The Impact of the Duration of Cardiac Troponin I Elevation on the Clinical Prognosis as Well as Incidence of New-Onset Atrial Fibrillation Respectively in Elderly Non-ST-Elevation Acute Myocardial Infarction Patients without PCI

心肌肌钙蛋白I升高持续时间对未接受经皮冠状动脉介入治疗(PCI)的老年非ST段抬高型急性心肌梗死患者的临床预后及新发房颤发生率的影响。

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Abstract

OBJECTIVE: This study aimed to investigate the impact of the duration of cardiac troponin I (TnI) elevation on the prognosis and incidence of new-onset atrial fibrillation (NOAF) in elderly patients with non-ST-elevation acute myocardial infarction (NSTE-AMI). METHODS: A total of 383 NSTE-AMI patients ≥75 years old were enrolled in this study and divided into two groups: in 194 cases, the duration of TnI elevation was ≥14 days (group 1), and in 189 cases, the duration of TnI elevation was <14 days (group 2). The patients were followed up for 60 months. The effect of TnI on prognosis was studied by cohort. The primary endpoint was a composite endpoint of cardiovascular death, reinfarction, ischemic stroke, and hospitalization for heart failure, and the secondary endpoint was all-cause death. A case-control study design was adopted to analyze the influencing factors of NOAF occurrence in Group 1 and Group 2. RESULTS: The median duration of follow-up was 26 months. Multivariate Cox's regression analysis revealed that the duration of TnI elevation ≥14 days and diuretic use were independent variables of the major composite endpoint (p < 0.01 for both), and the left ventricular ejection fraction and the duration of TnI elevation ≥14 days were independent related variables of all-cause death (p < 0.05). The duration of TnI elevation ≥14 days was correlated with the occurrence of NOAF, but, in the multivariate logistic regression model, only uric acid and high-sensitivity C-reactive protein were independently associated with NOAF (p < 0.05). CONCLUSION: The duration of TnI elevation ≥14 days was the independent correlation factor of the major composite endpoint and all-cause death; high sensitivity C-reactive protein and uric acid are independent risk factors for NOAF.

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