The Association Between the Hemodynamics in Anomalous Origins of Coronary Arteries and Atherosclerosis: A Preliminary Case Study Based on Computational Fluid Dynamics.

Bioengineering (Basel)

Department of Mechanics & Engineering, College of Architecture & Environment, Sichuan University, Chengdu 610065, China.

Published: November 2024

Patients with anomalous coronary artery origins (AOCA) exhibit a higher risk of atherosclerosis, where even minimal stenosis may lead to adverse cardiovascular events. However, the factors contributing to this heightened risk in AOCA patients remain unclear. This study aimed to investigate whether an AOCA patient is more prone to stenosis occurrence and its progression in view of hemodynamics. A patient whose left circumflex artery originated from the right coronary sinus with a mild stenosis in the left anterior descending (LAD) artery and a healthy individual were included in this study. Two additional models were developed by removing stenosis from the patient model and adding a corresponding stenosis to the healthy model. Additionally, the inlet flow waveforms for the left and right coronary arteries were swapped in both the patient and healthy models. Results indicated that the AOCA patient without stenosis demonstrated higher wall pressure (LAD: 95.57 ± 0.73 vs. 93.86 ± 0.50 mmHg; LCX: 94.97 ± 0.98 vs. 93.47 ± 0.56 mmHg; RCA: 96.23 ± 0.30 vs. 93.86 ± 0.46 mmHg) and TAWSS (LAD: 24.41 ± 19.53 vs. 13.82 ± 9.87 dyne/cm, < 0.0001; LCX: 27.21 ± 14.51 vs. 19.33 ± 8.78 dyne/cm) compared to the healthy individual, with similar trends also observed in stenotic conditions. Significant changes in the LCX flow distribution were also noted under varying pulsatile conditions (LCX: 18.28% vs. 9.16%) compared to the healthy individual. The high-pressure, high-shear hemodynamic environment in AOCA patients predisposes them to atherosclerosis, and the unique geometry exacerbates hemodynamic abnormalities when stenosis occurs. Clinicians should closely monitor AOCA patients with stenosis to prevent adverse cardiovascular events.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726885PMC
http://dx.doi.org/10.3390/bioengineering11121196DOI Listing

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