Association between tissue human neutrophil peptide 1–3 levels and cardiovascular phenotype: a prospective, longitudinal cohort study

Rami Abu Fanne*, Yaron Arbel, Ehud Chorin, Emad Maraga, Gabriel M. Groisman, Abd Alroof Higazi, Shmuel Banai

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Objective: Inflammation is associated with atherogenesis. Although a higher neutrophil count is associated with the plaque burden, the role of neutrophil activation is unclear. Human neutrophil peptides 1–3 (HNP1–3) are a risk factor for atherogenesis in bench models and are elevated in human atheromas. This study aimed to examine the association between skin HNP1–3 deposition and the severity of coronary artery disease (CAD), including long-term outcomes. Methods: HNP1–3 levels were immunohistochemically quantified in skin biopsies, which were prospectively taken from 599 consecutive patients before clinically indicated coronary angiography. Established cardiovascular risk factors and blood markers for atheroinflammation were obtained. CAD severity and the incidence of repeat revascularization and mortality at 48 months of follow-up were assessed in relation to HNP1–3 levels. Results: The risk of CAD was independently associated with age and HNP1–3 in the entire cohort (F = 0.71 and F = 7.4, respectively). Additionally, HNP1–3 levels were significantly associated with myocardial necrosis (R = 0.26). At the follow-up, high HNP1–3 levels negatively affected mortality (19.54%) and recurrent revascularization (8.05%). Conclusion: HNP1–3 tissue deposition is positively associated with the severity of CAD, myonecrosis, and long-term sequelae. HNP1–3 levels may be suppressed using colchicine.

Original languageEnglish
JournalJournal of International Medical Research
Volume50
Issue number10
DOIs
StatePublished - Oct 2022

Funding

FundersFunder number
Tel Aviv Medical Center

    Keywords

    • Inflammation
    • atherosclerosis
    • atherothrombosis
    • coronary artery disease
    • human neutrophil peptides 1–3
    • myocardial necrosis

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