Systemic inflammatory activation in patients with acute coronary syndrome secondary to nonatherosclerotic spontaneous coronary artery dissection

Pathological studies have suggested that local inflammation, particularly eosinophilic infiltration of the adventitia, could be related to nonatherosclerotic spontaneous coronary artery dissection (NA-SCAD). However, the role of systemic inflammation in the pathogenesis of NA-SCAD remains unknown. Our aim was to investigate systemic inflammatory activation in patients with an acute coronary syndrome (ACS) secondary to NA-SCAD. The institutional electronic medical database was reviewed, and 22 patients with NA-SCAD-ACS were identified after the review. Furthermore, 30 random patients with CAD-ACS and 30 random subjects without any history of CAD or ACS with demographic and clinical characteristics similar to those of NA-SCAD-ACS patients were identified from the institutional database to be included in the study. Patients with NA-SCAD-ACS and those with CAD-ACS both had higher white blood cell and neutrophil counts than controls. Neutrophil-lymphocyte ratio (NLR) and C-reactive protein (CRP) levels were only significantly higher in the NA-SCAD-ACS group [2.01 (1.54-6.17) for NLR and 0.70 (0.13-2.70) for CRP] than in the controls [1.55 (1.27-2.13), p=0.03 for NLR and 0.15 (0.10-0.43), p=0.049 for CRP]; however, there were no differences between the NA-SCAD-ACS and CAD-ACS groups [1.91 (1.41-2.78) for NLR and 0.41 (0.09-1.10) for CRP, p>0.05 for both comparisons] regarding all tested parameters. The degree of inflammatory activation in NA-SCAD-ACS patients was similar to, or even greater than, that in CAD-ACS patients; thus, suggesting a role of inflammation in the pathophysiology of NA-SCAD-ACS.