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.