Evaluative Value of Apelin-12 in Acute Myocardial Infarction

In acute myocardial infarction (MI), hypoxia, through the hypoxiainducible factor pathway, increases the level of apelin, protecting the myocardium from ischemia-reperfusion injury.

We aimed to evaluate the level of apelin-12 in the early and late phases of MI.

In this prospective observational study, 98 patients were randomly included with the following criteria: chest pain lasting for more than 30 minutes, a 12-lead ECG with ST-segment elevation, a rise of cardiac troponin I, and a primary percutaneous coronary intervention (PCI) within 12 hours. Blood samples were collected on the first day (early phase) and the seventh day (late phase) after reperfusion therapy. Continuous variables are expressed as mean ± standard deviation or median (range), while categorical variables are expressed as percentages. We compared the variables using the Wilcoxon test and evaluated the variability of apelin values with the Kruskal-Wallis test. We checked the degree of association and correlation between two variables with the Mann-Whitney test and Pearson correlation, respectively.

On the first day of the early phase after MI, the median apelin-12 level was 2.73 (0.46 –15.24), which was significantly higher than the seventh-day value of 2.32 (0.25 – 10.89) (P = 0.003 on Wilcoxon test). With the Kruskal-Wallis test, variability in apelin-12 values was noted on the first day relative to segmental wall motion abnormalities (P = 0.043) and on the seventh day relative to the number of coronary stenoses (P < 0.001). The Mann-Whitney test of the post-PCI final thrombolysis in MI (TIMI) flow grade (patients without reperfusion injury: TIMI 3; patients with reperfusion injury: TIMI ≤ 2) and the apelin-12 levels during the early phase of MI revealed a statistically significant difference (P = 0.002).

Differences in apelin-12 between the early and late phases may reflect the activity of the apelin-angiotensin receptor-like axis in patients with MI.