I. BACKGROUND

Cardiovascular diseases, of which myocardial infarction (MI) is the main cause of morbidity and mortality in Western countries, are now rapidly becoming more common in developing and underdeveloped countries [1]. Up to 3 million people worldwide suffer from MI and 1 million people die from this disease every year [2]. According to the World Health Organization in 2016, it is estimated that 31% of deaths in Vietnam are due to cardiovascular disease, more than half of which are coronary artery disease [3]. Research on biomarkers in patients with MI has made great progress in recent years and a solution to this problem is expected to be found in the near future, possibly in the form of multi-marker assessment [4]. There are many biomarkers studied in patients with myocardial infarction such as troponin, myoglobin, CK-MB, h-FAPB, IMA, etc. However, in general, their role is still limited because they are mainly studied in the acute phase. There is a clear correlation between inflammatory outcome signs and adverse outcomes in patients after acute myocardial infarction. In that general trend, periostin - an inflammatory biomarker in recent times promises to be an effective and necessary factor in accurately predicting disease progression, helping to choose treatment and is a target in preventive care of coronary artery disease [5]. ​​In the world, the role of periostin on the heart is increasingly studied in developed countries [6, 7]. In Vietnam, there is currently no research on the role of periostin in acute MI. Therefore, we conducted a study on the characteristics of serum periostin levels in patients with acute MI.

II. MATERIALS AND METHODS

2.1. Materials

The research subjects were divided into 2 groups: the group of patients diagnosed with acute MI and the remaining group was the control group. All patient groups and the control group were hospitalized and treated from September 2019 to March 2023.

Disease group: Including 153 patients diagnosed with acute MI treated at Hue Central Hospital and Vinh Long Hospital, including 55 patients with STEMI and 98 patients with NSTEMI.

Exclusion criteria for the disease group: moderate to severe valvular heart disease, concurrent inflammation, malignancy, hypertrophic cardiomyopathy, dilated cardiomyopathy, blood creatinine ≥ 4 mg/dL (353.6 µmol/L), disagreeing to participate in the study.

Control group: Including 153 healthy subjects who did not have acute MI (clinically no chest pain, hs-Troponin T within normal limits), who had regular health check-ups at Vinh Long hospital.

2.2. Methods

Study design: Analytical cross-sectional study. Non-probability, purposive sampling.

All patients will be clinically examined and assigned routine investigations during the patient’s hospital stay, except for serum periostin levels which is performed 5-7 days after MI (levels at first time). Patients will be periodically re-examined after discharge. After 3 months of MI, an echocardiogram (assessing LVEF parameters) and a second periostin blood test will be performed (levels at second time). Serum periostin concentration testing is performed by enzyme-linked immunosorbent assay, which is ELISA (Enzyme-Linked ImmunoSorbent Assay) and serum periostin concentration quantification is performed at the Department of Immunology, University of Medicine and Pharmacy, Hue University with the Human Periostin Kit from MyBioSource.com.

Data processing: Data were processed using SPSS version 26 (IBM SPSS Statistics for Windows, Version 26.0), Medcalc version 22.017 and Excel 2013 software.

III. RESULTS

The baseline characteristics are listed in Table 1. There was no difference in age, BMI and sex between the patient group and the control group, p > 0.05. The serum periostin level in acute MI patients was the highest, the control group's periostin level was the lowest, p < 0.001 (Table 2). Periostin level in Killip I group was lower than in the remaining group, the difference was statistically significant with p < 0.001 (Table 3). Mean serum periostin level in the LVEF < 50% group was significantly greater than that in the LVEF ≥ 50% group, p < 0.05 (Figure 1).

Table 1: Common characteristics between the disease group and the control group

Table 2: Periostin level between groups

a: periostin concentration in the first patient group, b: periostin concentration in the second patient group, c: periostin concentration in the control group

Table 3: Periostin levels at admission and general characteristics

Figure 1: Mean periostin level at admission between EF groups on echocardiography 3 months after MI

IV. DISCUSSION

Regarding the general characteristics of the study subjects, in our study there was no difference in the ratio of gender, BMI and age between the two groups of patients and the control group (Table 1), which is similar to the subjects of studies related to periostin after acute MI in the world [8]. There is a change in serum periostin concentration over time after acute MI, from 2016 to present, it has been shown that although periostin concentration has increased from the first day of injury, it only peaks after 5-7 days of illness and then gradually decreases [9]. That is the basis for us to choose the time for the first serum periostin test on the 5-7th day of MI, when the periostin concentration reaches its maximum value. In our study, the serum periostin concentration in patients with acute MI at the initial test was the highest, with a median of 149,37 ng/mL (Table 2). The second test 3 months after acute MI, the median serum periostin concentration decreased to 77.69 ng/mL, while the periostin concentration in the control group was the lowest, with a median of 63.04 ng/mL, compared with the reference value of normal serum periostin concentration of < 100 ng/mL according to Mybiosource.com - the manufacturer of the serum periostin test kit. The median periostin concentration in our control group was 63.04 ng/mL, not much different from the results of study of Evan Tan examining periostin levelsin Chinese adults with a median value of 57.0 ng/mL [10]. The study results were consistent with most previous literature [9], except Chi-Wen Cheng showed that periostin concentration decreased early after AMI, which is not similar to the natural progression of the disease and was not expected by the author himself [11]. However, the sample size in Chi-Wen Cheng's study was small (45 MI patients), so it is only for reference. Under normal conditions, serum periostin levels is very low, but when there is damage such as acute MI, periostin levels will increase rapidly. Research of Lin Ling et al(2014) recorded the median periostin concentration in acute MI patients as 188 ng/mL [12]. Periostin concentration peaked on days 5 to 7 after a acute MI and then gradually decreased over time [13]. Xinwei He et al studied patients with large-vessel atherosclerotic stroke, tested blood periostin levelsat 3 different times on days 1, 6, and 28 of stroke and found that periostin levelsbegan to increase from the first day of the disease, reached the highest concentration on day 6, and remained higher than normal after stroke for at least 28 days [14].

According to Caswell-Smith, periostin levels did not differ by age or common comorbidities other than respiratory diseases [15]. We noted no difference in serum periostin levels by age group (Table 3). In addition, there was no difference in periostin levels by BMI classification. This suggests that serum periostin levels are independent of age and body mass index. Meanwhile, periostin levels in the Killip I classification group were lower than in the Killip II-IV classification group, suggesting that serum periostin levels are more likely to correlate with disease severity. Regarding the difference of serum periostin in echocardiographic parameters after 3 months of MI: after the patient has an acute MI, periostin stimulates excessive myocardial remodeling, leading to a state of fibrotic scar tissue that does not function to replace the damaged myocardial area, which will reduce heart function, reduce LVEF, reduce cardiac contractility and lead to expansion of the size of the heart chamber, shown by an increase in the diameter of the heart chamber on echocardiography. The more periostin is produced, the more obvious the remodeling process becomes. The study results showed that the serum periostin concentration in the LVEF ≥ 50% group was much lower than that in the remaining group (Figure 1). This contributes to the demonstration that periostin is associated with cardiac remodeling after acute MI.

V. CONCLUSION

Serum periostin levels increase in acute myocardial infarction and decrease gradually post myocardial infarction. There is a difference in admission periostin levels between preserverd and reduced EF groups.

Ethics approval: This study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of Hue Central hospital.

Competing interests: The authors declare that they have no competing interests.