Background Factors affecting heart rate variability (HRV) in patients with atrial septal defect (ASD) have not been clarified. This study sought to identify those factors and establish a preliminary risk model. Methods A total of 154 patients with ASD who underwent transcatheter closure and met the study requirements were analyzed in this study. Moreover, 26 patients with patent foramen ovale (PFO) were enrolled in our study as a control group. All patients underwent echocardiography and ambulatory electrocardiography before and one day after the procedure. Results The standard deviation of all normal-to-normal (NN) intervals (SDNN) and the standard deviation of the averages of the NN intervals in all 5 min segments of the entire recording (SDANN) were significantly higher and the heart rate was lower after closure than before closure in patients with ASD (SDNN: 6.08, 95% CI 3.00 to 9.15, p < 0.001; SDANN: 7.57, 95% CI 4.50 to 10.64, p < 0.001; heart rate: -1.17, 95% CI − 2.86 to − 0.48, p = 0.006). Multiple regression analyses indicated that age, sex, defect diameter, heart rate and diabetes were significantly associated with HRV indices (SDNN: R2 = 0.415; P < 0.001). SDNN and SDANN had obvious correlations with right ventricular systolic pressure (SDNN: R = − 0.370, p < 0.001; SDANN: R = − 0.360, p < 0.001). Conclusions Factors affecting HRV in patients with ASD include age, sex, heart rate, defect size and diabetes. Furthermore, right ventricular systolic pressure plays an important role in the change in HRV.
Ginkgolide A (GA), a main terpenoid extracted from Ginkgo biloba, possesses biological activities such as anti-inflammatory, anti-tumor, and liver protection. However, the inhibitory effects of GA on septic cardiomyopathy remain unclear. This study aimed to explore the effects and mechanisms of GA in countering sepsis-induced cardiac dysfunction and injury. In lipopolysaccharide (LPS)-induced mouse model, GA alleviated mitochondrial injury and cardiac dysfunction. GA also significantly reduced the production of inflammatory and apoptotic cells, the release of inflammatory indicators, and the expression of oxidative stress-associated and apoptosis-associated markers, but increased the expression of pivotal antioxidant enzymes in hearts from LPS group. These results were consistent with those of in vitro experiments based on H9C2 cells. Database analysis and molecular docking suggested that FoxO1 was targeted by GA, as shown by stable hydrogen bonds formed between GA with SER-39 and ASN-29 of FoxO1. GA reversed LPS-induced downregulation of nucleus FoxO1 and upregulation of p-FoxO1 in H9C2 cells. FoxO1 knockdown abolished the protective properties of GA in vitro. KLF15, TXN2, NOTCH1, and XBP1, as the downstream genes of FoxO1, also exerted protective effects. We concluded that GA could alleviate LPS-induced septic cardiomyopathy via binding to FoxO1 to attenuate cardiomyocyte inflammation, oxidative stress, and apoptosis.
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