Carotid intraplaque neovascularization predicts coronary artery disease and cardiovascular events
European Society of Cardiology – European Heart Journal – April 12, 2019
It is thought that the majority of cardiovascular (CV) events are caused by vulnerable plaque. Such lesions are rupture prone, in part due to neovascularization. It is postulated that plaque vulnerability may be a systemic process and that vulnerable lesions may co-exist at multiple sites in the vascular bed. This study sought to examine whether carotid plaque vulnerability, characterized by contrast-enhanced ultrasound (CEUS)-assessed intraplaque neovascu-larization (IPN), was associated with significant coronary artery disease (CAD) and future CV events.
Methods and Results
We investigated carotid IPN using carotid CEUS in 459 consecutive stable patients referred for coronary angiog-raphy. IPN was graded based on the presence and location of microbubbles within each plaque (0, not visible; 1, peri-adventitial; and 2, plaque core). The grades of each plaque were averaged to obtain an overall score per pa¬tient. Coronary plaque severity and complexity was also determined angiographically. Patients were followed for 30 days following their angiogram. This study found that a higher CEUS-assessed carotid IPN score was associated with significant CAD (>_50% stenosis) (1.8 ± 0.4 vs. 0.5 ± 0.6, P < 0.0001) and greater complexity of coronary lesions (1.7 ± 0.5 vs. 1.3 ± 0.8, P < 0.0001). Furthermore, an IPN score >_1.25 could predict significant CAD with a high sen¬sitivity (92%) and specificity (89%). The Kaplan–Meier analysis demonstrated a significantly higher proportion of participants having CV events with an IPN score >_1.25 (P = 0.004).
Carotid plaque neovascularization was found to be predictive of significant and complex CAD and future CV events. CEUS-assessed carotid IPN is a clinically useful tool for CV risk stratification in high-risk cardiac patients.
Authors: Laura E. Mantella’, Kayla N. Colledanchise’, Marie-France Hétu2, Steven B. Feinstein3, Joseph Abunassar2, and Amer M. Johri’,2,*
1Department of Biomedical and Molecular Sciences, Queen’s University, 18 Stuart Street, Kingston, Ontario K7L 3N6, Canada; 2Department of Medicine, Cardiovascular Imaging Network at Queen’s (CINQ), Queen’s University, Kingston Health Sciences Centre, 76 Stuart Street, Kingston, Ontario K7L 2V7, Canada; and 3Department of Medicine, Rush University Medical Center, 1653 W Congress Pkwy, Chicago, IL, USA
European Heart Journal – Cardiovascular Imaging (2019) 0, 1–9 doi:10.1093/ehjci/jez070