Study On The Dynamic Changes Of Plasma BNP, CTnI, CKMB And IL-8 Levels And Relationship Of Those Markers With Heart Function In Patients With AVA Formation After AMI

Objective: Acute ventricular aneurysm (AVA) is a seriouscomplication of acute myocardial infarction (AMI) that may leadglobal left ventricular dysfunction, so it has a harmful influenceon the prognosis of patients with AMI. Many new evidencesshow that neuroendocrine activation play important roles in leftventricular remodeling (LVR) after acute myocardial infarction.Brain natriuretic peptide (BNP) is a neurohormone secretedmainly in the cardiac ventricles in response to volume expansionand pressure overload. BNP levels are increased markedly inpatients with AMI and may reflect the severity and prognosis ofheart failure. Cardiac troponin-I (cTnI) is a highly specific andsensitive marker of the cardiac damage that has been found inrecent years, so it has a important clinical value on the severitygrading and heart function estimation of AMI patients. Creatinekinase MB (CKMB) is also a specific and sensitive marker of thecardiac damage. Interleukin-8 (IL-8) is a powerful regulator ofimmunology and inflammation. Its peak time is earlier than thatof CKMB and cTnI in AMI, so IL-8 is one of the new referencemarkers of the diagnosis in early phase of AMI. These Markers 5英 文 摘 要play an important role in patients with AVA formation after AMI.This study is to investigate the dynamic changes of plasmaconcentrations of these markers and relationship of these markerswith heart function and prognosis in patients with AVA formationafter AMI. Methods: 62 patients who suffered from primary anterioracute myocardial infarction were enrolled in this study from Aug,2002 to Dec 2003, and were divided into AVA group and non-AVA group according to left ventricular angiography (LVG). Thediagnosis of AMI was according to the criterion of ACC/AHA: 1)New onset of chest pain lasting more than half an hour; 2) Theelectrocardiographic evidence of ST-segment elevation thatevolved into two or more bordering leads; 3) diagnostic elevationin creatine kinase (CK), CK-MB and /or positive Troponin T;Patients were excluded if they had the history of old myocardialinfarction, serious valvular heart disease, dilated andhypertrophic cardiomyopathy. The patients with medium orserious insufficiency of renal function and cancer were alsoexcluded. All patients were performed coronary angiography(CAG), percutaneous coronary intervention (PCI) and LVG, andthen divided into two groups according to the AVA formation.AVA was diagnosed according to the criterion of The CoronaryArtery Surgery Study (CASS) and Hirai. Left ventricular enddiastolic pressure (LVEDP) was recorded during LVG and all thepatients were performed equilibrium radionuclideangiocardiography (ERNA). The blood samples were obtained at 6英 文 摘 要the time of 6h, 12h, 18h, 1d, 2d, 3d, 5d, and 24w after the onsetof symptoms. ELISA determined the levels of plasma BNP.Immulite analyzer determined the levels of plasma cTnI andCKMB and the levels of plasma IL-8 were determined byradioimmunoassay. We used SAS 6.12 statistics software toanalysis all the data. Statistical significance was indicated by Pvalue <0.05. Results: 1. Clinical features: There were no significantdifferences about the age, sex, history of diabetes, hypertension,hyperlipidemia, smoking and drinking between the two groups.2. The BNP peak concentrations were higher in AVA group thanthose of non-AVA group(12.30±2.24ng/ml vs 9.92±2.54ng/ml,P<0.01). The peak time was earlier in AVA group than that ofnon-AVA group, peaking at 20.48±3.77h in AVA group and22.55±3.68h in non- AVA group. The BNP concentrations werealso higher in AVA group than those of non- AVA group at 7day(9.47±1.95ng/ml vs 6.65±1.56ng/ml, P<0.05)and 24week(5.36±1.43ng/ml vs 3.27±1.12ng/ml, P<0.05)3. The cTnIpeak concentrations were higher in AVA group than those ofnon-AVA group(161.59 ± 14.89ng/ml vs...