[Effect of distal ischemic preconditioning on cardiovascular events in adult patients with hip fracture one year after operation].

OBJECTIVE: To investigate the effect of remote ischemic preconditioning (RIPC) on major adverse cardiovascular events (MACE) in elderly patients with hip fracture 1 year after operation. METHODS: Total of 314 elderly patients with hip fracture of gradeⅡand Ⅲ for American Society of Anesthesiologists (ASA) were treated by surgical operation from April 2015 to May 2020 including 116 males and 198 females, the age ranged from 60 to 76 years old. The subjects were divided into intervention group and control group according to whether received RIPC. Among them, 157 cases in intervention group included 56 males and 101 females with an average age of (68.12±7.13) years old and 157 cases in control group included 60 males and 97 females with an average age of (68.24±7.05) years old. Both groups were given routine anesthesia. The intervention group was treated with RIPC on the basis of routine anesthesia. The MACE events 1 year after operation in two groups were compared and analyzed. RESULTS: The OR values of RIPC for myocardial infarction, heart failure, stroke, nonfatal cardiac arrest, coronary revascularization, severe arrhythmia, peripheral artery thrombosis, readmission of cardiovascular disease, and all-cause death in patients with hip fracture one year after operation were 1.269, 1.304, 0.977, 1.089, 1.315, 1.335, 0.896, 0.774, 1.191, respectively, but there was no significant difference (P>0.05). CONCLUSION: RIPC did not significantly affect and change the occurrence of major cardiovascular adverse events within 1 year after hip fracture surgery. The long term impact of RIPC on clinical cardiovascular outcomes in non cardiac surgery needs to be confirmed in appropriate randomized clinical trials.

Desmoplakin and clinical manifestations of desmoplakin cardiomyopathy.

ABSTRACT: Desmoplakin (DSP), encoded by the DSP gene, is the main desmosome component and is abundant in the myocardial tissue. There are three DSP isoforms that assume the role of supporting structural stability through intercellular adhesion. It has been found that DSP regulates the transcription of adipogenic and fibrogenic genes, and maintains appropriate electrical conductivity by regulating gap junctions and ion channels. DSP is essential for normal myocardial development and the maintenance of its structural functions. Studies have suggested that DSP gene mutations are associated with a variety of hereditary cardiomyopathy, such as arrhythmia cardiomyopathy, dilated cardiomyopathy (DCM), left ventricular noncompaction, and is also closely associated with the Carvajal syndrome, Naxos disease, and erythro-keratodermia-cardiomyopathy syndrome with skin and heart damage. The structure and function of DSP, as well as the clinical manifestations of DSP-related cardiomyopathy were reviewed in this article.

Overexpression of microRNA-590-3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF-κB signaling pathway by binding to RIPK1.

Ischemic heart disease is widely considered as a major health threat, which causes a high number of deaths every year worldwide. Much evidence has shown that oxidative stress (OS) is implicated in the pathogenesis of ischemia-reperfusion injury (IRI). This study aims to evaluate the effect of miR-590-3p on the OS of IRI mice through the nuclear factor kappa-B (NF-κB) signaling pathway by targeting receptor-interacting protein kinase 1 (RIPK1). IRI mouse models were established for extracting myocardial tissues and isolating myocardial cells. The expression of inflammatory related-factors was detected by enzyme-linked immunosorbent assay, and superoxide dismutase (SOD) and malondialdehyde (MDA) in tissues were determined. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were performed to assess the role of miR-590-3p in the expression of NF-κB-related factors and apoptosis-related factors. Besides, the regulatory effects of miR-590-3p on myocardial cell proliferation and apoptosis were also assessed. According to the obtained results, we found that IRI mice displayed higher expression of tumor necrosis factor-α, interleukin (IL)-6, and interferon-γ, lower expression of IL-10 in serum, a decreased SOD level, and an increased MDA level. In addition, RIPK1 was determined as a target gene of miR-590-3p. After transfection of overexpressed miR-590-3p or si-RIPK1, declined RIPK1, NF-κB, Toll-like receptor 4, caspase-3, FasL, p53, and c-myc levels, increased B-cell lymphoma-2 level, promoted cell proliferation, promoted cell cycle distribution and inhibited apoptosis of myocardial cells were found. Our study demonstrates that miR-590-3p can alleviate the OS of IRI mice through the inhibition of the RIPK1 and NF-κB signaling pathway. Thus, miR-590-3p represents a potential target for IRI repair.

