Elevated circulating IL-32 presents a poor prognostic outcome in patients with heart failure after myocardial
Wanling Xuan1, Weixing Huang1, Ruijie Wang1
1Department of Cardiology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China.
Insights
Interleukin-32 (IL-32) may predict adverse cardiac events in heart failure (HF) patients post-myocardial infarction (MI). Elevated IL-32 levels indicate a higher risk, suggesting its role in cardiac fibrosis and HF progression.
Area of Science:
- Cardiology
- Biomarker Discovery
- Cytokine Research
Background:
- Interleukin-32 (IL-32) is a newly identified proinflammatory cytokine.
- Limited data exist on IL-32's role as a biomarker in heart failure (HF).
- This study investigates IL-32's prognostic value in chronic HF patients post-myocardial infarction (MI).
Purpose of the Study:
- To assess the prognostic significance of IL-32 in patients with chronic heart failure following myocardial infarction.
- To explore the association between IL-32 levels and cardiac function, fibrosis, and adverse cardiac events.
- To investigate the potential role of IL-32 in cardiac remodeling and HF progression.
Main Methods:
- Prospective enrollment of 100 patients with chronic HF post-MI.
- Baseline measurement of IL-32, NT-proBNP, MMP-9, procollagen type I (PI), and type III (PIII).
- Follow-up for adverse cardiac events over 1.8 years; analysis using ROC curves, Kaplan-Meier statistics, and Cox regression.
Main Results:
- High IL-32 levels correlated with factors indicating deteriorated cardiac function and fibrosis.
- IL-32 was strongly expressed in cardiomyocytes from HF tissue.
- IL-32 predicted adverse cardiac events with an AUC of 0.72 (P<0.01) and was an independent predictor (HR 2.78, P=0.046).
- IL-32 exacerbated infarct size in a mouse model and upregulated pro-fibrotic markers in rat fibroblasts.
Conclusions:
- IL-32 shows potential as a novel predictor of adverse cardiac events in HF patients post-MI.
- The pro-fibrotic actions of IL-32 may contribute to adverse cardiac remodeling and HF progression.
Background:
Interleukin-32 (IL-32) is a newly discovered proinflammatory cytokine. However, there are limited data regarding IL-32 as a biomarker for heart failure (HF). In this study, we assessed the prognostic value of IL-32 in patients with chronic HF after myocardial infarction (MI).
Methods And Results:
Over a period of 1.8years, we prospectively enrolled 100 patients with chronic HF after MI. IL-32, NT-proBNP, Matrix metallopeptidase 9 (MMP-9), procollagen type I (PI) and type III (PIII) were measured at baseline. Study endpoint was adverse cardiac events. High IL-32 levels were associated with numerous factors that are related to deteriorate cardiac function and cardiac fibrosis. Strong expression of IL-32 was detected in human cardiomyocytes from HF tissue. ROC curve revealed the area under the curve of IL-32 for predicting negative outcome of HF was 0.72 (95% CI: 0.60-0.83, P<0.01). Kaplan-Meier statistics showed that the risk of adverse cardiac event was 5.75 fold (hazard ratio 5.75, 95% CI 1.53-21.58, P=0.009), which increased in the highest quartile (>296pg/mL). Cox regression analysis revealed IL-32 was an independent predictor for cardiac events (hazard ratio 2.78, 95% CI 1.02-7.57, P=0.046). Recombinant IL-32 significantly exacerbated infarct size in a mouse model of MI. IL-32 upregulated expression of MMP-9, PIII and transforming growth factor beta in rat fibroblasts.
Conclusion:
IL-32 might be a novel predictor of adverse cardiac event in patients with HF after MI. The pro-fibrotic effect of IL-32 may contribute to adverse cardiac remodeling and progression to HF.
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