Molecular mechanisms of coronary microembolization-induced MINOCA.

Abstract

Compared to classic myocardial infarction (cMI), myocardial infarction with non-obstructive coronary arteries (MINOCA) is characterized by symptoms consistent with acute coronary syndrome, but without demonstrable coronary obstruction. Therefore, its diagnosis remains challenging and often relies on cardiac magnetic resonance imaging (MRI), which is usually performed only days after the index event, leading to delayed diagnosis and initiation of therapy. Coronary microembolization (CME) has been described as one of the major pathologies underlying MINOCA. However, the molecular mechanisms of CME remain poorly understood, resulting in a lack of rapid diagnostic tools and specific therapy approaches. In this review, we describe the molecular underpinnings of CME-derived MINOCA: an inflammatory environment inducing significant cellular damage that is conserved between cMI and MINOCA. While we note that some of these inflammatory and cellular death pathways are shared with cMI, we dissect mechanistic distinctions in CME-derived MINOCA such as dysregulated immune responses and higher miRNA activity. Most importantly, as molecular treatments for MI are currently in late-stage clinical trials, we can thus differentiate which therapeutics may work better for MINOCA. Thus, these findings can be used as a roadmap for diagnostic biomarkers and targeted therapeutic approaches for MINOCA.