The relationship between systemic inflammation and increased left ventricular mass is partly mediated by noncalcified coronary artery disease burden in psoriasis
Objective: Increased left ventricular (LV) mass is an important precursor to heart failure. Inflammation plays an important role in increasing LV mass. However, the contribution of subclinical coronary artery disease (CAD) to the inflammation-LV mass relationship is unknown. In subjects with psorias...
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Elsevier
2021-09-01
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Series: | American Journal of Preventive Cardiology |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S2666667721000660 |
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doaj-53ab910eeae24ab3b68f90a805167670 |
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record_format |
Article |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Wunan Zhou Meron Teklu Vy Bui Grigory A. Manyak Promita Kapoor Amit K. Dey Alexander V. Sorokin Nidhi Patel Heather L. Teague Martin P. Playford Julie Erb-Alvarez Justin A. Rodante Andrew Keel Sujata M. Shanbhag Li-Yueh Hsu David A. Bluemke Marcus Y. Chen Marcus Carlsson Nehal N. Mehta |
spellingShingle |
Wunan Zhou Meron Teklu Vy Bui Grigory A. Manyak Promita Kapoor Amit K. Dey Alexander V. Sorokin Nidhi Patel Heather L. Teague Martin P. Playford Julie Erb-Alvarez Justin A. Rodante Andrew Keel Sujata M. Shanbhag Li-Yueh Hsu David A. Bluemke Marcus Y. Chen Marcus Carlsson Nehal N. Mehta The relationship between systemic inflammation and increased left ventricular mass is partly mediated by noncalcified coronary artery disease burden in psoriasis American Journal of Preventive Cardiology Inflammation Left ventricular mass Noncalcified coronary burden Cardiac computed tomography angiography |
author_facet |
Wunan Zhou Meron Teklu Vy Bui Grigory A. Manyak Promita Kapoor Amit K. Dey Alexander V. Sorokin Nidhi Patel Heather L. Teague Martin P. Playford Julie Erb-Alvarez Justin A. Rodante Andrew Keel Sujata M. Shanbhag Li-Yueh Hsu David A. Bluemke Marcus Y. Chen Marcus Carlsson Nehal N. Mehta |
author_sort |
Wunan Zhou |
title |
The relationship between systemic inflammation and increased left ventricular mass is partly mediated by noncalcified coronary artery disease burden in psoriasis |
title_short |
The relationship between systemic inflammation and increased left ventricular mass is partly mediated by noncalcified coronary artery disease burden in psoriasis |
title_full |
The relationship between systemic inflammation and increased left ventricular mass is partly mediated by noncalcified coronary artery disease burden in psoriasis |
title_fullStr |
The relationship between systemic inflammation and increased left ventricular mass is partly mediated by noncalcified coronary artery disease burden in psoriasis |
title_full_unstemmed |
The relationship between systemic inflammation and increased left ventricular mass is partly mediated by noncalcified coronary artery disease burden in psoriasis |
title_sort |
relationship between systemic inflammation and increased left ventricular mass is partly mediated by noncalcified coronary artery disease burden in psoriasis |
publisher |
Elsevier |
series |
American Journal of Preventive Cardiology |
issn |
2666-6677 |
publishDate |
2021-09-01 |
description |
Objective: Increased left ventricular (LV) mass is an important precursor to heart failure. Inflammation plays an important role in increasing LV mass. However, the contribution of subclinical coronary artery disease (CAD) to the inflammation-LV mass relationship is unknown. In subjects with psoriasis, a chronic inflammatory skin disease, we evaluated if systemic inflammation assessed by plasma glycoprotein A (GlycA) associated with LV mass measured on coronary CT angiography (CCTA). Additionally, we analyzed whether this relationship was mediated by early CAD assessed as noncalcified coronary burden (NCB). Methods: We performed an observational longitudinal study of 213 subjects with psoriasis free of known cardiovascular disease, 189 of whom were followed over one year. All participants had GlycA measurements by nuclear magnetic resonance spectroscopy and LV mass and NCB quantified by CCTA. Results: The cohort had a mean age of 50.3 (±12.9) years and 59% were male. There was moderate psoriasis severity and low cardiovascular risk. LV mass increased by GlycA tertiles [1st tertile:24.6 g/m2.7(3.8), 2nd tertile:25.5 g/m2.7(3.8), 3rd tertile:27.7 g/m2.7(5.5), p<0.001]. Both