Growth differentiation factor 15 is associated with left atrial/left atrial appendage thrombus in patients with nonvalvular atrial fibrillation

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Abstract

Background: There is evidence suggesting that growth differentiation factor 15 (GDF-15) appears to be associated with stroke in patients with atrial fibrillation (AF). AF-related thromboembolic stroke is predominantly attributed to the thrombus from the left atrium (LA) or left atrial appendage (LAA). Hypothesis: GDF-15 is related to LA/LAA thrombus in nonvalvular AF (NVAF) patients. Methods: A total of 894 patients with NVAF without anticoagulation therapy were included in this study. All patients routinely underwent transesophageal echocardiography for detection of LA/LAA thrombus. GDF-15 was measured by enzyme-linked immunosorbent assay. Logistic regression models were used to test for association. Results: LA/LAA thrombus was detected by transesophageal echocardiography in 69 (7.72%) patients with AF. The GDF-15 levels in the patients with LA/LAA thrombus were significantly higher than those without LA/LAA thrombus (log10 GDF-15: 2.989 ± 0.023 ng/L vs 2.831 ± 0.007 ng/L; P < 0.001). Logistic regression analysis showed that GDF-15 was an independent risk factor for LA/LAA thrombus (odds ratio [per quarter]: 1.799, 95% confidence interval: 1.381-2.344, P < 0.001) after adjusting for potential clinical risk factors. The optimal cutoff point for GDF-15 predicting LA/LAA thrombus was 809.9 ng/L (sensitivity, 75.3%; specificity, 61.5%), determined by ROC curve. The area under the curve was 0.709 (95% confidence interval: 0.644-0.770, P < 0.001). Conclusions: Elevated GDF-15 indicated a significantly increased risk for LA/LAA thrombus in NVAF patients. Thus, GDF-15 might be a potentially useful adjunct in discriminating LA/LAA thrombus in NVAF patients.

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Hu, X. F., Zhan, R., Xu, S., Wang, J., Wu, J., Liu, X., … Chen, L. (2018). Growth differentiation factor 15 is associated with left atrial/left atrial appendage thrombus in patients with nonvalvular atrial fibrillation. Clinical Cardiology, 41(1), 34–38. https://doi.org/10.1002/clc.22844

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