Physical activity and transitioning to retirement: evidence from the China health and retirement longitudinal study.

BACKGROUND: The impact of retirement on physical activity among older individuals remains ambiguous. This study aims to investigate the influence of retirement on physical activity and delineate the trajectories of physical activity changes during the retirement transition among elderly Chinese residents. Additionally, we endeavor to examine the factors that contribute to each trajectory. METHODS: This longitudinal cohort study used data from four surveys of the China Health and Retirement Longitudinal Study and included a sample of 428 individuals who underwent formal retirement and provided information on physical activity. We employed generalized estimating equation to explore the impact of the retirement transition on physical activity among Chinese older adults. Latent class growth analysis was used to identify distinct trajectories of physical activity, and binary logistic regression was performed to identify pre-retirement factors influencing changes in physical activity. RESULTS: Our findings indicate that retirement can lead to a decline in physical activity among older Chinese residents (OR = 0.85, 95%CI 0.75 ~ 0.97). We identified three distinct trajectories of physical activity during the retirement transition: Trajectory 1 - "sustained low level of physical activity" (7.94%); Trajectory 2 - "middle level of physical activity with gradual decline" (69.16%); Trajectory 3 - "sustained high level of physical activity with significant fluctuations" (22.90%). Furthermore, we discovered that individuals in the "middle level of physical activity and gradual decline" trajectory were more likely to have an annual income exceeding 40,000 yuan (OR = 9.69, 95%CI 1.12 ~ 83.63), reside in urban areas (OR = 2.27, 95%CI 1.14 ~ 4.52), and have a fondness for playing Mahjong (OR = 2.42, 95%CI 1.18 ~ 5.00) compared to those in the "sustained high level of physical activity with significant fluctuations" trajectory. Additionally, having an annual income exceeding 40,000 yuan (OR = 19.67, 95%CI 1.30 ~ 298.61) predicted membership in the "sustained low level of physical activity" trajectory when compared to the "sustained high level of physical activity with significant fluctuations" trajectory. CONCLUSION: Retirement represents a substantial milestone in the life course and is associated with notable alterations in physical activity patterns. Among older Chinese residents, the trajectories of physical activity during the retirement transition exhibit diverse paths and are influenced by pre-retirement factors, including annual income, residential location, and hobbies. The findings of this study have important implications for the formulation of policies aimed at promoting healthy aging among individuals approaching retirement age.

Lansoprazole-induced osteoporosis via the IP3R- and SOCE-mediated calcium signaling pathways.

BACKGROUND: Many clinical studies have shown a correlation between proton pump inhibitors (PPIs) and osteoporosis or fractures. The purpose of this study was to establish a murine model of chronic oral PPI administration to verify whether PPIs caused bone metabolic impairment and investigate the relevant molecular mechanism underlying the effects of PPIs on MC3T3-E1 murine osteoblasts. METHODS: A lansoprazole-induced bone loss model was used to investigate the damaging effects of PPIs. In vivo, immunohistochemistry, Hematoxylin-Eosin (HE) staining, micro-CT analysis, and blood biochemical analyses were used to evaluate the effect of lansoprazole on bone injury in mice. In vitro, the effects of lansoprazole and related signaling pathways in MC3T3-E1 cells were investigated by CCK-8 assays, EdU assays, flow cytometry, laser confocal microscopy, patch clamping, reverse transcription-quantitative polymerase chain reaction and Western blotting. RESULTS: After 6 months of lansoprazole gavage in ICR mice, the micro-CT results showed that compared with that in the vehicle group, the bone mineral density (BMD) in the high-dose group was significantly decreased (P < 0.05), and the bone microarchitecture gradually degraded. Biochemical analysis of bone serum showed that blood calcium and phosphorus were both decreased (P < 0.01). We found that long-term administration of lansoprazole impaired skeletal function in mice. In vitro, we found that lansoprazole (LPZ) could cause calcium overload in MC3T3-E1 cells leading to apoptosis, and 2-APB, an inhibitor of IP3R calcium release channel and SOCE pathway, effectively blocked increase in calcium caused by LPZ, thus protecting cell viability. CONCLUSIONS: Longterm administration of LPZ induced osteoporotic symptoms in mice, and LPZ triggered calcium increases in osteoblasts in a concentration-dependent manner. Intracellular calcium ([Ca2+]i) persisted at a high concentration, thereby causing endoplasmic reticulum stress (ERS) and inducing osteoblast apoptosis.

