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Page 2 of 22 Andò et al. Vessel Plus 2023;7:15 https://dx.doi.org/10.20517/2574-1209.2023.26

community. The efficacy of rotational atherectomy in improving procedural success for the treatment of calcified
lesions has been widely demonstrated. The advent of new technologies -especially of intravascular lithotripsy
(IVL)-, the application of techniques and materials initially developed for as complex procedures as chronic total
occlusions (CTO), the increasing experience of contemporary operators and the introduction of latest generation
drug-eluting stents (DES) with excellent technical and structural properties, are further contributing to improving
outcomes of current PCI for calcific lesions.

Keywords: Coronary artery calcifications, percutaneous coronary intervention, drug-eluting stents, rotational
atherectomy, intravascular lithotripsy, intravascular ultrasound, optical coherence tomography

INTRODUCTION
Severe coronary artery calcifications (CAC), already identified by Andreas Grüntzig as one of the main
[1]
limitations to the feasibility of coronary balloon angioplasty , are a challenge for the contemporary
interventional cardiologist as well for several reasons: first, the growing demand for diagnostic procedures
and interventions in elderly patients who carry CAC because of aging; in addition, the general prognostic
improvement after percutaneous coronary intervention (PCI) and the reduction in the incidence of
restenosis with latest generation drug-eluting stents (DES) are expanding the indications to PCI to
[2]
increasingly complex anatomies . In the last decade, the renewed interest in tools for ablation or
modification of calcified plaques paved the way to the development of new technologies and to technical
and procedural improvements of those already existing, with the ultimate aim to optimize the mechanic
effects of balloon angioplasty and the expansion and apposition of DES to the vessel wall.

EPIDEMIOLOGY AND PROGNOSTIC ROLE OF CORONARY ARTERY CALCIFICATIONS
All patients with cardiovascular disease virtually have a certain amount of CAC. Therefore, the assessment
of CAC provides additional prognostic information over traditional risk factor-based assessment in
predicting mortality risk . The presence of CAC is epidemiologically associated with a higher
[3]
[4]
cardiovascular risk profile , while prognostically, they are independent predictors of stent thrombosis and
target vessel revascularization one year after PCI . In an individual analysis of approximately 6,300 patients
[5]
from 7 randomized trials of DES, it was demonstrated that the prevalence of severely calcified coronary
[6]
lesions is associated with a higher incidence of incomplete revascularization and higher mortality .
Moreover, in a more recent analysis of 19,833 patients from 18 randomized trials, the negative prognostic
impact of coronary artery calcification remained evident across a 5-year follow-up, an effect that was only
mitigated by second-generation DES . Therefore, calcified coronary lesions, in addition to being
[7]
particularly frequent in contemporary practice, represent a negative prognostic indicator regardless of the
clinical presentation or the type of DES implanted . These negative outcomes are related not only to
[8,9]
comorbidities but also to the greater technical complexity of PCI in calcified lesions, which represent an
obstacle to the progression of stents through the coronary arteries and, in any case, reduce their expansion
capacity; CAC can indeed damage the DES polymer and consequently alter the normal distribution kinetics
and the uniformity of release of the anti-proliferative drug [10,11] . This results in an often-suboptimal
procedural result and an increased risk of complications such as intrastent restenosis or stent thrombosis.
Beyond this, CAC also increases the risk of acute procedural complications such as stent loss, dissection,
and coronary artery perforation .
[12]

BIOLOGY AND HISTOLOGY OF CORONARY CALCIFICATIONS
Vascular calcification is an active biological process that reflects systemic inflammation finely regulated by
cellular interaction mechanisms . Histologically, vascular calcifications can be localized both in the tunica
[13]