Pan-Immune-Inflammation Value as an Independent Indicator of Isolated Coronary Artery Ectasia

MakaleAçık Erişim
  • SDG 3 · Sağlık ve Kaliteli Yaşam

Özet

Objective: Coronary artery ectasia (CAE) is increasingly recognized as an active inflammatory vascular disorder rather than a benign anatomical variant. The pan-immune-inflammation value (PIV) is a novel biomarker integrating neutrophil, monocyte, platelet, and lymphocyte counts, providing a comprehensive measure of systemic inflammation. This study aimed to evaluate the association between PIV and CAE and to compare their diagnostic performance with that of conventional inflammatory indices. Method: In this retrospective case-control study, 17,538 patients who underwent elective coronary angiography between 2018 and 2024 were screened. A total of 228 patients with isolated CAE and 296 age-, sex-, and Body Mass Index (BMI)-matched controls with normal coronary arteries were included. Hematologic and biochemical parameters were analyzed, and inflammatory indices were calculated. Logistic regression and receiver operating characteristic (ROC) analyses were performed to identify independent predictors and assess diagnostic performance. Results: Patients with CAE had significantly higher PIV levels compared to controls (801.6 [504.4-1301.8] vs. 491.8 [302.4-872.7], P < 0.001). In multivariable logistic regression, log-transformed PIV remained independently associated with CAE (odds ratio [OR]: 1.987, 95% confidence interval [CI]: 1.057-3.737, P = 0.033), along with hypertension, triglycerides, high-density lipoprotein (HDL) cholesterol, and serum creatinine. PIV demonstrated the highest discriminative ability among all inflammatory indices (area under the curve [AUC]: 0.674, 95% CI: 0.623-0.722), and correlated strongly with the Systemic Immune-Inflammation Index (SII), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and Systemic Inflammation Response Index (SIRI) (P = 0.75-0.94). Conclusion: Elevated PIV levels are independently associated with CAE, reflecting the pivotal role of systemic inflammation in its pathogenesis. Given its simplicity and availability, PIV may serve as a practical adjunctive marker for identifying patients at risk of CAE, warranting validation in larger prospective studies.

Anahtar Kelimeler

RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/gumushane/16324Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.5543/tkda.2025.51336Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorTunca, Cagatay
dc.contributor.authorÖzkan, Mehmet Taha
dc.contributor.authorErgin, Berin Nur
dc.contributor.authorGök, Saner Bahadir
dc.contributor.authorTas, Alperen
dc.contributor.authorKürklü, Haci Ali
dc.contributor.authorAkbuga, Kursat
dc.contributor.authorTanik, Veysel Ozan
dc.contributor.authorÖzlek, Bulent
dc.date.accessioned2026-10-22T10:29:13.259000968Z
dc.date.available2026-10-22T10:29:13.259000968Z
dc.date.issued2026-01
dc.description.abstractObjective: Coronary artery ectasia (CAE) is increasingly recognized as an active inflammatory vascular disorder rather than a benign anatomical variant. The pan-immune-inflammation value (PIV) is a novel biomarker integrating neutrophil, monocyte, platelet, and lymphocyte counts, providing a comprehensive measure of systemic inflammation. This study aimed to evaluate the association between PIV and CAE and to compare their diagnostic performance with that of conventional inflammatory indices. Method: In this retrospective case-control study, 17,538 patients who underwent elective coronary angiography between 2018 and 2024 were screened. A total of 228 patients with isolated CAE and 296 age-, sex-, and Body Mass Index (BMI)-matched controls with normal coronary arteries were included. Hematologic and biochemical parameters were analyzed, and inflammatory indices were calculated. Logistic regression and receiver operating characteristic (ROC) analyses were performed to identify independent predictors and assess diagnostic performance. Results: Patients with CAE had significantly higher PIV levels compared to controls (801.6 [504.4-1301.8] vs. 491.8 [302.4-872.7], P < 0.001). In multivariable logistic regression, log-transformed PIV remained independently associated with CAE (odds ratio [OR]: 1.987, 95% confidence interval [CI]: 1.057-3.737, P = 0.033), along with hypertension, triglycerides, high-density lipoprotein (HDL) cholesterol, and serum creatinine. PIV demonstrated the highest discriminative ability among all inflammatory indices (area under the curve [AUC]: 0.674, 95% CI: 0.623-0.722), and correlated strongly with the Systemic Immune-Inflammation Index (SII), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and Systemic Inflammation Response Index (SIRI) (P = 0.75-0.94). Conclusion: Elevated PIV levels are independently associated with CAE, reflecting the pivotal role of systemic inflammation in its pathogenesis. Given its simplicity and availability, PIV may serve as a practical adjunctive marker for identifying patients at risk of CAE, warranting validation in larger prospective studies.
dc.identifier.doi10.5543/tkda.2025.51336
dc.identifier.eissn1308-4488
dc.identifier.issn1016-5169
dc.identifier.issue1
dc.identifier.pmid41408779
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/gumushane/16324
dc.identifier.volume54
dc.identifier.wosWOS:001668885600006
dc.language.isoen
dc.publisherKARE PUBL
dc.relation.ispartofTURK KARDIYOLOJI DERNEGI ARSIVI-ARCHIVES OF THE TURKISH SOCIETY OF CARDIOLOGY
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAtherosclerosis
dc.subjectcoronary artery ectasia
dc.subjectinflammatory biomarkers
dc.subjectpan-immune-inflammation value
dc.subjectsystemic inflammation
dc.subject.classificationCardiac & Cardiovascular Systems
dc.subject.classificationCardiovascular System & Cardiology
dc.subject.otherPATHOGENESIS
dc.subject.otherASSOCIATION
dc.subject.otherACID
dc.titlePan-Immune-Inflammation Value as an Independent Indicator of Isolated Coronary Artery Ectasia
dc.typeArticle
dspace.entity.typePublication
rdl.citation.openalex2
rdl.citation.wos4
rdl.oa.statusgold
rdl.oa.urlhttps://doi.org/10.5543/tkda.2025.51336
rdl.sdgSDG03
rdl.source.indexWOS
rdl.wos.indexEmerging Sources Citation Index (ESCI)