Imatinib-induced hepatotoxicity via oxidative stress and activation of NLRP3 inflammasome: an in vitro and in vivo study.

Imatinib (IM), a milestone drug used in the field of molecular targeted therapy, has been reported to cause serious adverse liver effects, including liver failure and even death. Immune-mediated injury and mitochondrial dysfunction are involved in drug-induced liver injury. However, the mechanism of IM-induced hepatotoxicity remains unclear and warrants further study. In our study, Sprague Dawley rats were administered IM by gavage with 50 mg/kg body weight (BW) once daily for 10 days. Drug-induced liver injury accompanied by inflammatory infiltration was observed in rats following IM exposure, and the expression of NOD-like receptor protein 3 (NLRP3) inflammasome-related proteins was significantly increased compared with that of the control. HepG2 cells were exposed to 0-100 µM IM for 24 h. The results showed that IM decreased cell viability in a dose-dependent manner. Moreover, IM induced a state of obvious oxidative stress and activation of nuclear factor kappa B (NF-κB) in cells, which resulted in the activation of NLRP3 inflammasomes, including caspase 1 cleavage and IL-1ß release. These results were significantly reduced after the use of the antioxidants N-acetyl-l-cysteine or the NF-κB inhibitor pyrrolidine di-thio-carbamate. Furthermore, NLRP3 knockdown significantly reduced the release of inflammatory cytokines and improved cell viability. In summary, our data demonstrated that oxidative stress and NLRP3 inflammasome activation are involved in the process of IM-induced hepatotoxicity. The results of this study provide a reference for the prevention and treatment of IM-induced hepatotoxicity.

Overexpression of GAS5 inhibits abnormal activation of Wnt/ß-catenin signaling pathway in myocardial tissues of rats with coronary artery disease.

OBJECTIVE: The aim of this study is to investigate the clinical value of long noncoding RNA growth arrest-specific transcript 5 (LncRNA GAS5) in the diagnosis of coronary artery disease (CAD) and its protective effect on myocardial injury in rats with CAD. METHODS: Patients with CAD and healthy controls were selected to measure the expression of GAS5, and further to perform the correlation analysis and ROC curve. In addition, the rat models of CAD were also established to observe the effect of GAS5 on hyperlipidemia, myocardial injury, cardiomyocyte apoptosis, oxidative stress, and inflammatory injury of rats with CAD, and the effect of the Wnt/ß-catenin signaling pathway was also determined. RESULTS: Overexpression of GAS5 in CAD rats determines improvement of hyperlipidemia, attenuation of myocardial injury, inhibition of cardiomyocyte apoptosis, oxidative stress, inflammatory injury, and abnormal activation of the Wnt/ß-catenin signaling pathway in myocardial tissues. CONCLUSION: Our study demonstrates that downregulation of GAS5 is found in CAD, and overexpression of GAS5 inhibits abnormal activation of the Wnt/ß-catenin signaling pathway in myocardial tissues of CAD rats.

Upregulation of lncRNA VDR/CASC15 induced by facilitates cardiac hypertrophy through modulating miR-432-5p/TLR4 axis.

