Abstract
Background: Mechanisms underlying coronary microvascular dysfunction (CMD), a known cause of ischemia with non-obstructive coronary arteries (INOCA), are not well understood. Methods: In a prospective cohort study, we investigated the whole-blood transcriptome of 28 female patients with INOCA who underwent clinically indicated invasive coronary angiography to identify pathways relevant to the pathophysiology of CMD. Results: Four protein coding genes related to cell signaling and metabolism were differentially expressed and 47 transcriptomic pathways related to cell signaling, metabolism, inflammation, and sex hormone signaling were primarily upregulated with greater coronary microvascular dysfunction. Conclusion: Our findings support the hypothesis that inflammation leads to maladaptive microvascular remodeling and fibrosis, contributing to the pathogenesis of CMD.