Cardiometabolic predictors of high-risk CCTA phenotype in a diverse patient population

Introduction: Low-attenuation non-calcified plaque (LAP) burden and vascular inflammation by pericoronary adipose tissue (PCAT) measured from coronary CT angiography (CCTA) have shown to be predictors of cardiovascular outcomes. We aimed to investigate the relationships of cardiometabolic risk facto...

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Main Authors: Toshiki Kuno, Javier Arce, Michael Fattouh, Sharmila Sarkar, John P Skendelas, Jonathan Daich, Aldo L Schenone, Lili Zhang, Carlos J Rodriguez, Salim S Virani, Piotr J Slomka, Leslee J Shaw, Eric E Williamson, Daniel S Berman, Mario J Garcia, Damini Dey, Leandro Slipczuk
Format: Article
Language:English
Published: Elsevier 2023-09-01
Series:American Journal of Preventive Cardiology
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2666667723001198
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author Toshiki Kuno
Javier Arce
Michael Fattouh
Sharmila Sarkar
John P Skendelas
Jonathan Daich
Aldo L Schenone
Lili Zhang
Carlos J Rodriguez
Salim S Virani
Piotr J Slomka
Leslee J Shaw
Eric E Williamson
Daniel S Berman
Mario J Garcia
Damini Dey
Leandro Slipczuk
author_facet Toshiki Kuno
Javier Arce
Michael Fattouh
Sharmila Sarkar
John P Skendelas
Jonathan Daich
Aldo L Schenone
Lili Zhang
Carlos J Rodriguez
Salim S Virani
Piotr J Slomka
Leslee J Shaw
Eric E Williamson
Daniel S Berman
Mario J Garcia
Damini Dey
Leandro Slipczuk
author_sort Toshiki Kuno
collection DOAJ
description Introduction: Low-attenuation non-calcified plaque (LAP) burden and vascular inflammation by pericoronary adipose tissue (PCAT) measured from coronary CT angiography (CCTA) have shown to be predictors of cardiovascular outcomes. We aimed to investigate the relationships of cardiometabolic risk factors including lipoprotein(a) and epicardial adipose tissue (EAT) with CCTA high-risk imaging biomarkers, LAP and vascular inflammation. Methods: The patient population consisted of consecutive patients who underwent CCTA for stable chest pain and had a complete cardiometabolic panel including lipoprotein(a). Plaque, PCAT and EAT were measured from CT using semiautomated software. Elevated LAP burden and PCAT attenuation were defined as ≥4% and ≥70.5 HU, respectively. The primary clinical end-point was a composite of myocardial infarction, revascularization or cardiovascular death. Results: A total of 364 consecutive patients were included (median age 56 years, 64% female); the majority of patients were of Hispanic (60%), and the rest were of non-Hispanic Black (21%), non-Hispanic White (6%) and non-Hispanic Asian (4%) race/ethnicity. The prevalence of elevated LAP burden and PCAT attenuation was 31 and 18%, respectively, while only 8% had obstructive stenosis. There were significant differences in plaque characteristics among different racial/ethnic groups (p<0.001). Lipoprotein(a) correlated with LAP burden in Hispanic patients. Patients with elevated LAP were older, more likely to be have diabetes, hypertension, hyperlipidemia and smoke with higher CAC and EAT volume (all P<0.05). Patients with elevated LAP were more likely to develop the primary clinical outcome (p<0.001) but those with elevated PCAT were not (p=0.797). Conclusion: The prevalence of LAP and PCAT attenuation were 31 and 18%, respectively. Lipoprotein(a) levels correlated with LAP burden in Hispanic patients. Age, male sex, hypertension and hyperlipidemia increased the odds of elevated LAP, which showed prognostic significance.
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spelling doaj.art-99bcbe62bb5d439ca0f19af55f817afa2023-09-28T05:26:37ZengElsevierAmerican Journal of Preventive Cardiology2666-66772023-09-0115100578Cardiometabolic predictors of high-risk CCTA phenotype in a diverse patient populationToshiki Kuno0Javier Arce1Michael Fattouh2Sharmila Sarkar3John P Skendelas4Jonathan Daich5Aldo L Schenone6Lili Zhang7Carlos J Rodriguez8Salim S Virani9Piotr J Slomka10Leslee J Shaw11Eric E Williamson12Daniel S Berman13Mario J Garcia14Damini Dey15Leandro Slipczuk16Cardiology Division, Montefiore Medical Center, Montefiore Medical Center/Albert Einstein Colalege of Medicine, Cardiology Division. 111 E210th, Bronx, NY 10467, United StatesCardiology Division, Montefiore Medical Center, Montefiore Medical Center/Albert Einstein Colalege of Medicine, Cardiology Division. 111 E210th, Bronx, NY 10467, United StatesCardiology Division, Montefiore Medical Center, Montefiore Medical Center/Albert Einstein Colalege of Medicine, Cardiology Division. 111 E210th, Bronx, NY 10467, United StatesCardiology Division, Montefiore Medical Center, Montefiore Medical Center/Albert Einstein Colalege of Medicine, Cardiology Division. 111 E210th, Bronx, NY 10467, United StatesCardiothoracic and Vascular Surgery Department, Montefiore Medical Center/Albert Einstein College of Medicine, Bronx, NY, United StatesCardiology Division, Montefiore Medical Center, Montefiore Medical Center/Albert Einstein Colalege of Medicine, Cardiology Division. 