eISSN: 1897-4295
ISSN: 1734-9338
Advances in Interventional Cardiology/Postępy w Kardiologii Interwencyjnej
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SCImago Journal & Country Rank
 
3/2022
vol. 18
 
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abstract:
Original paper

The role of temporal changes of pro-inflammatory cytokines in the development of adverse cardiac remodeling after ST-elevation myocardial infarction

Mehmet Sait Altintas
1
,
Nilnur Eyerci
2
,
Serkan Sivri
3
,
Mehmet Ali Felekoglu
4
,
Orhan Karayigit
5
,
Bekir Demirtas
6
,
Murat Gok
7
,
Omer Faruk Ates
8

1.
Department of Cardiology, Istanbul Training and Research Hospital, Istanbul, Turkey
2.
Department of Medical Biology, Kafkas University Faculty of Medicine, Kars, Turkey
3.
Department of Cardiology, Kirsehir State Hospital, Kirsehir, Turkey
4.
Department of Cardiology, Atakent Hospital, Yalova, Turkey
5.
Department of Cardiology, Yozgat City Hospital, Yozgat, Turkey
6.
Department of Cardiology, Cankiri State Hospital, Cankiri, Turkey
7.
Department of Cardiology, Edirne Sultan Murat I State Hospital, Edirne, Turkey
8.
Department of Radiology, Sakarya University Faculty of Medicine, Sakarya, Turkey
Adv Interv Cardiol 2022; 18, 3 (69): 217–227
Online publish date: 2022/11/08
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Introduction
Increasing evidence supports the view that pro-inflammatory cytokines play a role in fibrosis after myocardial infarction (MI). It has been suggested that interleukin (IL)-12p40, a pro-inflammatory cytokine, can induce interferon  (IFN-) and matrix metalloproteinase (MMP). However, the role of IL-12p40 in adverse cardiac remodeling (AR) after ST-elevation MI (STEMI) is unclear. Aim: To examine the role of temporal changes of pro-inflammatory cytokines in the development of post-STEMI AR.

Material and methods
A total of 43 patients with STEMI for the first time ever were prospectively analyzed. In cardiac magnetic resonance imaging at 6 months after STEMI, a decrease of left ventricular end-diastolic volume by ≥ 12% was defined as reverse cardiac remodeling (RR), and a 12% increase was defined as AR. Cytokine concentrations were measured on the first day (baseline) and 2 weeks after STEMI.

Results
Mean IL-12p40 (59.1 ±14.5 vs. 46.7 ±9.1 pq/ml, p = 0.001), median IFN- (20.4 vs. 16.2 pq/ml, p = 0.048) and median MMP-2 (33866 vs. 20691 pq/ml, p = 0.011) baseline concentrations were higher in AR than RR. In patients with AR, IL-12p40 level was lower at 2 weeks than baseline (p < 0.001). There was a positive correlation between the baseline concentrations of IL-12p40, IFN-, MMP-2, C-reactive protein and infarct size (p < 0.05). Increased IL-12p40 and MMP-2 baseline levels were independently associated with AR (OR = 1.14, p = 0.010; OR = 1.08, p = 0.035).

Conclusions
In the initial phase of MI, greater release of pro-inflammatory cytokines was associated with increased MMP-2 levels. Elevated expression of IL-12 and MMP-2 had an independent association with AR. This may be related to the excessive inflammatory response in the initial phase of MI.

keywords:

matrix metalloproteinase, IL-12p40, interferons, myocardial infarction, cardiac remodeling

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