Ectodysplasin A is associated with the presence and severity of coronary artery disease and poor long-term clinical outcome in patients presenting with ST-elevation myocardial infarction

ABSTRACT

Objectives

Hepatokines are proteins secreted by hepatocytes and many hepatokines such as fetuin A/B, selenoprotein P have been shown to play a role in the pathogenesis of many metabolic dysfunctions such as diabetes, insulin resistance, hypertension, and metabolic syndrome by showing autocrine, paracrine and systemic effects. Ectodysplasin A (EDA) is a recently discovered hepatokine that plays a role in the development of ectodermal structures. In recent studies, it has been revealed that EDA may be associated with the pathogenesis of non-alcoholic liver disease, insulin resistance, Type 2 diabetes mellitus. The close relationship between these metabolic diseases and coronary artery disease (CAD), which may be associated with insulin resistance, has been well documented in previous studies. However, until now, there is no study examining the relationship of EDA with CAD and its effect on long-term outcomes. In this study, we aim to reveal this relationship on patients presenting with ST elevation myocardial infarction (STEMI).

Methods

EDA levels of 544 patients who applied to the study with STEMI and 544 people without coronary artery disease were included in the control group, and the patients with STEMI were followed for median of 33.7 ± 6.8 months.

Results

We found that EDA levels were significantly higher in patients with STEMI and that EDA levels were proportional to the severity of CAD (p < 0.001) also EDA levels may be an independent predictor of poor clinical outcome in patients with STEMI.

Conclusion

These results suggest that EDA is closely related to the presence and severity of CAD.

KEYWORDS:

• Hepatokine
• Ectodysplasin A
• coronary artery disease
• ST elevation myocardial infarction
• Long-term clinical outcome

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

The authors report no financial support.