Kramer J. Wahlberg, Cyrus Thomas-Walker, Bradley J. Tompkins, Juvena Hitt, Allen B. Repp, William Hopkins
{"title":"The Association of P2Y12 Inhibitor Pretreatment With Length of Stay Among Patients With Acute Coronary Syndrome Who Underwent Coronary Artery Bypass Graft Surgery: A Cohort Study","authors":"Kramer J. Wahlberg, Cyrus Thomas-Walker, Bradley J. Tompkins, Juvena Hitt, Allen B. Repp, William Hopkins","doi":"10.1155/cdr/8959128","DOIUrl":"https://doi.org/10.1155/cdr/8959128","url":null,"abstract":"<p><b>Introduction:</b> Recent clinical practice guidelines do not recommend routine P2Y<sub>12</sub> inhibitor pretreatment for patients with non-ST-elevation acute coronary syndromes (NSTE-ACS) treated with an early invasive strategy based upon clinical trial data suggesting no improvement in clinical outcomes and increased risk of bleeding. A subset of patients with NSTE-ACS who receive pretreatment and subsequently require coronary artery bypass graft (CABG) surgery may require lengthy P2Y<sub>12</sub> inhibitor washout to reduce periprocedural bleeding risk, potentially prolonging hospitalization and increasing costs. We sought to study the association of P2Y<sub>12</sub> inhibitor pretreatment on value-based outcomes including length of stay, cost, and discharge destination.</p><p><b>Methods:</b> We conducted a retrospective cohort study of patients presenting with NSTE-ACS who underwent CABG at a tertiary academic medical center between 2019 and 2021. We assessed the frequency of P2Y<sub>12</sub> inhibitor pretreatment over the study period and compared risk-adjusted length of stay, cost of hospitalization, and discharge destination among patients who did or did not receive pretreatment.</p><p><b>Results:</b> One hundred eighty-eight patients met inclusion criteria, and 77% received pretreatment. The rate of pretreatment decreased significantly over the study period (<i>p</i> < 0.001). Pretreatment was associated with longer preoperative length of stay (4.2 ± 1.6 vs. 3.4 ± 2.5 days, <i>p</i> = 0.019), with no significant difference in postoperative or total length of stay. There was no difference in cost of hospitalization or likelihood of discharge to home following CABG.</p><p><b>Conclusion:</b> Among patients presenting with NSTE-ACS who underwent inpatient CABG, P2Y<sub>12</sub> inhibitor pretreatment was associated with longer preoperative length of stay, but no difference in total length of stay, cost of hospitalization, or discharge destination in this observational, single-center study.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/8959128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143801515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Thrombospondin-1 Silencing Ameliorates Osteoblastic Differentiation of Aortic Valve Interstitial Cells via Inhibiting Nuclear Factor-κB Pathway","authors":"Qing Li, Chengxiang Song, Zisong Wei, Junli Li, Hao Zhou, Shuoding Wang, Hongde Li, Haoran Yang, Qiang Luo, Mao Chen","doi":"10.1155/cdr/3845211","DOIUrl":"https://doi.org/10.1155/cdr/3845211","url":null,"abstract":"<p><b>Objective:</b> Calcific aortic valve disease (CAVD) is a progressive cardiovascular condition driven by the osteogenic differentiation of valve interstitial cells (VICs), with no effective drug therapies currently available. Hence, our objective is to investigate the impact of thrombospondin-1 (TSP-1) silencing on CAVD progression.</p><p><b>Methods:</b> In vitro experiments were employed using human primary VICs with TSP-1 knockdown, cultured in osteogenic induction medium, and followed by analyses including western blot, alkaline phosphatase staining, alizarin red staining, immunofluorescence, and flow cytometry. In vivo experiments used two murine models of CAVD to determine the role of TSP-1 silencing on aortic valve calcification.</p><p><b>Results:</b> We observed that silencing of TSP-1 reduced the osteogenic differentiation of VICs. Subsequent experiments demonstrated that TSP-1 knockdown suppressed nuclear factor-<i>κ</i>B (NF-<i>κ</i>B)–mediated inflammation during osteoblastic differentiation of VICs. Consistent findings were also observed in two murine models of CAVD.</p><p><b>Conclusions:</b> The present study has shown that TSP-1 silencing could mitigate the development of CAVD by inhibiting NF-<i>κ</i>B-mediated inflammation. We propose that targeting TSP-1-mediated NF-<i>κ</i>B pathway could provide a potential therapeutic method for treating CAVD.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/3845211","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143793774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xuechen Cui, Yuan Wang, Xuening Li, Hong Li, Ruihua Yin, Yue Liu, Aijun Ma, Shaonan Yang
