ArticleNorthern clinics of Istanbul2018
Systemic inflammatory activation in patients with acute coronary syndrome secondary to nonatherosclerotic spontaneous coronary artery dissection.
Article in Northern clinics of Istanbul, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Pericoronary Adipose Tissue Attenuation in Patients with Spontaneous Coronary Artery Dissection According to Emotional Versus Physical Triggers: An Analysis from the INSIGHT-SCAD Study.Journal of cardiovascular development and disease · 2026Article
- Genetic Association of Circulating Proteins and Gene Transcripts With Spontaneous Coronary Artery Dissection.Circulation. Genomic and precision medicine · 2026Article
- Spontaneous Coronary Artery Dissection (SCAD): Unveiling the Enigma of the Unexpected Coronary Event.Current atherosclerosis reports · 2025Review
- Spontaneous Coronary Artery Dissection: A Narrative Review of Epidemiology and Public Health Implications.Medicina (Kaunas, Lithuania) · 2025Review
- Spontaneous coronary artery dissection in regions of non-Western populations: a systematic literature search and scoping review.European heart journal open · 2025Review
- Genetics architecture of spontaneous coronary artery dissection in an Italian cohort.Frontiers in cardiovascular medicine · 2024Article
- Pathophysiology of spontaneous coronary artery dissection: hematoma, not thrombus.Frontiers in cardiovascular medicine · 2023Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivePathological 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.
methodsThe 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.
resultsPatients 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.
conclusionThe 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.
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