Associations between Inflammatory Markers and Global Systolic Function Measured by MRI: The Multi-Ethnic Study of Atherosclerosis (MESA)
Amir Ali Rahsepar1, Mohammadali Habibi2, Cheeling Chan3, Nadine kawel2, Kiang Liu3, Joao Lima2, and James Carr1

1Radiology, Northwestern University, Chicago, IL, United States, 2Cardiology, Johns Hopkins University, Baltimore, MD, United States, 3Preventive medicine, Northwestern University, Chicago, IL, United States

Synopsis

In this cross-sectional study, we investigated the associations between Inflammatory markers and global systolic function measured by MRI in The Multi-Ethnic Study of Atherosclerosis (MESA).

Introduction

Epidemiological studies have supported the role of inflammation in cardiovascular disease [1]. Cardiac magnetic resonance imaging (MRI), is known as the gold standard to evaluate cardiac function and structure. We aimed to determine the cross-sectional associations between specific combinations of inflammatory markers and cardiac function and structure among participants of the Multi-Ethnic Study of Atherosclerosis (MESA) who were free of cardiovascular disease.

Methods

At baseline, 2093 participants (mean age 61, 53% women) with Interleukin-2 (IL-2), Interleukin-6 (IL-6), tumor necrosis factors-α (TNF-α), and cardiac MRI measures (Left ventricular (LV) end-systolic and -diastolic volumes, ejection fraction (EF), and cardiac output) were included. Standardized MRI protocol was followed across all field centers and cardiac MRI images were transmitted using DICOM transfer protocol to a MESA central reading center. Participants were first classified into IL-6, IL-2, and TNF-α groups based on tertiles of each inflammatory marker within the entire cohort. A priori, participants were categorized into one of three groups, ranging from low to high levels of inflammatory markers, depending on the number of individual inflammatory marker in the lowest and highest tertiles for each corresponding inflammatory marker: Low (at least 2 measures in the lowest tertile and no markers in the highest tertile), Middle ((a) fewer than 2 measures in the highest or lowest tertile or (b) one marker in the highest tertile with one or more of the remaining markers in the lowest tertile), and High (at least 2 measures in the highest tertile and no marker in the lowest tertile). Linear regression models were used for the analyses, and the low inflammatory marker group was used as the reference.

Results

Participants in the high inflammatory marker group were associated with older age, higher BMI, higher blood pressure, more diabetes, higher total cholesterol, lower HDL cholesterol, higher prevalence of CAC>10, and were less educated. Multivariable linear regression models for individual marker showed that IL-6 had more prominent role in reducing the cardiac function indices compared to IL-2 and TNF-α. After adjusting for age, sex, race, education, physical activity, cigarette smoking, diabetes, BMI, systolic blood pressure, anti-hypertensive medication use, HDL cholesterol, total cholesterol, statin use, and prevalence of CAC>10, participants in higher inflammatory marker group had significantly reduced LV end diastolic volume, stroke volume, and EF compared to those in very low levels of inflammatory marker group (Table). Regression analysis showed that IL-6 had more prominent role in reducing the cardiac function indices compared to IL-2 and TNF-α.

Conclusion

Among asymptomatic individuals without documented cardiovascular disease, high levels of inflammation are associated with significantly reduced diastolic volume, stroke volume and EF compared to those with very low levels of inflammation. These population-based findings implicate the role inflammation in the pathogenesis of cardiovascular disease and help to determine whether future medical therapy targeted reduction of inflammation prevents decline in cardiac function in individuals with cardiovascular disease.

Acknowledgements

MESA Family is conducted and supported by the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with MESA investigators. Support is provided by grants and contracts R01HL071051, R01HL071205, R01HL071250, R01HL071251, R01HL071258, R01HL071259, UL1-RR-025005, by the National Center for Research Resources, Grant UL1RR033176, and the National Center for Advancing Translational Sciences, Grant UL1TR000124.

References

[1] Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 2005.

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Proc. Intl. Soc. Mag. Reson. Med. 24 (2016)
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