Sustained cardiac hypertrophy has threatened human health. With the development of human genome project, non-coding RNAs (ncRNAs) have attracted more and more attentions of researchers. As a subgroup of ncRNAs, long non-coding RNAs (lncRNAs) has been widely studied in human diseases, including cardiac hypertrophy. According to search results of bioinformatics website, lncRNA CASC15 potentially participates in the course of cardiac hypertrophy. According to the result of qRT-PCR, CASC15 expression was upregulated when cardiomyocytes were treated with Ang-II. Moreover, CASC15 was highly expressed in cardiac hypertrophic model. Upregulation of CASC15 was accompanied with some hypertrophic responses. To explore the specific biological function of CASC15 in cardiac hypertrophy, loss-of-function experiments were conducted in Ang-II-induced cardiomyocytes. Results of immunofluorence staining revealed that cell surface area enlarged by Ang-II was decreased when CASC15 was silenced. The expression levels of hypertrophic factors were attenuated by knockdown of CASC15. To detect the molecular mechanism by which CASC15 regulates the progression of cardiac hypertrophy, mechanism experiments were designed and carried out. It was found that CASC15 was activated by the transcription factor VDR. Furthermore, CASC15 can upregulate TLR4 by competitively binding miR-432-5p. In conclusion, Upregulation of lncRNA CASC15 induced by VDR facilitates cardiac hypertrophy via miR-432-5p/TLR4 axis.

[The predictive value of mild renal insufficiency on the prognosis of patients with acute coronary syndrome].

OBJECTIVE: To investigate the predictive value of mild renal insufficiency on the endpoint events in patients with acute coronary syndrome (ACS). METHODS: A total of 552 patients with ACS were enrolled in the present study. According to the levels of estimated glomerular filtration rate (eGFR), patients were divided into two groups, normal renal function (eGFR ≥ 90 ml×min(-1)×1.73 m(-2)) and mild renal insufficiency (60 ≤ eGFR<90 ml×min(-1)×1.73 m(-2)). The primary and secondary events were collected and analyzed through the present prospective follow-up study. RESULTS: The patients in mild renal insufficiency group had a higher incidence of the primary endpoint events than normal renal function group [31 cases (12.6%) vs 15 cases (4.9%), P = 0.001]. There was no difference of the secondary endpoint events incidence in the two groups. The incidence rate of all-cause mortality [8.9% (22 cases) vs 2.2% (7 cases), P < 0.001] and cardiac death [6.5% (16 cases) vs 1.3% (4 cases), P = 0.001] was higher in mild renal insufficiency group, but there was no statistical difference of incidence rate of no fatal stroke and myocardial infarction in the two groups. The results of COX regression analysis showed that the incidence of primary endpoint events in patients with mild renal dysfunction was 2.265 folds (95%CI 1.076-4.771, P = 0.031) of patients with normal renal function. Further analysis indicated that the predictive value of mild renal insufficiency was only for all-cause mortality (HR 3.118, 95%CI 1.197-8.125, P = 0.020), not for heart failure and revascularization. According to the Kaplan-Meier curves results, the incidences of the primary endpoint events (P = 0.004) and all-cause mortality (P = 0.001) were higher in mild renal insufficiency group than in normal renal function group. CONCLUSION: Mild renal insufficiency has important predictive value for primary endpoint events in patients with ACS.

Circ-JA760602 promotes the apoptosis of hypoxia-induced cardiomyocytes by transcriptionally suppressing BCL2.

Acute myocardial infarction (AMI) is myocardial necrosis caused by the complete or partial obstruction of a coronary artery. Circular RNAs (circRNAs) have been proven as regulators in the progression of various human diseases, including AMI. However, the role of novel circ-JA760602 in AMI remains unknown. Here, we investigated the role of circ-JA760602 in modulating the apoptosis of hypoxia-induced AMI cells using the AC16 cardiomyocyte in vitro cell model. The expression of circ-JA760602 in AC16 cardiomyocytes subjected to hypoxia was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was measured by cell counting kit-8 (CCK-8) assay. Apoptosis of cardiomyocytes was evaluated by TUNEL assay and flow cytometry analysis. The cellular location of circ-JA760602 was identified through fluorescence in situ hybridization (FISH) assay and subcellular fractionation assay. The downstream molecular mechanisms of circ-JA760602 were demonstrated by luciferase reporter assay, RNA binding protein immunoprecipitation (RIP) assay and chromatin immunoprecipitation (ChIP) assay. Rescue assays were performed to demonstrate the effects of BCL2 knockdown on circ-JA760602 silencing-mediated cardiomyocyte apoptosis. Circ-JA760602 expression was elevated after hypoxia treatment. Knockdown of circ-JA760602 enhanced viability and curbed apoptosis of hypoxia-treated cardiomyocytes. EGR1 and E2F1 could activate BCL2 transcription. Cytoplasmic circ-JA760602 bound with EGR1 and E2F1 to thus inhibit their nuclear translocation. BCL2 knockdown reversed the effects of circ-JA760602 silencing on the apoptosis of hypoxia-treated AC16 cells. Circ-JA760602 promotes hypoxia-induced apoptosis of cardiomyocytes by binding with EGR1 and E2F1 to inhibit the transcriptional activation of BCL2.