Predictive value of serum uric acid on cardiovascular disease and all-cause mortality in urban Chinese patients.

BACKGROUND: The association between increased serum uric acid (SUA) levels and cardiovascular risk has been debated for decades. Several large studies have provided conflicting results regarding the clinical significance of elevated SUA levels in cardiovascular disease (CVD) or cerebrovascular disease. The aim of this study was to investigate the relationship between SUA and CVD and all-cause mortality and their potential diagnostic value. METHODS: A total of 3570 in-patients ranging in age from 56 to 95 years (mean (67.36 +/- 11.36) years) were selected from 20 hospitals in Beijing and Shanghai. A carefully designed questionnaire was used to gather baseline data of each patient. All patients were divided into two main groups according to their SUA levels: high SUA and normal SUA groups. Serum indices and other important parameters were measured. RESULTS: Compared with normal SUA group, high SUA group had significant difference in systolic blood pressure (SBP), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), body mass index (BMI), and age (P < 0.05 or P < 0.01). High SUA prevailed in female and patients with history of essential hypertension, while history of smoking and diabetes showed no significant difference between two groups. All-cause and CVD mortality occurred more frequently in high SUA group than in normal SUA group. In the accumulative survival analysis, high SUA group had lower survival rate than normal SUA group both in CVD and all-cause mortality. COX regression analysis indicated that the history of smoking, age and high SUA were independent risk factors for the development of CVD. CONCLUSIONS: These preliminary observations suggest that patients with high SUA levels would face higher risk of mortality. SUA measurement may be applied as a routine predictor for clinical assessment.

[The relation between angiotensin II receptors 1 and 2, and CYP11B2 and atrial structural remodeling in patients with atrial fibrillation].

OBJECTIVE: To investigate the relation between of the angiotensin II receptors 1 and 2 (AT1-R and AT2-R), and aldosterone (Ald) synthetase CYP11B2 gene expression and atrial structural remodeling. METHODS: Thirty-eight patients were divided into three groups: sinus rhythm (SR) group (n = 11), paroxysmal atrial fibrillation (pAF) group (n = 13, with a duration of AF < 6 months), and constant atrial fibrillation (cAF) group (n = 14, with a duration of AF > 6 months) and underwent open thoracic surgery. 500 mg of tissue of right appendage was taken during the off-pump operation (tissue of left appendage was also taken in 8 patients of the cAF group). The levels of AT1-R, AT2-R, and CYP11B2 were detected. With semiquantitative polymerase chain reaction. Immunohistochemistry was used to localize AT1-R. RESULTS: The mean diameter of the left atrium of the cAF group was (5.8 +/- 0.6) cm, significantly greater than those of the pAF and SR groups (4.2 +/- 0.7) cm and (3.3 +/- 0.4) cm respectively, (both P < 0.01). However, there was not significant difference in the mean diameter of left atrium between the pAF and SR groups (P > 0.05). The CYP11B2R mRNA expression of the cAF group was 0.41 +/- 0.03, significantly higher than those of the pAF and SR groups (0.27 +/- 0.09 and 0.23 +/- 0.01 respectively, both P < 0.05). The AT1-R mRN expression level of the cAF group was 1.03 +/- 0.04, significantly lower than that of the SR group (0.90 +/- 0.10, P < 0.05). The AT2-R mRNA expression level of the cAF group was 1.16 +/- 0.16, significantly higher than that of the SR group (0.90 +/- 0.10, P < 0.05). In the SR group the AT1-R protein expression was mainly seen in the cellular membrane of the atrial cardiac muscle cells and rarely seen in the fibroblasts and vascular sooth muscle cells, however, in the pAF group AT1-R positive staining was seen in the cellular membrane, cytoplasm of the atrial cardiac cells, fibroblasts, and vascular sooth muscle cells, and the AT1-R positive staining of the cAF group was stronger than that of the pAF group and weaker then that of the SR group. CONCLUSION: The atrial structural remodeling is mediated by tissue RAS. The downregulation of AT1-R mRNA is probably an excessive reaction of atrial myocardium to tissue Ang II, while the upregulation of AT2-R mRNA is probably an adaptive and compensatory reaction of atrial myocardium to tissue Ang II. The regulation of AT-R may occur at the level of transcription and translation of the protein synthesis. In the cAF and pAF patients, the increase of the gene expression of CYP11B2 shows that Ald may be involved in the pathophysiological process of atrial remodeling in AF.