TY - JOUR
T1 - Coronary artery plaque rupture and erosion
T2 - Role of wall shear stress profiling and biological patterns in acute coronary syndromes
AU - Russo, Giulio
AU - Pedicino, Daniela
AU - Chiastra, Claudio
AU - Vinci, Ramona
AU - Lodi Rizzini, Maurizio
AU - Genuardi, Lorenzo
AU - Sarraf, Mohammad
AU - d'Aiello, Alessia
AU - Bologna, Marco
AU - Aurigemma, Cristina
AU - Bonanni, Alice
AU - Bellantoni, Antonio
AU - D'Ascenzo, Fabrizio
AU - Ciampi, Pellegrino
AU - Zambrano, Aniello
AU - Mainardi, Luca
AU - Ponzo, Myriana
AU - Severino, Anna
AU - Trani, Carlo
AU - Massetti, Massimo
AU - Gallo, Diego
AU - Migliavacca, Francesco
AU - Maisano, Francesco
AU - Lerman, Amir
AU - Morbiducci, Umberto
AU - Burzotta, Francesco
AU - Crea, Filippo
AU - Liuzzo, Giovanna
N1 - Funding Information:
CC, DG and UM acknowledge funding from the Ministry of Education, Universities and Research through Fondo Integrativo Speciale per la Ricerca FISR 2019—FISR2019_03221 CECOMES .
Funding Information:
Dr. Russo received fellowship training grant from EAPCI, sponsored by Edwards Lifesciences and speaker's fee from Abiomed.
Funding Information:
This work was supported by PRIN 2017 , Prot. 2017WJBKKW_001 .
Publisher Copyright:
© 2022 The Author(s)
PY - 2023/1/1
Y1 - 2023/1/1
N2 - Aims: Wall shear stress (WSS) is involved in coronary artery plaque pathological mechanisms and modulation of gene expression. This study aims to provide a comprehensive haemodynamic and biological description of unstable (intact-fibrous-cap, IFC, and ruptured-fibrous-cap, RFC) and stable (chronic coronary syndrome, CCS) plaques and investigate any correlation between WSS and molecular pathways. Methods and results: We enrolled 24 CCS and 25 Non-ST Elevation Myocardial Infarction-ACS patients with IFC (n = 11) and RFC (n = 14) culprit lesions according to optical coherence tomography analysis. A real-time PCR primer array was performed on peripheral blood mononuclear cells for 17 different molecules whose expression is linked to WSS. Computational fluid dynamics simulations were performed in high-fidelity 3D-coronary artery anatomical models for three patients per group. A total of nine genes were significantly overexpressed in the unstable patients as compared to CCS patients, with no differences between IFC and RFC groups (GPX1, MMP1, MMP9, NOS3, PLA2G7, PI16, SOD1, TIMP1, and TFRC) while four displayed different levels between IFC and RFC groups (TNFα, ADAMTS13, EDN1, and LGALS8). A significantly higher WSS was observed in the RFC group (p < 0.001) compared to the two other groups. A significant correlation was observed between TNFα (p < 0.001), EDN1 (p = 0.036), and MMP9 (p = 0.005) and WSS values in the RFC group. Conclusions: Our data demonstrate that IFC and RFC plaques are subject to different WSS conditions and gene expressions, suggesting that WSS profiling may play an essential role in the plaque instability characterization with relevant diagnostic and therapeutic implications in the era of precision medicine.
AB - Aims: Wall shear stress (WSS) is involved in coronary artery plaque pathological mechanisms and modulation of gene expression. This study aims to provide a comprehensive haemodynamic and biological description of unstable (intact-fibrous-cap, IFC, and ruptured-fibrous-cap, RFC) and stable (chronic coronary syndrome, CCS) plaques and investigate any correlation between WSS and molecular pathways. Methods and results: We enrolled 24 CCS and 25 Non-ST Elevation Myocardial Infarction-ACS patients with IFC (n = 11) and RFC (n = 14) culprit lesions according to optical coherence tomography analysis. A real-time PCR primer array was performed on peripheral blood mononuclear cells for 17 different molecules whose expression is linked to WSS. Computational fluid dynamics simulations were performed in high-fidelity 3D-coronary artery anatomical models for three patients per group. A total of nine genes were significantly overexpressed in the unstable patients as compared to CCS patients, with no differences between IFC and RFC groups (GPX1, MMP1, MMP9, NOS3, PLA2G7, PI16, SOD1, TIMP1, and TFRC) while four displayed different levels between IFC and RFC groups (TNFα, ADAMTS13, EDN1, and LGALS8). A significantly higher WSS was observed in the RFC group (p < 0.001) compared to the two other groups. A significant correlation was observed between TNFα (p < 0.001), EDN1 (p = 0.036), and MMP9 (p = 0.005) and WSS values in the RFC group. Conclusions: Our data demonstrate that IFC and RFC plaques are subject to different WSS conditions and gene expressions, suggesting that WSS profiling may play an essential role in the plaque instability characterization with relevant diagnostic and therapeutic implications in the era of precision medicine.
KW - Acute coronary syndrome
KW - Computational fluid dynamics
KW - Personalized medicine
KW - Plaque erosion
KW - Plaque rupture
KW - Shear stress
KW - Vulnerable plaque
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U2 - 10.1016/j.ijcard.2022.10.139
DO - 10.1016/j.ijcard.2022.10.139
M3 - Article
C2 - 36343795
AN - SCOPUS:85141807898
SN - 0167-5273
VL - 370
SP - 356
EP - 365
JO - International Journal of Cardiology
JF - International Journal of Cardiology
ER -