Association of systemic immune-inflammation index (SII) with presence of isolated coronary artery ectasia
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1st Cardiology Department, Haseki Training and Research Hospital, University of Health Sciences Turkey, Istanbul, Turkey
Submission date: 2021-03-31
Final revision date: 2021-07-03
Acceptance date: 2021-07-21
Publication date: 2021-09-20
Arch Med Sci Atheroscler Dis 2021;6(1):152–157
The systemic immune-inflammation index (SII) has been developed based on the calculation of N×P/L (N, P and L represent neutrophil count, platelet count and lymphocyte count, respectively), and it is widely used as a marker of inflammation and an indicator of cardiovascular outcomes in patients with coronary artery disease. We examined a possible association between SII and the presence of isolated coronary artery ectasia (CAE).

Material and methods:
In this retrospective case-control study, a total of 4400 patients who underwent elective coronary angiography between June 2015 and July 2020 were retrospectively screened. Following the application of exclusion criteria, our study population consisted of 139 CAE patients and 141 age- and gender-matched subjects who proved to have normal coronary angiograms.

The median value of SII was found to be statistically significantly higher in patients with CAE (p < 0.01). SII level ≥ 809 measured on admission had 48% sensitivity and 82% specificity in predicting isolated CAE in ROC curve analysis. In this ROC analysis, the predictive powers of neutrophil-to-lymphocyte ratio (NLR) and SII in determining the presence of ectasia were compared, and the predictive power of SII was significantly stronger than N/L ratio (p = 0.003). In the multivariate analysis, hyperlipidaemia (OR = 1.978, 95% CI: 1.168–3.349, p = 0.01), smoking (OR = 1.86, 95% CI: 1.090–3.127, p = 0.023) N/L ratio (OR = 1.192, 95% CI: (1.114–1.997, p = 0.07) and SII (OR = 1.002, 95% CI: 1.001–1.003, p < 0.01) were independent predictors of the presence of isolated CAE.

SII is a readily available clinical laboratory value that is associated with the presence of isolated CAE. Our findings may indicate a common pathophysiological mechanism between CAE and coronary artery disease.