Why the study?
Do endothelial function, oxidative stress, and inflammatory markers differ between patients with chronic coronary slow flow phenomenon and healthy controls?
Do endothelial function, oxidative stress, and inflammatory markers differ between patients with chronic coronary slow flow phenomenon and healthy controls?
Endothelial dysfunction, inflammation, and oxidative stress do not appear to be the primary mechanisms driving microvascular dysfunction in chronic coronary slow flow phenomenon.
Findings do not support endothelial dysfunction or inflammation as primary CSFP drivers; leaves open alternative microvascular mechanisms for prospective study.
The coronary slow flow phenomenon (CSFP) is associated with coronary microvascular dysfunction although the responsible mechanisms are unknown. This study compared endothelial function assessed by changes in augmentation index (AIx) following endothelium-independent (glyceryl trinitrate, GTN) and endothelium-dependent vasodilators (salbutamol), in 40 stable CSFP patients and 23 age-matched healthy controls. Plasma concentrations of inflammatory proteins (myeloperoxidase and high-sensitivity C-reactive protein), oxidative stress biomarkers (malondialdehyde and homocysteine), and asymmetric dimethylarginine levels were also determined. There were no differences between CSFP and controls in response to salbutamol (AIx: -2.28 ± 0.88% vs. -3.22 ± 0.70%, p = 0.4) or GTN (AIx: -11.30 ± 0.75% vs. -13.30 ± 1.00%, p = 0.12). Similarly, there were no differences in the measured biomarkers. Thus, alternate mechanisms to the assessed endothelial function, inflammatory and oxidative stress processes should be explored to explain the microvascular dysfunction in CSFP patients.
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Kennedy et al. (2012) studied this question.
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