Adropin - A new player in energy regulation predicts long-term prognosis of patients with acute myocardial infarction.

Background: As a novel energy homeostasis regulator, Adropin not only plays a vital part in meditating energy metabolism, but also has a certain correlation with atherosclerotic diseases. The purpose of this study was to evaluate the effect of Adropin on the long-term prognosis of patients with acute myocardial infarction (AMI). Methods: 162 recruited patients with AMI were divided into low Adropin group (Adropin<166.3 pg/mL, n = 82) and high Adropin group (Adropin≥166.3 pg/mL, n = 80), according to the mean value of serum Adropin level. Patients were followed up and major adverse cardiac events (MACEs) were recorded. The Kaplan-Meier method and Cox regression model were used to evaluate the survival of patients and the related factors of cardiac events. Results: Diabetes was more common in low Adropin group than that in high Adropin group (P < 0.05). Patients were followed up for an average of 50.3 ± 19.2 months. MACEs occurred in 37 patients (22.8%), including 6 cardiac deaths (3.7%), 14 recurrent myocardial infarction (8.6%) and 17 rehospitalization of heart failure (10.5%). The incidence of recurrent myocardial infarction in low Adropin group was higher than that in high Adropin group (13.4% vs 3.8%, P < 0.05). There was no significant difference in the overall incidence of MACE, cardiac death and rehospitalization of heart failure between the two groups. Kaplan-Meier method (log rank test) analysis results showed that patients with low Adropin had lower survival rate without recurrent myocardial infarction (log rank P = 0.035). Conclusion: Low Adropin level was associated with an increased risk of long-term recurrent myocardial infarction in patients with AMI.

Relationship between red blood cell-related indices and coronary artery calcification.

BACKGROUND: Red blood cell (RBC) indices such as RBC count and RBC distribution width (RDW) are associated with heart failure and coronary artery disease, but the relationship between RBC indices and coronary artery calcification (CAC) is unclear. This study aimed to investigate RBC indices' correlation with, and predictive value for, the presence and severity of CAC. METHODS: In this study, 1257 hospitalized patients who received a coronary computed tomography angiography examination were finally selected. Patients were classified into a control group (without CAC, n = 655) and a calcification group (with CAC, n = 602) according to their CAC score. The calcification group was further divided into a low calcification group, medium calcification group, and high calcification group. RESULTS: In the calcification group, the RBC count was lower, and the RDW-standard deviation (SD) and RDW-coefficient of variation (CV) were higher, than those in the control group (P < .05). In the high calcification group, the RBC count was significantly lower, and the RDW-SD and RDW-CV were significantly higher, than those in the low calcification group (P < .05). Multivariate logistic regression analysis showed that RBC count, RDW-SD, and RDW-CV were independent predictors of CAC presence. Furthermore, multivariate logistic regression analysis also showed that RBC count and RDW-SD were independent predictors of severe CAC. CONCLUSIONS: RBC indices were significantly associated with the presence and severity of CAC, indicating that these RBC indices have the potential to be predictors of CAC.

Adropin Inhibits Vascular Smooth Muscle Cell Osteogenic Differentiation to Alleviate Vascular Calcification via the JAK2/STAT3 Signaling Pathway.

Vascular calcification is characterized as the deposition of hydroxyapatite mineral in the form of calcium-phosphate complexes in the vasculature. Transdifferentiation between vascular smooth muscle cells (VSMCs) and osteoblast-like cells is considered essential in the progression of vascular calcification. The pathophysiological mechanisms underlying vascular calcification and VSMC osteogenic differentiation remain to be fully elucidated, and the development of novel therapies is required. In the present study, PCR and western blot analysis were conducted to quantify the mRNA and protein expression levels of calcification-associated markers (bone morphogenetic protein 2, alkaline phosphatase, osteoprotegerin, osteocalcin, and runt-related transcription factor 2) and adropin in VSMCs and rat vascular tissues. The calcification of VSMCs was assessed using alizarin red staining. Moreover, adropin expression levels in VSMCs were analyzed using immunofluorescence. Lentiviral transfection and small interfering RNA were used for overexpression and knockdown of adropin in VSMCs, respectively. The results demonstrated that adropin alleviated vascular calcification in vivo. Moreover, adropin also inhibited osteogenic differentiation and the calcification of VSMCs in vitro. Notably, results of the present study revealed that the tyrosine protein kinase JAK2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway played a key role in the aforementioned inhibition. In conclusion, the results of the present study demonstrated that adropin inhibited VSMC osteogenic differentiation to alleviate vascular calcification via the JAK2/STAT3 signaling pathway.

Association of cystatin C with coronary artery calcification in patients undergoing multidetector computed tomography.

