engleski

The impact of apelin level on the incidence of major adverse cardiac events after myocardial infarction with ST elevation

Background: During acute myocardial infarction, phosphorylated TnI levels, Ca2+ sensitivity and ATPase activity are decreased in the myocardium, and the elevation in Ca2+ levels activates protease I (calpain I), leading to the proteolytic degradation of troponins. Concurrently, hypoxia enhanced the expression of hypoxia inducible factor 1 alpha (HIF-1a) increasing the level of apelin, which limits infarct size, and improves myocardial function. Methods: In this prospective observational study, 100 consecutive patients meeting the following criteria were included: continuous chest pain lasting > 30 min, an electrocardiogram (ECG) with ST-segment elevation (measured at the J-point) ≥ 2.5 mm in men < 40 years, ≥ 2 mm in men ≥ 40 years, or ≥ 1.5mm in women in leads V2-V3 and/or ≥ 1mm in other leads [in the absence of left ventricular (LV) hypertrophy or left bundle branch block (LBBB)], rise of specific biomarkers such as troponin I and the MB fraction of creatine kinase (CKMB), and patients who underwent reperfusion therapy. The levels of apelin-12, creatine kinase (CK), the MB fraction of creatine kinase (CKMB), troponin I, NT-proBNP, CRP, triglycerides, LDL and HDL cholesterol, and other routine laboratory parameters are measured. In particular, we evaluated the levels of apelin-12 and troponin I on the first and seventh days after reperfusion therapy in all patients. Results: There was variability in apelin values on the first day (Kruskal-Wallis test) relative to segmental wall motion abnormalities (SWMAs) (p=0.046) and on the seventh day relative to different numbers of coronary lesions and stenoses (p<0.001). Based on the Mann-Whitney test, the relationship between apelin-12 and the final TIMI grade flow in the acute phase of myocardial infarction was statistically significant (p=0.001). Apelin-12 was inversely correlated with troponin I levels (Spearman’s correlation = −0.40) with a p value <0.001. There was variability in the apelin values on the seventh day (Kruskal- Wallis test) based on major adverse cardiac events (MACE) (p = 0.012). Using ROC curve analyses, a cut-off value of >2.2 for the association of apelin with MACE was determined, and the AUC was 0.71 (95% CI, 0.58– 0.84). Survival analysis using the Kaplan-Meier method showed a lower rate of MACE among patients with apelin levels >2.2 (p = 0.002), and the ROC curve analysis showed a statistically significant difference in the area under the curve (p = 0.004). Pearson’s correlation between apelin-12 and creatine kinase-MB on the first day in patients without reperfusion injury was characterized with a p value <0.003, while between apelin-12 and NT- proBNP on the seventh day in patients without reperfusion injury p value was -0.042. Conclusion: The increase level of apelin during acute phase of myocardial infarction indicate a protective effect from reperfusion injury while low level of apelin during non-acute phase of myocardial infarction is found to be inversely associated with number of coronary stenoses. Apelin-12 influences troponin I levels in the acute phase of STEMI, whereas during the non-acute phase, low apelin levels were associated with high rate of MACE. In STEMI patients undergoing reperfusion therapy, apelin-12 was associated with creatine kinase-MB depending reperfusion injury determining role of apelin in creatine kinase system.

apelin ; major adverse cardiac events ; myocardial infarction

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