Plenary 1. Mon 31 May – talk 4, Renu Virmani

Coronary artery calcification and its progression: what does it really mean? Renu Virmani, Baltimore, USA

Atherosclerosis: metabolism dysfunction drives inflammation in the vessels

Renu Virmani is President of CVPath Institute, Gaithersburg, and Clinical Professor, Department of Pathology at Georgetown University; University of Maryland-Baltimore; George Washington University, and Vanderbilt University, USA. MD. She is recognized as one of the leaders in the search for diagnostic and treatment therapies for vulnerable plaque. Dr. Virmani received her MD from Lady Hardinge Medical College, Delhi University, New Delhi, India. Currently, Dr. Virmani is a member of the American Heart Association, the US and Canadian Academy of Pathology, and is a Fellow of the American College of Cardiology.

Coronary artery calcification is a clinical marker of atherosclerosis, starting as microcalcifications and evolving to larger calcium fragments which eventually become sheet-like deposits. These changes occur concurrently with the progression of atherosclerotic plaque. Formerly considered a passive age-related process, coronary artery calcification is now recognized as an active process associated with atherosclerosis, and as a marker of the state of atherosclerotic plaque stability. Indeed, multiple cohort and population studies have shown that coronary artery calcium scoring is effective and reproducible in predicting the risk for cardiovascular disease, supporting a role in informing individualized risk management.

However, it has been suggested that the effect of calcification might be biphasic. Microcalcification, or spotty calcification, represents an active stage of vascular calcification correlated with inflammation. Plaque rupture has been shown to correlate positively with the number of spotty calcifications, and inversely with the number of large calcifications. Calcification of differential amounts, sizes, shapes, and positions may play differential roles in plaque homeostasis, which is further impacted by the environment surrounding the calcification. The interactive effects of these important factors influencing calcification and plaque is inadequately understood and merits further study. 

Recent references

Abdelrahman KM, Chen MY, Dey AK, Virmani R, Finn AV, Khamis RY, Choi AD, Min JK, Williams MC, Buckler AJ, Taylor CA, Rogers C, Samady H, Antoniades C, Shaw LJ, Budoff MJ, Hoffmann U, Blankstein R, Narula J, Mehta NN. Coronary computed tomography angiography from clinical uses to emerging technologies: JACC State-of-the-Art Review. J Am Coll Cardiol 2020;76:1226-1243.

Tomaniak M, Katagiri Y, Modolo R, de Silva R, Khamis RY, Bourantas CV, Torii R, Wentzel JJ, Gijsen FJH, van Soest G, Stone PH, West NEJ, Maehara A, Lerman A, van der Steen AFW, Lüscher TF, Virmani R, Koenig W, Stone GW, Muller JE, Wijns W, Serruys PW, Onuma Y. Vulnerable plaques and patients: state-of-the-art. Eur Heart J 2020;41:2997-3004.

Ferraro RA, van Rosendael AR, Lu Y, Andreini D, Al-Mallah MH, Cademartiri F, Chinnaiyan K, Chow BJW, Conte E, Cury RC, Feuchtner G, de Araújo Gonçalves P, Hadamitzky M, Kim YJ, Leipsic J, Maffei E, Marques H, Plank F, Pontone G, Raff GL, Villines TC, Lee SE, Al’Aref SJ, Baskaran L, Cho I, Danad I, Gransar H, Budoff MJ, Samady H, Stone PH, Virmani R, Narula J, Berman DS, Chang HJ, Bax JJ, Min JK, Shaw LJ, Lin FY. Non-obstructive high-risk plaques increase the risk of future culprit lesions comparable to obstructive plaques without high-risk features: the ICONIC study. Eur Heart J Cardiovasc Imaging 2020;21:973-980.

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