{"title":"A Positive Feedback Loop Between CXCL16 and the Inflammatory Factors IL-17A and TGF-β Promotes Large Artery Atherosclerosis by Activating the STAT3/NF-κB Pathway","authors":"Xuechen Cui, Yuan Wang, Xuening Li, Hong Li, Ruihua Yin, Yue Liu, Aijun Ma, Shaonan Yang","doi":"10.1155/cdr/2973633","DOIUrl":"https://doi.org/10.1155/cdr/2973633","url":null,"abstract":"<p>CXC chemokine ligand 16 (CXCL16) expression is often observed in studies related to atherosclerosis (AS). However, the process by which CXCL16 promotes AS is still unknown. CXCL16 has the potential to be a therapeutic target for atherosclerotic disease, and we studied whether CXCL16 expression in carotid atherosclerotic plaques is correlated with plaque stability. The results revealed that the expression level of CXCL16 in unstable plaques was greater than that in stable plaques (<i>p</i> < 0.05). In an in vitro model, CXCL16 promoted the expression of interleukin-17A (IL-17A) and transforming growth factor-<i>β</i> (TGF-<i>β</i>) and the release of STAT3/NF-<i>κ</i>B pathway-associated proteins by regulating the expression of IL-17A, TGF-<i>β</i>, and CXCL16. In conclusion, there is a positive feedback regulatory pathway between inflammatory factors and CXCL16 during the progression of carotid AS. Inflammatory factors and CXCL16 promote each other’s expression and activate the STAT3/NF-<i>κ</i>B pathway to promote carotid AS. CXCL16 is highly expressed in carotid atherosclerotic plaques, affecting plaque stability and further leading to the development of AS-related diseases such as ischaemic stroke. Thus, we hypothesise that CXCL16 is a potential therapeutic target for treating AS and AS-related diseases.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/2973633","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143689961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Effect of Vitamin D3 Injection Combined With High-Intensity Interval Training on Excessive Autophagy in the Heart Tissue of Type 2 Diabetes–Induced Rats: An Analysis of the mTOR–Beclin-1–Fyco-1–Cathepsin D Pathway","authors":"Hadi Golpasandi, Mohammad Rahman Rahimi","doi":"10.1155/cdr/8817195","DOIUrl":"https://doi.org/10.1155/cdr/8817195","url":null,"abstract":"<p><b>Introduction:</b> This study investigated the effect of vitamin D3 injection combined with high-intensity interval training on cell signaling pathways involved in excessive autophagy, specifically the mTOR (mechanistic target of rapamycin)–Beclin-1–Fyco-1 (FYVE and coiled-coil domain-containing protein 1)–cathepsin D pathway, in the heart tissue of Type 2 diabetes–induced rats.</p><p><b>Method:</b> In this experimental study, 32 male Wistar rats were fed a high-fat diet for 6 weeks to induce Type 2 diabetes, followed by a single subcutaneous injection of 35 mg/kg streptozotocin (STZ). The rats were then randomly assigned to one of four groups: (1) diabetes control (DC), (2) diabetes + HIIT (DT), (3) diabetes + vitamin D3 (DV), and (4) diabetes + HIIT + vitamin D3 (DTV). HIIT sessions were conducted for 8 weeks, five times per week, at an intensity of 85%–95% of maximum running speed (<i>V</i><sub>max</sub>), while vitamin D3 was administered weekly via subcutaneous injection at a dose of 10,000 IU/kg. Twenty-four hours after the intervention period, heart and left ventricular tissues were collected for analysis of the levels of autophagy signaling proteins mTOR, phosphorylated mechanistic target of rapamycin (pmTOR), Beclin-1, Fyco-1, and cathepsin D.</p><p><b>Results:</b> Two-way ANOVA revealed that Type 2 diabetes significantly increased the levels of Beclin-1, Fyco-1, and cathepsin D (<i>p</i> < 0.001) while significantly reducing the levels of mTOR and pmTOR (<i>p</i> < 0.001). HIIT, vitamin D3 injection, and their combined treatment significantly decreased the levels of Beclin-1, Fyco-1, and cathepsin D and increased the levels of mTOR and pmTOR compared to the diabetes control group (<i>p</i> < 0.001).</p><p><b>Conclusion:</b> Type 2 diabetes increases autophagy in the left ventricle, marked by altered levels of key autophagy proteins. HIIT and vitamin D3 injections mitigate these effects by enhancing mTOR signaling and reducing excessive autophagy. These interventions show promise as nonpharmacological strategies to improve cardiac health in Type 2 diabetes and could be incorporated into clinical and rehabilitation programs.