His bundle pacing versus right ventricular pacing: A comparative study.

BACKGROUND: Pacing is the most effective and dependable method for treating complete atrioventricular block (AVB). OBJECTIVE: The purpose of this study is to investigate the use of His bundle pacing (HBP) in patients with atrioventricular block. METHODS: Patients who underwent HBP or right ventricular pacing (RVP) were enrolled and divided into two groups: the HBP group and the RVP group, respectively. We compared baseline clinical data, fluoroscopy duration, operation duration, pacing electrode parameters during the operation or follow-up, baseline QRS duration, and pacing QRS duration. RESULTS: HBP was attempted in 48 patients and was successful in 34 patients who were included in the HBP group. In addition, 30 RVP patients were included in the RVP group. Fluoroscopy duration and operation duration were significantly longer in the HBP group compared to the RVP group. Compared to the RVP group, the HBP group had a higher pacing threshold, a lower R wave amplitude, and a shorter pacing QRS duration. At 6 months of follow-up, the pacing threshold remained higher, the R wave amplitude was significantly lower, and the end-diastolic diameter of the left ventricle was smaller in the HBP group. CONCLUSION: HBP was safe and effective for atrioventricular block despite the longer fluoroscopy and operation duration in the HBP group when compared to the RVP group.

Circ-TLR4 promotes cardiac hypertrophy through recruiting FUS to stabilize TLR4 mRNA.

BACKGROUND: Cardiac hypertrophy is an adaptive and compensatory mechanism preserving cardiac output during detrimental stimuli. Circular RNAs (circRNAs) have been illustrated to exert important implications in the pathogenesis of multiple cardiovascular diseases (CVD) including demonstrated cardiac hypertrophy. Toll-like receptor 4 (TLR4) has been previously reported to be a crucial regulator in inflammatory response and cardiac hypertrophy. However, the role of circular isoforms derived from TLR4 in cardiac hypertrophy remains unclear. METHODS: Expression of circ-TLR4 and TLR4 in cardiomyocytes was detected by RT-qPCR. The indicators of cardiac hypertrophy responses, including cell surface area, atrial natriuretic factor (ANF), B-type natriuretic peptide (BNP) and ß-myosin heavy chain (ß-MHC) were measured by immunofluorescence staining and western blot. RIP assay was used to validate the interaction between circ-TLR4 and TLR4. RESULTS: Circ-TLR4 and TLR4 was up-regulated in cellular models of cardiac hypertrophy. Circ-TLR4 knockdown attenuated angiotensin II (Ang II)-induced hypertrophy responses in cardiomyocytes. Moreover, circ-TLR4 positively regulated TLR4 expression through recruiting FUS to stabilize TLR4 mRNA. Furthermore, TLR4 overexpression rescued the cardiac responses mediated by circ-TLR4 silencing. CONCLUSION: Circ-TLR4 promotes cardiac hypertrophy through recruiting FUS to stabilize TLR4 mRNA.

Corosolic acid and its structural analogs: A systematic review of their biological activities and underlying mechanism of action.

