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Published on: August 17, 2022
Inflammation, endothelial cell activation, and coronary microvascular dysfunction in women with chest pain and no
Oscar C Marroquin1, Kevin E Kip, Suresh R Mulukutla
1Cardiovascular Institute, Department of Epidemiology, University of Pittsburgh, Pittsburgh, PA, USA. marroquinoc@upmc.edu
Insights
Coronary microvascular dysfunction in women with chest pain and no obstructive coronary artery disease (CAD) is not linked to inflammation or endothelial activation. These findings suggest inflammation may not drive this condition.
Area of Science:
- Cardiology
- Vascular Biology
- Inflammation Research
Background:
- Coronary artery microvascular dysfunction (CMD) is common in women with chest pain and non-obstructive coronary artery disease (CAD).
- Elevated inflammatory and endothelial activation markers are observed in patients with chest pain and non-obstructive CAD.
- The link between inflammation, endothelial activation, and CMD remains unclear.
Purpose of the Study:
- To investigate the association between markers of inflammation and endothelial cell activation and coronary flow reserve (CFR) in women with chest pain and non-obstructive CAD.
- To determine if inflammation or endothelial activation plays a role in the pathophysiology of CMD in this patient group.
Main Methods:
- Utilized data from the NHLBI WISE study, including 94 women with chest pain and non-obstructive CAD.
- Assessed catheterization-based coronary flow reserve (CFR).
- Measured serum levels of inflammatory markers (e.g., high-sensitivity C-reactive protein, IL-6, IL-18) and endothelial activation markers (e.g., soluble intracellular adhesion molecule-1).
Main Results:
- Coronary flow reserve (CFR) showed no significant correlation with any measured inflammatory or endothelial activation markers.
- Median levels of these markers did not differ between women with abnormal CFR and those with normal coronary microvascular function.
- Multivariable analyses confirmed no association between inflammation/endothelial activation markers and CFR.
Conclusions:
- Coronary microvascular dysfunction in women with chest pain and without obstructive CAD is not associated with systemic markers of inflammation or endothelial cell activation.
- These findings suggest that inflammation and endothelial activation may not be key players in the development of CMD in this specific population.
Background:
Coronary artery microvascular dysfunction is prevalent in women with chest pain in the absence of obstructive coronary artery disease (CAD) and is manifested by attenuated coronary flow reserve (CFR). Markers of inflammation and endothelial cell activation have been found to be elevated in patients with chest pain but without CAD. The relationship between inflammation, endothelial activation, and CFR is not known.
Methods:
Ninety-four women with chest pain in the absence of obstructive angiographic CAD underwent catheterization-based assessment of CFR and measurement of levels of inflammatory markers (n = 78) and endothelial cell activation in the NHLBI WISE study.
Results:
Coronary flow reserve did not correlate with levels of C-reactive protein (high-sensitivity C-reactive protein) (rs = -0.07, P = .53), interleukin (IL)-6 (rs = -0.12, P = .31), IL-18 (rs = 0.14, P = .23), tumor necrosis factor alpha (rs = -0.09, P = .43), transforming growth factor beta1 (rs = 0.02, P = .84), and soluble intracellular adhesion molecule-1 (rs = 0.04, P = .68). Median levels of markers of inflammation and endothelial cell activation did not differ between the 57 women with abnormal CFR (< 2.5) and the 37 women with normal coronary microvascular function (high-sensitivity C-reactive protein 0.32 vs 0.25 mg/dL, P = .80; IL-6 2.89 vs 2.39 pg/mL, P = .63; IL-18 218 vs 227 pg/mL, P = .59; tumor necrosis factor alpha 2.7 vs 2.4 pg/mL, P = .43; transforming growth factor beta1 9928 vs 12436 pg/mL, P = .76; soluble intracellular adhesion molecule-1 286 vs 287 pg/mL, P = .95). Multivariable models demonstrated no evidence of associations between markers of inflammation and of endothelial cell activation and CFR.
Conclusions:
Coronary microvascular dysfunction is not associated with markers of inflammation and endothelial cell activation in women with chest pain in the absence of obstructive CAD. These results suggest that inflammation and endothelial cell activation may not play a pathophysiological role in coronary microvascular dysfunction.
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