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/8817195","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143688887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Comprehensive Analysis Based on Genes Associated With Cuproptosis, Ferroptosis, and Pyroptosis for the Prediction of Diagnosis and Therapies in Coronary Artery Disease","authors":"Yongyi Zhang, Zhehan Guo, Renkui Lai, Xu Zou, Liuling Ma, Tianjin Cai, Jingyi Huang, Wenxiang Huang, Bingcheng Zou, Jinming Zhou, Jinxin Li","doi":"10.1155/cdr/9106621","DOIUrl":"https://doi.org/10.1155/cdr/9106621","url":null,"abstract":"<p>Coronary artery disease (CAD) is a complex condition influenced by genetic factors, lifestyle, and other risk factors that contribute to increased mortality. This study is aimed at evaluating the diagnostic potential of genes associated with cuproptosis, ferroptosis, and pyroptosis (CFP) using network modularization and machine learning methods. CAD-related datasets GSE42148, GSE20680, and GSE20681 were sourced from the GEO database, and genes related to CFP genes were gathered from MsigDB and FerrDb datasets and literature. To identify diagnostic genes linked to these pathways, weighted gene coexpression network analysis (WGCNA) was used to isolate CAD-related modules. The diagnostic accuracy of key genes in these modules was then assessed using LASSO, SVM, and random forest models. Immunity and drug sensitivity correlation analyses were subsequently performed to investigate possible underlying mechanisms. The function of a potential gene, STK17B, was analyzed through western blot and transwell assays. Two CAD-related modules with strong correlations were identified and validated. The SVM model outperformed LASSO and random forest models, demonstrating superior discriminative power (AUC = 0.997 in the blue module and AUC = 1.000 in the turquoise module), with nine key genes identified: CTDSP2, DHRS7, NLRP1, MARCKS, PELI1, RILPL2, JUNB, STK17B, and SLC40A1. Knockdown of STK17B inhibited cell migration and invasion in human umbilical vein endothelial cells. In summary, our findings suggest that CFP genes hold potential as diagnostic biomarkers and therapeutic targets, with STK17B playing a role in CAD progression.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/9106621","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143622664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Clinical and Echocardiographic Risk Factors of Adverse Outcomes in Young Patients With Dilated Cardiomyopathy","authors":"Mengwan Li, Wenheng Liu, Shouling Mi, Meng Wang, Yanli Wang, Qilong Guo, Zhexun Lian, Junhua Ge","doi":"10.1155/cdr/2122089","DOIUrl":"https://doi.org/10.1155/cdr/2122089","url":null,"abstract":"<p><b>Purpose:</b> This study is aimed at identifying clinical and echocardiographic factors associated with all-cause mortality or heart transplantation (HTx) in young patients with dilated cardiomyopathy (DCM).</p><p><b>Methods:</b> We conducted a retrospective analysis of hospitalized patients (aged 18–45 years) diagnosed with DCM between January 2012 and December 2022. All patients underwent a 2-year medical therapy for heart failure, followed by at least 1 year of follow-up. Clinical and echocardiographic data were collected at baseline and after the 2-year treatment period. Multivariate Cox proportional hazards regression with a backward stepwise method was used to identify risk factors for all-cause mortality or HTx.</p><p><b>Results:</b> The study cohort comprised 67 patients. Over a median follow-up of 38 months (range 18–50), 15 patients died and 24 underwent HTx. Significant risk factors for all-cause mortality/HTx included smoking, digoxin use, elevated N-terminal pro-brain natriuretic peptide (NT-proBNP, ≥ 5678 pg/mL), higher C-reactive protein (CRP, ≥ 3.0 mg/L), higher uric acid (UA, ≥ 570 <i>μ</i>mol/L), lower left ventricular ejection fraction (LVEF, ≤25%), and enlarged end-diastolic left ventricular diameter (LVD, ≥ 65 mm). Among these, elevated CRP (hazard ratio, HR = 6.727, <i>p</i> < 0.001) and enlarged LVD (HR = 3.038, <i>p</i> = 0.007) were the strongest independent risk factors, irrespective of other risk factors. Moreover, each 5 mm annual increase in end-systolic left atrial diameter (LAD, HR = 3.641, <i>p</i> < 0.001) and each unit annual increase in Ln(NT-proBNP) (HR = 4.069, <i>p</i> < 0.001) were the strongest predictors of all-cause mortality/HTx, even after accounting for the effects of body mass index, duration of treatment, and baseline CRP level.