BACKGROUND: The corosolic acid (CA), also known as plant insulin, is a pentacyclic triterpenoid extracted from plants such as Lagerstroemia speciosa. It has been shown to have anti-diabetic, anti-inflammatory and anti-tumor effects. Its structural analogs ursolic acid (UA), oleanolic acid (OA), maslinic acid (MA), asiatic acid (AA) and betulinic acid (BA) display similar individual pharmacological activities to those of CA. However, there is no systematic review documenting pharmacological activities of CA and its structural analogues. This study aims to fill this gap in literature. PURPOSE: This systematic review aims to summarize the medical applications of CA and its analogues. METHODS: A systematic review summarizes and compares the extraction techniques, pharmacokinetic parameters, and pharmacological effects of CA and its structural analogs. Hypoglycemic effect is one of the key inclusion criteria for searching Web of Science, PubMed, Embase and Cochrane databases up to October 2020 without language restrictions. 'corosolic acid', 'ursolic acid', 'oleanolic acid', 'maslinic acid', 'asiatic acid', 'betulinic acid', 'extraction', 'pharmacokinetic', 'pharmacological' were used to extract relevant literature. The PRISMA guidelines were followed. RESULTS: At the end of the searching process, 140 articles were selected for the systematic review. Information of CA and five of its structural analogs including UA, OA, MA, AA and BA were included in this review. CA and its structural analogs are pentacyclic triterpenes extracted from plants and they have low solubilities in water due to their rigid scaffold and hydrophobic properties. The introduction of water-soluble groups such as sugar or amino groups could increase the solubility of CA and its structural analogs. Their biological activities and underlying mechanism of action are reviewed and compared. CONCLUSION: CA and its structural analogs UA, OA, MA, AA and BA are demonstrated to show activities in lowering blood sugar, anti-inflammation and anti-tumor. Their oral absorption and bioavailability can be improved through structural modification and formulation design. CA and its structural analogs are promising natural product-based lead compounds for further development and mechanistic studies.

Pharmacogenetic and safety analysis of cinacalcet hydrochloride in healthy Chinese subjects.

BACKGROUND: Our study aims to explore the effect of genetics on the pharmacodynamics (PD) and pharmacokinetics (PK) of cinacalcet in healthy Chinese subjects; to investigate the effect of dietary factors on cinacalcet, and to evaluate the safety of cinacalcet under fasting and non-fasting conditions using a bioequivalence trial. METHODS: We investigated the relationship of cinacalcet PK with single nucleotide polymorphisms (SNPs) of CYP3A4, CYP1A2 and CYP2D6, and of cinacalcet PD with SNPs of calcium-sensitive receptors (CASR) and vitamin D receptors (VDR) in 65 healthy Chinese subjects recruited to participate in this study. Our study was a phase I, open-label, randomized, two-period, two-sequence crossover, a single-center clinical study designed under both fasting and non-fasting conditions to investigate the effect of dietary factors on cinacalcet. Plasma cinacalcet concentrations were analyzed using a validated HPLC-MS/MS assay. Clinical laboratory tests evaluated safety. Thirteen SNPs of CASR, VDR, and CYP genes were selected for pharmacogenetic analysis. RESULTS: CYP3A4 rs4646437 was found to be associated with the PK of cinacalcet under fasting conditions (P<0.01). Subjects carrying T alleles of rs4646437 appeared to metabolize cinacalcet poorly. The Cmax and AUC of subjects in the non-fasting group were significantly higher (P<0.0001) than those in the fasting group. The Tmax, CL/F, and Vd/F in the fasting group were significantly higher (P<0.0001) than those in the non-fasting group. In the fasting group, the geometric least square mean ratios (T/R) of the Cmax and AUC0-t were 109.89% and 105.33%, and the corresponding 90% CIs were 98.36-122.79% and 98.04-113.15%, respectively. In the non-fasting group, the T/R of the Cmax and AUC0-t were 100.74% and 99.09%, and the corresponding 90% CIs were 92.65-109.54% and 94.79-103.58%, respectively. All adverse events (AEs) were mild, and no serious adverse events (SAEs) occurred during the bioequivalence trial. CONCLUSIONS: Following our investigation, we reached the following conclusions: CYP3A4 rs4646437 may affect cinacalcet PK; the reference and test preparations of cinacalcet were bioequivalent under fasting and non-fasting conditions and were safe to use; and dietary factors had a significant effect on the PK of cinacalcet, in that exposure to the drug increased when cinacalcet was taken after eating.