GlycA (β=0.24, p = 0.001) and NCB (β=0.50, p<0.001) associated with LV mass in models adjusted for age, sex, hypertension, hypertension therapy, lipid therapy, biologic therapy for psoriasis, waist:hip ratio, psoriasis disease duration and severity. In multivariable-adjusted mediation analyses, NCB accounted for 32% of the GlycA-LV mass relationship. Finally, over one year, change in NCB independently associated with change in LV mass (β=0.25, p = 0.002). Conclusions: Both systemic inflammation and coronary artery NCB were associated with LV mass beyond cardiovascular risk factors in psoriasis. Furthermore, a substantial proportion of the inflammatory-LV mass relationship was mediated by NCB. These findings underscore the possible contribution of early coronary artery disease to the relationship between systemic inflammation and LV mass. |
topic |
Inflammation Left ventricular mass Noncalcified coronary burden Cardiac computed tomography angiography |
url |
http://www.sciencedirect.com/science/article/pii/S2666667721000660 |
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doaj-53ab910eeae24ab3b68f90a8051676702021-08-24T04:07:55ZengElsevierAmerican Journal of Preventive Cardiology2666-66772021-09-017100211The relationship between systemic inflammation and increased left ventricular mass is partly mediated by noncalcified coronary artery disease burden in psoriasisWunan Zhou0Meron Teklu1Vy Bui2Grigory A. Manyak3Promita Kapoor4Amit K. Dey5Alexander V. Sorokin6Nidhi Patel7Heather L. Teague8Martin P. Playford9Julie Erb-Alvarez10Justin A. Rodante11Andrew Keel12Sujata M. Shanbhag13Li-Yueh Hsu14David A. Bluemke15Marcus Y. Chen16Marcus Carlsson17Nehal N. Mehta18National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesRadiology and Imaging Sciences, Clinical Center, National Institutes of Health, Bethesda, MD, United StatesDepartment of Radiology, University of Wisconsin School of Medicine and Public Health, Madison, WI, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United StatesNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United States; Corresponding author at: Lasker Senior Investigator, Chief, Section of Inflammation and Cardiometabolic Diseases, National Heart, Lung and Blood Institute, National Institutes of Health, 10 Center Drive, Clinical Research Center, Room 5-5140, Bethesda, MD 20892, USA.Objective: Increased left ventricular (LV) mass is an important precursor to heart failure. Inflammation plays an important role in increasing LV mass. However, the contribution of subclinical coronary artery disease (CAD) to the inflammation-LV mass relationship is unknown. In subjects with psoriasis, a chronic inflammatory skin disease, we evaluated if systemic inflammation assessed by plasma glycoprotein A (GlycA) associated with LV mass measured on coronary CT angiography (CCTA). Additionally, we analyzed whether this relationship was mediated by early CAD assessed as noncalcified coronary burden (NCB). Methods: We performed an observational longitudinal study of 213 subjects with psoriasis free of known cardiovascular disease, 189 of whom were followed over one year. All participants had GlycA measurements by nuclear magnetic resonance spectroscopy and LV mass and NCB quantified by CCTA. Results: The cohort had a mean age of 50.3 (±12.9) years and 59% were male. There was moderate psoriasis severity and low cardiovascular risk. LV mass increased by GlycA tertiles [1st tertile:24.6 g/m2.7(3.8), 2nd tertile:25.5 g/m2.7(3.8), 3rd tertile:27.7 g/m2.7(5.5), p<0.001]. Both GlycA (β=0.24, p = 0.001) and NCB (β=0.50, p<0.001) associated with LV mass in models adjusted for age, sex, hypertension, hypertension therapy, lipid therapy, biologic therapy for psoriasis, waist:hip ratio, psoriasis disease duration and severity. In multivariable-adjusted mediation analyses, NCB accounted for 32% of the GlycA-LV mass relationship. Finally, over one year, change in NCB independently associated with change in LV mass (β=0.25, p = 0.002). Conclusions: Both systemic inflammation and coronary artery NCB were associated with LV mass beyond cardiovascular risk factors in psoriasis. Furthermore, a substantial proportion of the inflammatory-LV mass relationship was mediated by NCB. These findings underscore the possible contribution of early coronary artery disease to the relationship between systemic inflammation and LV mass.http://www.sciencedirect.com/science/article/pii/S2666667721000660InflammationLeft ventricular massNoncalcified coronary burdenCardiac computed tomography angiography |