Abstract
BackgroundDuring acute myocardial infarction, phosphorylated TnI levels, Ca2+ sensitivity and ATPase activity are decreased in the myocardium, and the subsequent elevation in Ca2+ levels activates protease I (caplain I), leading to the proteolytic degradation of troponins. Concurrently, the levels of apelin and APJ expression are increased by limiting myocardial injury.MethodsIn this prospective observational study, 100 consecutive patients with ST-elevation acute myocardial infarction were included. Patients meeting the following criteria were included in our study: (1) continuous chest pain lasting for >30 min, (2) observation of ST-segment elevation of more than 2 mm in two adjacent leads by electrocardiography (ECG), (3) increased cardiac troponin I levels, and (4) patients who underwent reperfusion therapy. We evaluated the levels of apelin-12 and troponin I on the first and seventh days after reperfusion therapy in all patients.ResultsApelin-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).ConclusionThe influence of apelin levels on troponin levels in the acute phase of STEMI is inversely correlated, whereas in the non-acute phase, low apelin values were associated with a high rate of MACE.
Highlights
During acute myocardial infarction, phosphorylated TnI levels, Ca2+ sensitivity and Adenosine triphosphatase (ATPase) activity are decreased in the myocardium, and the subsequent elevation in Ca2+ levels activates protease I, leading to the proteolytic degradation of troponins
After acute myocardial infarction, the left ventricle undergoes a series of changes in shape, size, and thickness, which is referred to as ventricular remodelling; it precedes the development of clinically evident major adverse cardiac events (MACE) by months to years
The aims of this study were to evaluate the influence of apelin on troponin levels and the rate of major adverse cardiac events (MACE) in ST-Segment elevation myocardial infarction (STEMI) patients
Summary
During acute myocardial infarction, phosphorylated TnI levels, Ca2+ sensitivity and ATPase activity are decreased in the myocardium, and the subsequent elevation in Ca2+ levels activates protease I (caplain I), leading to the proteolytic degradation of troponins. The role of hypoxia in the release of apelin, ischaemia reperfusion injury, and the action of apelin in cardiac contractility remains unclear. Apelin and the cardiovascular system The gene for the APJ receptor is located on chromosome 11 and encodes a G-protein coupled receptor that is recognized only by apelin [4, 5]. APJ receptor expression is high in the heart, lung, kidney, cerebellum and vascular endothelium. In the heart, this receptor is expressed on a number of cell types, including the endothelium, smooth muscle and myocytes. The apelin gene is located on the human X chromosome, which, in response to hypoxia, encodes a 77-amino-acid preproprotein that is cleaved by endopeptidases into a biologically active peptide such as apelin-12 [6].
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