Human cytomegalovirus promotes the activation of TGF-ß1 in human umbilical vein endothelial cells by MMP-2 after endothelial mesenchymal transition.

BACKGROUND: Human cytomegalovirus (HCMV) infection is one of the risk factors of cardiovascular disease; the most important pathological change is the change of vascular endothelial cell (VEC) function, but its mechanism is still unclear. Transforming growth factor ß1 (TGF-ß1) is an important cytokine associated with fibrosis; it can induce the occurrence of endothelial mesenchymal transition (EndMT) in VECs, which means endothelial cells acquire the characteristics and phenotypes of mesenchymal cells and secrete molecules associated with the deposition and remodeling of the extracellular matrix. Many in vivo and in vitro studies have shown that HCMV infection promotes the secretion and activation of TGF-ß1. OBJECTIVES: This study aims to observe the changes of endothelial cells after HCMV infection and EndMT occurrence induced by TGF-ß1 and to explore the possible mechanism of HCMV infection in the pathogenesis of cardiovascular disease. MATERIAL AND METHODS: Immunofluorescence staining, reverse transcription polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), and immunoprecipitation methods were used in this study to analyze the changes in morphology and gene expression. RESULTS: We found that EndMT-related morphological and gene expression changes occurred in human umbilical vein endothelial cells (HUVECs) infected and uninfected with HCMV after treatment with TGF-ß1. Human umbilical vein endothelial cells infected with HCMV, which are treated with TGF-ß1, can activate the extracellular potential TGF-ß1 by activating matrix metalloproteinase 2 (MMP-2). CONCLUSIONS: Our findings provide a molecular basis for the association between HCMV infection, TGF-ß1 and cardiovascular disease.

Predicting in-hospital death in patients with type B acute aortic dissection.

The outcome of patients with acute type B aortic dissection (BAAD) is largely dictated by whether or not the case is "complicated." The purpose of this study was to investigate the risk factors leading to in-hospital death among patients with BAAD and then to develop a predictive model to estimate individual risk of in-hospital death.A total of 188 patients with BAAD were enrolled. Risk factors for in-hospital death were investigated with univariate and multivariable logistic regression analysis. Significant risk factors were used to develop a predictive model.The in-hospital mortality rate was 9% (17 of 188 patients). Univariate analysis revealed 7 risk factors to be statistically significant predictors of in-hospital death (P < .1). In multivariable analysis, the following variables at admission were independently associated with increased in-hospital mortality: hypotension (odds ratio [OR], 4.85; 95% confidence interval [CI], 1.12-18.90; P = .04), ischemic complications (OR, 8.24; 95% CI, 1.25-33.85; P < .001), renal dysfunction (OR, 12.32; 95% CI, 10.63-76.66; P < .001), and neutrophil percentage ≥80% (OR, 5.76; 95% CI, 2.58-12.56; P = .03). Based on these multivariable results, a reliable and simple prediction model was developed, a total score of 4 offered the best point value.Independent risk factors associated with in-hospital death can be predicted in BAAD patients. The prediction model could be used to identify the prognosis for BAAD patients and assist physicians in their choice of management.

miR-23 regulates cell proliferation and apoptosis of vascular smooth muscle cells in coronary heart disease.

BACKGROUND: Aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) play an important role in the pathogenesis of cardiovascular diseases including coronary heart disease (CHD). MicroRNAs has reported play critical roles in VSMCs function. The present study was to investigate the effects of microRNA­23 (miR-23) on VSMCs and uncover its potential mechanism. METHODS: Cell viability was detected by CCK-8 assay. Cell apoptosis was measured by flow cytometry. Dual luciferase reporter assay was conducted to verify whether BCL2L11 is a target gene of miR-23. The protein levels of BCL2L11 and caspase-3 were detect by quantitative real time PCR and western blot. RESULTS: Our results showed that the expression of miR-23 was upregulated in peripheral blood of CHD patients compared with controls. Overexpression of miR-23 promoted VSMCs proliferation and inhibited VSMCs apoptosis. Downregulation of miR-23 suppressed VSMCs proliferation and promoted VSMCs apoptosis. In addition, we identified BCL2L11 was a direct gene of miR-23. Overexpression of miR-23 decreased the levels of BCL2L11 and caspase-3, and downregulate of miR-23 increased the levels of BCL2L11and caspase-3 in VSMCs. CONCLUSION: Our findings suggest that miR-23 plays a crucial role in controlling VSMCs proliferation and apoptosis by targeting BCL2L11.

