Coronary Artery Ectasia: Review of the Non-Atherosclerotic Molecular and Pathophysiologic Concepts

Abstract

Coronary artery ectasia (CAE) is frequently encountered in clinical practice, conjointly with atherosclerotic CAD (CAD). Given the overlapping cardiovascular risk factors for patients with concomitant CAE and atherosclerotic CAD, a common underlying pathophysiology is often postulated. However, coronary artery ectasia may arise independently, as isolated (pure) CAE, thereby raising suspicions of an alternative mechanism. Herein, we review the existing evidence for the pathophysiology of CAE in order to help direct management strategies towards enhanced detection and treatment.

Keywords: CAD; coronary artery aneurysm; coronary artery ectasia; cytokine; lipidome.

Figure 1

Proposed cytokine-mediated pathways resulting in CAE. IL-2 = Interleukin-2; IL-4 = Interleukin-4; IL-6 = Interleukin-6; Th2 = T-helper 2; CAE = coronary artery ectasia; SMC = smooth muscle cells; and M2 = M2 macrophages.

Figure 2

Schematic of proposed pathways underlying vascular remodelling in the pathogenesis of CAE. Proposed triggers such as e.g., viral or Gut microbial metabolites are not included in the figure. IFN-γ = interferon gamma; IFN-α = interferon alfa; IL-6 = interleukin-6; IL-8 = interleukin-8; IL-1β = interleukin 1-beta; CRP = c-reactive protein; ICAM1 = Intercellular Adhesion Molecule 1; VCAM1 = Vascular Cell Adhesion Molecule 1; MMP = Matrix Metalloproteinases; SMC = smooth muscle cells; NO = nitric oxide; ECM = extracellular matrix; SM = sphingomyelin; PC = phosphatidylcholine; FAs = fatty acids; and miRNA = microribonucleic acids.