IMR Press / RCM / Volume 23 / Issue 2 / DOI: 10.31083/j.rcm2302058
Open Access Original Research
Coronary artery cavitation as a trigger for atherosclerotic plaque progression: a simplified numerical and computational fluid dynamic demonstration
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1 Division of Cardiology, Department of Specialistic Medicine, Rovigo General Hospital, 45100 Rovigo, Italy
2 Department of Translational Medicine, University of Ferrara, 44121 Ferrara, Italy
3 Department of Cardiology, West Vicenza Hospital, 36014 Arzignano, Italy
4 Cardiovascular Research, Methodist Hospital, Merrillville, IN 46410, USA
*Correspondence: (Gianluca Rigatelli)
These authors contributed equally.
Academic Editor: Peter A. McCullough
Rev. Cardiovasc. Med. 2022, 23(2), 58;
Submitted: 23 July 2021 | Revised: 19 October 2021 | Accepted: 21 October 2021 | Published: 12 February 2022
(This article belongs to the Special Issue Coronary Artery Atherosclerosis: Translation from Basic to Clinic)
Copyright: © 2022 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

Backgrounds: Coronary cavitation is supposed to be generated by both concentric and eccentric coronary artery stenosis which propagates downstream the vessel, creating microbubbles which exploded when the fluid pressure was lower than the vapor pressure at a local thermodynamic state. Objective: To assess, using numerical and computational fluid dynamic analysis (CFD), the potential of cavitation to both induce damage to coronary artery endothelium and to promote atherosclerotic plaque progression. Methods: We retrospectively reviewed the data 12 consecutive patients evaluated between 1st January 2013 and 1st January 2014 with an isolated hemodynamically significant Left Main (LM) disease. The patient specific geometries have been reconstructed. Bubble velocity has been calculated in accordance with Newton’s second law. Both the forces arising from the bubbles’ interaction with the continuous phase and impact with the endothelium have been evaluated. The impact of turbulence on the motion of bubbles have been modelled with a dispersion model. Results: Among the 12 patients retrospectively analysed [8 males, mean age 68.2 ± 12.8 years old], the mean LM stenosis was 72.3 ± 3.6%. As expected, in all subjects, LM stenoses induced cavitation which propagates downstream the vessel creating microbubbles. The higher concentration of vapor region was detected before the carina (within 0.8 to 1.3 cm from the stenosis). Due to the pressure gradient generated by the stenosis, formation of a re-entry jet which penetrates each bubble generated a shock wave. Before the carina, the mean bubbles radius observed was 4.2 ± 1.4 μm, which generated a mean peak pressure of 3.9 ± 0.5 MPa when they explode. Conclusion: The cavitation phenomenon is effectively generated in a model of LM bifurcation and instantaneous pressure-peaks due to collapses of vapor bubbles resulted in a measurable dynamic load on vessel wall potentially able to induce endothelial damage.

Coronary artery disease
Fig. 1.
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