Sphingomyelin in erythrocyte membranes increases the total cholesterol content of erythrocyte membranes in patients with acute coronary syndrome.

OBJECTIVES: To investigate whether the sphingomyelin content of erythrocyte membranes (SEM) is changed in patients with acute coronary syndrome (ACS) and determine the correlation between SEM and the total cholesterol content of erythrocyte membranes (CEM). METHODS: The SEM and CEM levels were measured in 354 patients undergoing coronary artery angiography in three different groups: ACS patients (n=199), patients with stable angina pectoris (SAP) (n=82), and controls (n=73). RESULTS: The SEM levels in the ACS group were significantly higher than those of the SAP group. The SEM levels were correlated positively with the CEM levels in patients with coronary artery disease. Multivariable logistic regression analysis showed that patients with higher levels of both SEM and CEM had an 8.569-fold greater risk of developing ACS than other patients, after adjusting for all potential confounding variables. CONCLUSION: Elevated SEM and CEM levels showed both independent and combined correlations with the occurrence of ACS and were positively correlated with each other in patients with coronary artery disease. These data suggest that the increased levels of SEM may play a role in the progression to plaque instability in ACS and may be the mechanisms underlying elevated levels of CEM in patients with ACS.

Total cholesterol content of erythrocyte membranes in acute coronary syndrome: correlation with apolipoprotein A-I and lipoprotein (a).

OBJECTIVES: Recent studies reported that total cholesterol erythrocyte membrane (CEM) levels were associated with the presence of acute coronary syndrome (ACS). However, little is known about the mechanisms of CEM elevation in these patients. The aim of this study was to investigate the association between CEM and the circulating lipid profile to delineate the possible mechanisms of CEM elevation in patients with ACS. METHODS: CEM levels, serum concentrations of triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, lipoprotein (a), apolipoprotein A-I (Apo A-I), apolipoprotein B (Apo B), and high-sensitive C-reactive protein levels were measured in 418 Chinese patients undergoing coronary artery angiography, including ACS (n=311) and stable angina pectoris (n=107). RESULTS: CEM levels in the ACS group were significantly higher (median, 129.82; interquartile range, 110.99-156.54 µg/mg, P<0.001) compared with the stable angina pectoris group (median, 80.88; interquartile range, 66.69-98.57 µg/mg). Multivariable logistic regression analyses showed a significantly independent relationship between CEM levels and the presence of ACS (odds ratio, 10.257; 95% confidence interval, 5.380-19.556, P<0.001). CEM levels were positively correlated with plasma lipoprotein (a) levels (r=0.175; P<0.001) and negatively correlated with serum Apo A-I levels (r=-0.149; P=0.002). CONCLUSION: CEM levels are closely associated with the occurrence of ACS as an independent determinant. The correlation of CEM with lipoprotein (a) and Apo A-I suggests that changes to these lipid proteins could be one possible mechanism for CEM increase in patients with ACS.

Total cholesterol content of erythrocyte membranes levels are associated with the presence of acute coronary syndrome and high sensitivity C-reactive protein.

In this study we assessed whether total cholesterol content of erythrocyte membranes (CEM) was associated with the presence of acute coronary syndrome (ACS) and high sensitivity C-reactive protein (hs-CRP). Consecutive angina patients were assessed; 98 had ACS and 45 had stable angina pectoris (SAP). CEM in the ACS group was significantly higher compared with the SAP group (p< 0.05). Multiple logistic regression analyses revealed a significant independent relation between CEM and the presence of ACS (OR 24.990, p<0.001). CEM was positively correlated with serum hs-CRP levels (r=0.328, p<0.001). These findings suggest a potential role of CEM as a marker of vulnerable plaque.