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Andò et al. Vessel Plus 2023;7:15 https://dx.doi.org/10.20517/2574-1209.2023.26 Page 3 of 22

intima, representing a component of the atherosclerotic plaque ultimately responsible for vascular events,
and in the tunica media, where they assume a more often circumferential appearance linked to the presence
[14]
of elastic tissue and where they cause an increase in stiffness and decrease vascular compliance . Overall,
intimal calcifications are a dynamic phenomenon that can be considered as the barometer of the
atherosclerotic process : during the early stages of intimal thickening, calcified spots are associated with
[15]
plaque instability, while in more advanced fibrocalcific lesions, confluent regions of calcification are
observed with calcified sheets or plates where collagen matrix and necrotic core itself are calcified and
associated with more stable atherosclerosis phenotypes, representing a final response to atherosclerotic
damage . Fracture in calcified sheets can lead to the formation of nodular calcification. Such nodules may
[16]
prompt discontinuation of the endothelial lining, thus extending into the lumen, and promoting fibrin
[15]
deposition and acute luminal thrombosis . In pathological studies, calcified nodules are the underlying
[15]
mechanism in 2% to 7% of coronary thrombosis . Importantly, different types of calcified nodules can be
identified at either pathology or intravascular imaging, such as eruptive and non-eruptive calcific nodules,
and their management remains a matter of debate . Calcifications of the tunica media are very common in
[17]
patients with chronic kidney disease, especially in vessels typically spared by atherosclerosis, and they are
often not associated with the narrowing of the vessel lumen . The microscopic appearance of calcifications
[18]
can be amorphous, i.e., devoid of any tissue architecture, but can even assume a chondro-osseous
architecture, which presupposes a phenotypic change of the vascular smooth muscle cells into mesenchymal
stem cells . After DES implantation in calcified lesions, the same mechanisms, such as calcium sheet
[16]
formation and reformation of calcified nodules inside DES, may be involved in DES failure.

EVALUATION OF CORONARY CALCIFICATIONS
Coronary calcifications can be detected by various diagnostic methods, in particular computed tomography
(CT), angiography and intravascular imaging techniques. Intravascular ultrasound (IVUS) and optical
coherence tomography (OCT) are the most used techniques. They allow a very accurate assessment of the
calcium burden and its distribution and eccentricity, information that allows planning an individualized
strategy for lesion preparation and optimization of stent implantation.

Coronary computed tomography angiography
[19]
CT is the most sensitive method for detecting coronary calcium . It is mainly used in elective conditions to
stratify medium and long-term cardiovascular risk through the calcium score (volumetric quantification of
calcium) of the coronary arteries . Apart from the general prognostic data, there are no currently
[20]
established criteria for planning and guiding a specific interventional treatment based on the CT scan. A
Korean group has proposed a new “calcification remodeling index” based on coronary CT scans, in addition
to better known criteria such as calcium score, calcification volume or the number of quadrants involved in
the calcification arc, to predict the use of rotational atherectomy during PCI .
[21]

Coronary angiography
Angiography is highly specific but lacks sensitivity compared with coronary CT and intravascular imaging
for identifying coronary calcium. In the pivotal 1995 study by Gary Mintz, coronary angiography was
indeed able to identify calcium in only 38% of cases, and sensitivity was even less for mild levels of
[22]
calcification . CAC are angiographically identified as linear radiopaque areas that follow the contour of the
coronary artery in a synchronous motion with cardiac contraction prior to opacification with contrast
[Figure 1]. They are defined as severe when both sides of the arterial wall are identified during cardiac
movement in the absence of contrast dye . It has been observed that those coronary calcifications that are
[23]
not visible angiographically, and therefore can be identified only with IVUS or OCT, do not appear to limit
[24]
stent expansion . Consequently, the presence of angiographically visible calcium, i.e., a thick calcification,
is likely to remain a good predictor of incomplete stent expansion. During contrast injection, calcium