| Objectives: current statistics show that, as an immense health problem, the morbidity of acute myocardial infarction(AMI) in china is ascending. Medical therapies and revisualization by percutaneous coronary intervention or coronary by-pass surgery have reduced the mortality major adverse cardiovascular events and significantly. However, many of the treated patients still have angina or heart failure symptoms, many hospitalisations and a poor prognosis. Left ventricular remodeling after acute myocardial infarction(AMI) is associated with all these adverse prognosis. Acute myocardial infarction(AMI) leads to molecular, structural, geometrical and functional changes in the heart in a process known as ventricular remodeling. Inflammation plays an important role in all stages of the initiation and progression of atherosclerosis including myocardial infarction and remodeling. Inflammation is triggered by tissue injury, it mediates wound healing and scar formation. An intense organized inflammatory response is triggered after myocardial ischemia and necrosis, and involves all components of the innate immunity, affecting both cardio-myocytes and non-cardio-myocyte cells. Therefore, inflammatory biomarker could be prognostic biomarkers in IHD. Epidemiological and clinical studies have shown strong and consistent relationship between biomarkers of inflammation, evaluated by high sensitivity C-reactive protein(hs-CRP),and risk of cardiovascular events in patients with IHD. However, when using hs-CRP in general population studies, then hs-CRP does not always seem to have a significant prognostic value in detecting future cardiovascular disease. YKL-40 is a 40 k Da plasma glycoprotein and a member of the “mammalian chitinase-like proteinsâ€. YKL-40 is regarded as an acute phase protein, since its plasma concentration increases more than 25% following aninflammatory stimulus, but YKL-40 is different from and independent of Creactive protein(CRP). Elevated plasma YKL-40 levels are seen in patients with diseases characterized by inflammation and ongoing tissue remodeling such as cancer, ischemic cardiovascular diseases, diabetes, chronic obstructive pulmonary disease, asthma, rheumatoid arthritis, inflammatory bowel disease, pneumonia, and liver fibrosis. As an inflammation factor YKL-40 is elevated in different stage of coronary artery disease. Elevated plasma concentration of YKL-40(also named chitinase-3-like-1) is emerging as a new biomarker of cardiovascular disease.YKL-40 is secreted by macrophages, including those in atherosclerotic plaques, neutrophils, and vascular smooth muscle cells. That plasma YKL-40 is increased early in patients with ST-elevation myocardial infarction(STEMI). It is not known whether plasma YKL-40 is related to infarct size and recovery of ventricular function. So it is necessary to investigate the association of serum YKL-40 level with ventricular remodeling in acute myocardial infarction patient.Methods: 78 cases of patients with acute ST segment elevation myocardial infarction were chosen between September 2013 and December 2014 in the second hospital of Hebei medical university. The included object of study Based on cardiovascular disease branch of Chinese medical association in 2011 myocardial infarction diagnostic criteria. Anteriorly myocardial infarction, heart failure and other heart disease can lead structural changes, such as high blood pressure for a long time, congenital heart disease, heart valve disease, renal insufficiency, abnormal liver function or a history of chronic hepatitis, arthritis, cancer, asthma, and autoimmune diseases, recently there are all sorts of infected patients were excluded. Venous blood samples were drawn at intervals during the index admission(0-12 h, 12-24 h, 24-48 h,48-72 h, 72-96 h, and >96 h) from the onset of chest pain until discharge in 78 patients with AMI. Serum YKL-40 was measured using enzyme-linked immune-sorbent assay. Acute myocardial infarction after admission in accordance with the guide of conventional treatment,thrombolysis indications given thrombolysis, patients with emergency PTCA conditions in the second hospital, Hebei medical university international give corresponding treatment. All of the patients without taboo, give the standard drug therapy. 30 subjects with stable coronary artery disease were chosen as control. Stable coronary heart disease diagnose refer to ESC 2013 guide for stable coronary heart diseases. Peripheral venous blood would be taken in first 24 hours, YKL-40 was measured using enzyme-linked immune-sorbent assay. Collect all the general clinical data, including name, gender, age, height, weight, smoking history, past medical history(high blood pressure, diabetes, hyperlipidemia and other cardiovascular disease risk factors), regular routine blood, blood biochemistry, electrocardiogram, chest radiograph and ECG to exceed examination. Echocardiographic(ECG) assessment of LV volumes, LV ejection fraction(LVEF), and wall motion index score were assessed before discharge and follow-up(median 180, range 153-207 days) for patients. Application of SPSS 19.0 statistical package analysis, measurement data are first to normality test, standard deviation of the normal distribution expressed as mean ± standard deviation, the count data expressed as a percentage. Repeated measurement data mean compared using analysis of variance of repeated measurement data, measured data before and after comparison mean using matching t test. Obey the normal distribution of each variable comparing with Pearson correlation between linear correlation analyses, P < 0.05 statistically significant.Result: 1 This study enrolled 78 cases of patients with ST-elevated acute myocardial infarction, male(57.7%), mean age(52.6 ±9.2), 30 patients with stable coronary heart disease, male(56.7%), average age(53.8 ± 7.2). Age and sex between the group of acute myocardial infarction and the stable coronary heart disease have no statistical significance(P > 0.05).2 Acute myocardial infarction patients serum YKL-40 after myocardial infarction 0-12 hours(234.41±43.33), 12 to 24 hours(220.65 ±46.06) is the maximal, present a peak, and no statistical difference between two groups(P = 0.702). 24 hours later fall to a plateau, the serum levels of YKL-40,24-48 hours(96 ±28.39), 48-72 hours(92.49±27.56), 72-96 hours(99.73±21.74) and >96 hours(97.35± 21.4), and each group of 24 hours later have no statistical difference(each P<0.001). 3 Peak of serum YKL-40 in patients with acute myocardial infarction(0-12 hours(234.41 ±43.33 respective) and the number of white blood cells(R = 0.24, P = 0.24) and number of neutrophils(R = 0.235, P = 0.235) are positive correlation. 4 Peak of serum YKL-40 in patients with acute myocardial infarction(0-12 hours respective) and LVEF in admission(R=-0.327 P=0.003) showed a negative correlation, and admission ventricular wall motion index were positively correlated(R = 0.157, P = 0.157). And the changes of left ventricular end-diastolic volume(Δ LVEDV 9.67± 23.83) from admission and follow-up were positively correlated(R = 0.361, P = 0.361). 5 Plateau of serum YKL-40 in patients with acute myocardial infarction(12-24 hours respective) and 6 month follow-up LVEF(41.67±7.11) showed a positively correlation(R=0.23 P= 0.043), and 6 month follow-up ventricular wall motion index were negative correlated(R=-0.311 P=0.019). And the changes of left ventricular end-diastolic volume(Δ LVEDV 9.67± 23.83) from admission and follow-up were negative correlated(R=-0.462 P<0.001).Conclusion: Serum YKL-40 is elevated following AMI. YKL-40 is related to LV remodeling and functions following AMI. Higher early levels of YKL-40 positively associate with the LV remodeling and circulating WBC levels. In contrast, higher plateau levels later after AMI are negative associated with relative preservation of LV remodeling. |