</p><p><b>Conclusions:</b> Intensive monitoring and medical care may be beneficial for young adult DCM patients with defined risk factors such as smoking, elevated NT-proBNP and CRP, lower LVEF, and enlarged LV diameter. Our findings suggest that personalized intensive monitoring and medical care based on identified risk factors may improve outcomes in young adult DCM patients.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/2122089","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143571409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cysteine-Rich Protein 61 (CCN1) Deficiency Alleviated Cardiac Remodeling in 5/6 Nephrectomized Mice by Suppressing the MAPK Signaling Pathway","authors":"Yihan Zhao, Liang Gu, Yunxuan Chen, Yibei Lin, Jincheng Xing, Diyan Xu, Zhen Su, Zhouqing Huang","doi":"10.1155/cdr/6813183","DOIUrl":"https://doi.org/10.1155/cdr/6813183","url":null,"abstract":"<p><b>Background:</b> With the progression of chronic kidney disease (CKD), we can often observe cardiac remodeling, fibrosis, and cardiac failure in patients. Cysteine-rich protein 61 (CCN1) is an extracellular matrix protein that plays a reuse role in cardiac remodeling. However, whether CCN1 participates in the crosslink between the heart and kidney in CKD and the potential mechanism remains unknown.</p><p><b>Methods:</b> We constructed a mouse model of CKD by 5/6 nephrectomy (5/6 Nx). Hematoxylin–eosin staining (H&E), Masson’s trichrome staining, and Sirius red staining were used to observe cardiac morphology and fibrosis. H9c2 cells were treated with si-CCN1 or si-NC or mitogen-activated protein kinase (MAPK)–related inhibitors or agonist before being cultured with 5/6 Nx mouse serum. The relative protein level was detected by Western blotting.</p><p><b>Results:</b> We observed that CCN1 expression was markedly enhanced in the serum and heart tissues, accompanied by disordered myocardial arrangement, obvious cardiac fibrosis, hypertrophy, and decreased cardiac systolic function reflected by echocardiography. The relative markers collagen 1 (COL-1), transforming growth factor-<i>β</i> (TGF-<i>β</i>), heavy-chain cardiac myosin (MyHC), and atrial natriuretic peptide (ANP) presented an increase in expression. In vivo and in vitro, after the knockdown of CCN1, the above results in the CKD group or CKD serum group were reversed; in addition, the MAPK signaling pathway was obviously activated due to 5/6 Nx, which was abolished by CCN1 inhibition. CCN1 silencing or MAPK pathway inhibition also decreased the expression of myocardial fibrosis and hypertrophy markers in H9c2 cells, while MAPK-related agonist partly reversed the effect of CCN1 inhibition.</p><p><b>Conclusion:</b> Our in vivo and in vitro study showed that specific CCN1 deficiency markedly alleviated cardiac remodeling in 5/6 Nx mice through the inhibition of the MAPK pathway.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/6813183","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143497192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Urine Output as a Novel Predictor for In-Hospital Mortality in Acute Pulmonary Embolism Patients: Training With the MIMIC Database and Validation With Independent Cohort","authors":"Wenjia Ai, Fangfei Li, Qilin Yang, Jingluo Qiu, Aiqiang Zhou, Yinqian Huang, Baohui Xu, Zhihui Zhang","doi":"10.1155/cdr/7907049","DOIUrl":"https://doi.org/10.1155/cdr/7907049","url":null,"abstract":"<p><b>Background:</b> Identifying high-risk patients with acute pulmonary embolism is vital for improving disease prognosis. However, current guidelines and research on risk factors are insufficient to meet clinical needs. This study was aimed at exploring novel risk factors to predict in-hospital mortality.</p><p><b>Methods:</b> We utilized a patient cohort from the Medical Information Mart for Intensive Care Version IV (MIMIC-IV) database as training cohort. Major analyses included screening risk factors for in-hospital mortality, correlation analysis via smooth curve fitting, multivariate Cox regression, and subgroup analysis. The findings were further validated with our own institute patient cohort.</p><p><b>Results:</b> Among 1463 adult patients with acute pulmonary embolism in the MIMIC-IV database, the overall in-hospital mortality rate was 17.8%. A nonlinear correlation was observed between urine output and in-hospital mortality. A urine discharge less than 0.85 mL/kg/h was used as the threshold and was negatively associated with the risk for in-hospital death. Compared to patients with urine value < 0.5 mL/kg/h, the risk for in-hospital mortality reduced by 36% and 48% in patients with urine values of 0.5–0.85 mL/kg/h and > 0.85 mL/kg/h, with the hazard ratios of 0.64 (0.47, 0.87) and 0.52 (0.38, 0.72), respectively. This association remained significant in the subgroup analysis after adjusting for age, gender, hypotension, and low oxygen saturation. Our validation patient cohort (<i>n</i> = 151) further confirmed the strong association of the urine value with in-hospital mortality and consistent cutoff value.