ABSTRACT: Cystatin C is associated with atherosclerosis, but the relationship between cystatin C and coronary artery calcification (CAC) is uncertain. The purpose of this study was to evaluate the predictive value of cystatin C on the occurrence and severity of CAC.A total of 1447 hospitalized patients with coronary computed tomography angiography were selected in this study. According to the CAC score (CACS), patients were divided into calcification group (with CAC, n = 749) and control group (without CAC, n = 698). The calcification group was further divided into low calcification group (CACS < 100, n = 407), medium calcification group (CACS 100-400, n = 203), and high calcification group (CACS≥400, n = 139).Patients with CAC had higher cystatin C level than those in control group (P < .05). With the increase of calcification score, the cystatin C level showed an upward trend. The cystatin C level in the high calcification group was significantly higher than those in the low and medium calcification group (P < .05). ROC curve analysis showed that cystatin C had a high predictive value for the occurrence of CAC [area under the curve 0.640, 95% confidence interval (95% CI) 0.591-0.690, cut-off value 0.945 mg/L, sensitivity 0.683, specificity 0.558, P < .05] and severe CAC (area under the curve 0.638, 95% CI 0.550-0.762, cut-off value 0.965 mg/L, sensitivity 0.865, specificity 0.398, P < .05). Multivariate logistic regression analysis showed that cystatin C was an independent predictor of severe CAC (AOR 3.748, 95% CI 1.138-10.044, P < .05).Cystatin C was significantly associated with the occurrence and severity of CAC, suggesting that cystatin C had the potential as a predictor of CAC.

Obesity paradox in pulmonary hypertension due to left ventricular systolic dysfunction.

OBJECTIVE: Pulmonary hypertension (PH) due to left ventricular systolic dysfunction (PH-HFrEF) is a common heart disease with poor prognosis. In this study, we explored the risk factors for PH-HFrEF and investigated the related factors affecting the prognosis of PH-HFrEF patients. METHODS: The study recruited consecutive patients with PH-HFrEF and systolic pulmonary artery pressure (sPAP) of more than 40 mm Hg with left ventricular ejection fraction (LVEF) of less than 45% on echocardiography. Patients with left ventricular systolic dysfunction (HFrEF) but without PH (sPAP < 30 mmHg and LVEF < 45%) were chosen as the control group. Patients were followed up for 18 months, and major adverse cardiac events (MACE) were recorded. RESULTS: In total, 93 patients with PH-HFrEF formed the study group and 93 LVEF-matched patients with HFrEF were enrolled as controls. Body mass index (BMI) in PH-HFrEF patients was significantly lower compared with the control group (p < 0.05). Multivariate logistic regression analysis revealed that low BMI was an independent predictor of the presence of PH in patients with HFrEF (p < 0.05). There were 23 (24.7%) MACE in the PH-HFrEF group and 18 (19.4%) MACE in the control group. Cox regression analysis showed that low BMI was an independent predictor of MACE occurrence in the PH-HFrEF group (p < 0.05). CONCLUSION: Low BMI appear to be significantly associated with PH occurrence in patients with HFrEF, and is an independent predictor of MACE in patients with PH-HFrEF.

Puerarin alleviates coronary heart disease via suppressing inflammation in a rat model.

BACKGROUND: Puerarin shows inhibitory effects on inflammation in chronic heart failure (CHF), but its efficacy in coronary heart disease (CHD) remained vague. METHODS: Rat CHD model was constructed, and serum parameters were determined using a blood liquid biochemical analyzer. Also, contents of creatine kinase (CK), creatine kinase MB isoenzyme (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin (cTnT) were measured using colorimetry. Histological examination was conducted with Hematoxylin-Eosin (H&E) staining, and cardiac function was assessed by Echocardiography. Cell apoptosis was detected using Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Relative expressions were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed. RESULTS: In CHD rats, the levels of TC, LDL and TG and the expressions of matrix metalloproteinase-9 (MMP-9), CD40 ligand (CD40L), tumor necrosis factor-α (TNF-α) and C-reactive protein (CRP) were increased while HDL level was decreased, accompanied with inflammatory cell infiltration and cardiac malfunction. Also, the contents of CK, CK-MB, LDH and cTnT, the percentage of apoptotic cells, the expressions of Bcl-2 associated X protein (Bax), cleaved Caspase-3, TNF-α, Interleukin-ß (IL-ß), IL-6 and Lipoprotein-associated Phospholipase A2 (Lp-PLA2) expressions and the levels of oxidized-(ox-)LDL and malondialdehyde (MDA) were upregulated, while the level of super oxidase dismutase (SOD) and the expressions of B cell lymphoma-2 (Bcl-2) and vascular endothelial growth factor (VEGF) were downregulated. However, Puerarin ameliorated the effects of CHD model construction, suppressed nuclear factor-(NF-)κB expression, and enhanced the expressions of Farnesoid X Receptor (FXR), phosphorylated-AKT (p-AKT) and phosphorylated-signal transducer and activator of transcription 3 (p-STAT3). CONCLUSION: Puerarin alleviated CHD in rats via inhibiting inflammation, providing possible method for CHD treatment.