamic changes, and therefore increase the risk of stroke. Besides, IAC or CAC indicates atherosclerosis, which is one of the main causes of stroke. It is worth noting that besides the total amount of calcification, the morphology, distribution, and size (large or small) of calcification can also impact on the risk of stroke. Intimal calcification and medial calcification have distinct implications and should be studied separately.