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

INTRODUCTION[|]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.[¤]METHODS[|]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. [¤]RESULTS[|]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.[¤]DISCUSSION AND CONCLUSION[|]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.[¤]