111 E210th, Bronx, NY 10467, United StatesCardiology Division, Montefiore Medical Center, Montefiore Medical Center/Albert Einstein Colalege of Medicine, Cardiology Division. 111 E210th, Bronx, NY 10467, United StatesCardiology Division, Montefiore Medical Center, Montefiore Medical Center/Albert Einstein Colalege of Medicine, Cardiology Division. 111 E210th, Bronx, NY 10467, United StatesCardiology Division, Montefiore Medical Center, Montefiore Medical Center/Albert Einstein Colalege of Medicine, Cardiology Division. 111 E210th, Bronx, NY 10467, United StatesOffice of the Vice Provost (Research), The Aga Khan University, Karachi, Pakistan; Division of Cardiology, The Texas Heart Institute/Baylor College of Medicine, Houston, TX, United StatesDivision of Cardiology, The Texas Heart Institute/Baylor College of Medicine, Houston, TX, United StatesDepartments of Medicine (Cardiology) and Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, NY, United StatesMayo Clinic, Rochester, MN, United StatesDivision of Cardiology, The Texas Heart Institute/Baylor College of Medicine, Houston, TX, United StatesCardiology Division, Montefiore Medical Center, Montefiore Medical Center/Albert Einstein Colalege of Medicine, Cardiology Division. 111 E210th, Bronx, NY 10467, United StatesDepartment of Imaging, Cedars-Sinai Medical Center, Biomedical Imaging Research Institute, Los Angeles, CA, United States; Corresponding authors.Cardiology Division, Montefiore Medical Center, Montefiore Medical Center/Albert Einstein Colalege of Medicine, Cardiology Division. 111 E210th, Bronx, NY 10467, United States; Corresponding authors.Introduction: Low-attenuation non-calcified plaque (LAP) burden and vascular inflammation by pericoronary adipose tissue (PCAT) measured from coronary CT angiography (CCTA) have shown to be predictors of cardiovascular outcomes. We aimed to investigate the relationships of cardiometabolic risk factors including lipoprotein(a) and epicardial adipose tissue (EAT) with CCTA high-risk imaging biomarkers, LAP and vascular inflammation. Methods: The patient population consisted of consecutive patients who underwent CCTA for stable chest pain and had a complete cardiometabolic panel including lipoprotein(a). Plaque, PCAT and EAT were measured from CT using semiautomated software. Elevated LAP burden and PCAT attenuation were defined as ≥4% and ≥70.5 HU, respectively. The primary clinical end-point was a composite of myocardial infarction, revascularization or cardiovascular death. Results: A total of 364 consecutive patients were included (median age 56 years, 64% female); the majority of patients were of Hispanic (60%), and the rest were of non-Hispanic Black (21%), non-Hispanic White (6%) and non-Hispanic Asian (4%) race/ethnicity. The prevalence of elevated LAP burden and PCAT attenuation was 31 and 18%, respectively, while only 8% had obstructive stenosis. There were significant differences in plaque characteristics among different racial/ethnic groups (p<0.001). Lipoprotein(a) correlated with LAP burden in Hispanic patients. Patients with elevated LAP were older, more likely to be have diabetes, hypertension, hyperlipidemia and smoke with higher CAC and EAT volume (all P<0.05). Patients with elevated LAP were more likely to develop the primary clinical outcome (p<0.001) but those with elevated PCAT were not (p=0.797). Conclusion: The prevalence of LAP and PCAT attenuation were 31 and 18%, respectively. Lipoprotein(a) levels correlated with LAP burden in Hispanic patients. Age, male sex, hypertension and hyperlipidemia increased the odds of elevated LAP, which showed prognostic significance.http://www.sciencedirect.com/science/article/pii/S2666667723001198High-risk plaqueCT coronary angiogramRisk factorsPCATLAPEpicardial adipose tissue
spellingShingle Toshiki Kuno
Javier Arce
Michael Fattouh
Sharmila Sarkar
John P Skendelas
Jonathan Daich
Aldo L Schenone
Lili Zhang
Carlos J Rodriguez
Salim S Virani
Piotr J Slomka
Leslee J Shaw
Eric E Williamson
Daniel S Berman
Mario J Garcia
Damini Dey
Leandro Slipczuk
Cardiometabolic predictors of high-risk CCTA phenotype in a diverse patient population
American Journal of Preventive Cardiology
High-risk plaque
CT coronary angiogram
Risk factors
PCAT
LAP
Epicardial adipose tissue
title Cardiometabolic predictors of high-risk CCTA phenotype in a diverse patient population
title_full Cardiometabolic predictors of high-risk CCTA phenotype in a diverse patient population
title_fullStr Cardiometabolic predictors of high-risk CCTA phenotype in a diverse patient population
title_full_unstemmed Cardiometabolic predictors of high-risk CCTA phenotype in a diverse patient population
title_short Cardiometabolic predictors of high-risk CCTA phenotype in a diverse patient population
title_sort cardiometabolic predictors of high risk ccta phenotype in a diverse patient population
topic High-risk plaque
CT coronary angiogram
Risk factors
PCAT
LAP
Epicardial adipose tissue
url http://www.sciencedirect.com/science/article/pii/S2666667723001198
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