</p><p><b>Conclusion:</b> Our study revealed a negative association of urine output with in-hospital mortality in acute pulmonary embolism patients, with the optimal urine output being significantly higher than the value of other critical illnesses.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/7907049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143489949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Impacts of CD36 Variants on Plasma Lipid Levels and the Risk of Early-Onset Coronary Artery Disease: A Systematic Review and Meta-Analysis","authors":"Zhi Luo, Lingwei Lv","doi":"10.1155/cdr/8098173","DOIUrl":"https://doi.org/10.1155/cdr/8098173","url":null,"abstract":"<p><b>Background:</b> Recent studies have indicated that cluster of differentiation 36 (CD36) is closely linked to dyslipidemia and early-onset coronary artery disease (EOCAD). This study is aimed at investigating the impacts of <i>CD36</i> gene variants on lipid profiles and EOCAD risk.</p><p><b>Methods:</b> PubMed, Cochrane Library, Central, CINAHL, and ClinicalTrials.gov were searched until June 15, 2024.</p><p><b>Results:</b> In total, 25 studies (11,494 individuals) were included for the analysis. The A allele carriers of the rs1761667 variant had higher high-density lipoprotein cholesterol (HDL-C) levels and higher EOCAD risk than noncarriers. In contrast, the G allele carriers of the rs1049673 and rs3211956 variants had lower low-density lipoprotein cholesterol (LDL-C) levels and lower EOCAD risk than noncarriers. Subgroup analysis indicated that the antiatherosclerotic impact and reduced EOCAD risk were primarily observed in Chinese with rs1049673 and rs3211956.</p><p><b>Conclusions:</b> The rs1761667, rs1049673, and rs3211956 variants of the <i>CD36</i> gene have significant impacts on lipid levels and may serve as genetic markers for the risk of EOCAD primarily in Chinese. The impacts of <i>CD36</i> variants on EOCAD risk are mediated, at least partly, by dyslipidemia. Genetic screening of <i>CD36</i> gene variants may be helpful for early intervention or prevention of EOCAD in individuals with high risk factors.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/8098173","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143481355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Acute Effects of Motor Imagery Combined With Action Observation Breathing Exercise on Cardiorespiratory Responses, Brain Activity, and Cognition: A Randomized, Controlled Trial","authors":"Ebrar Atak, Amine Ataç","doi":"10.1155/cdr/6460951","DOIUrl":"https://doi.org/10.1155/cdr/6460951","url":null,"abstract":"<p>Breath and brain activity have been integral to daily life since time immemorial. Cognition and cardiorespiratory responses are closely interlinked, necessitating further investigation into their dynamics. The potential benefits of combining motor imagery (MI) and action observation (AO) based breathing exercises in rehabilitation have not been fully explored. This study was aimed at assessing the acute effects of MI combined with AO on cognitive function and cardiorespiratory responses. Thirty-three healthy adults were randomized into MI combined with AO breathing (MI+AO), active respiratory exercise (ARE), and control groups, with equal distribution across groups. Electroencephalography (EEG) data were collected using a Muse EEG headband, and cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) while imagining activities were measured via the Kinesthetic and Visual Imagery Questionnaire (KVIQ). Significant improvements in the Timed Up and Go (TUG) test and systolic blood pressure were observed in the ARE group (<i>p</i> < 0.05), alongside improvements in MoCA and KVIQ scores (<i>p</i> < 0.05). EEG data revealed significant decreases in delta and theta power at the temporoparietal (TP) location in the ARE group (<i>p</i> < 0.05). These findings suggest that MI and AO, when combined with respiratory exercises, may serve as effective passive strategies to support cognition and cardiorespiratory function, particularly in individuals who struggle to actively participate in pulmonary rehabilitation.</p><p><b>Trial Registration:</b> ClinicalTrials.gov identifier: NCT06099483</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/6460951","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}