ArticleClinical cardiology2021
The association of interferon-alpha with development of collateral circulation after artery occlusion.
Article in Clinical cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 1 citations in OpenAlex.
- Role of physiological ischemia training in suppressing ventricular remodeling and ventricular arrhythmia in patients after myocardial infarction: a randomized controlled trial.American journal of translational research · 2024Article
- The association of interferon-alpha with development of collateral circulation after artery occlusion.Clinical cardiology · 2021Article
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6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPrevious studies have demonstrated that interferon (IFN) signaling is enhanced in patients with poor collateral circulation (CC). However, the role and mechanisms of IFN-alpha in the development of CC remain unknown.
methodsWe studied the serum levels of IFN-alpha and coronary CC in a case-control study using logistics regression, including 114 coronary chronic total occlusion (CTO) patients with good coronary CC and 94 CTO patients with poor coronary CC. Restricted cubic splines was used to flexibly model the association of the levels of IFN-alpha with the incidence of good CC perfusion restoration after systemic treatment with IFN-alpha was assessed in a mice hind-limb ischemia model.
resultsCompared with the first IFN-alpha tertile, the risk of poor CC was higher in the third IFN-alpha tertile (OR: 4.79, 95% CI: 2.22-10.4, p < .001). A cubic spline-smoothing curve showed that the risk of poor CC increased with increasing levels of serum IFN-alpha. IFN-alpha inhibited the development of CC in a hindlimb ischemia model. Arterioles of CC in the IFN-alpha group were smaller in diameter than in the control group.
conclusionPatients with CTO and with poor CC have higher serum levels of IFN-alpha than CTO patients with good CC. IFN-alpha might impair the development of CC after artery occlusion.
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