Cardiology Plus最新文献

{"title":"Metabolism, inflammation, and cardiovascular diseases from basic research to clinical practice.","authors":"Zihang Huang, Aijun Sun","doi":"10.1097/CP9.0000000000000037","DOIUrl":"10.1097/CP9.0000000000000037","url":null,"abstract":"","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"4-5"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/52/b4/cp9-8-4.PMC10178914.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9492946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of in-hospital evolocumab therapy on lipoprotein(a) in patients with acute myocardial infarction: a retrospective cohort study and a propensity score matching analysis.","authors":"Ge Gao,&nbsp;Tao Zheng,&nbsp;Beidi Lan,&nbsp;Weiying Hui,&nbsp;Shi Chen,&nbsp;Zuyi Yuan,&nbsp;Yue Wu,&nbsp;John Y L Chiang,&nbsp;Tao Chen","doi":"10.1097/CP9.0000000000000036","DOIUrl":"10.1097/CP9.0000000000000036","url":null,"abstract":"<p><p>Elevated lipoprotein(a) is associated with an increased risk of atherosclerotic cardiovascular disease. Evolocumab, a proprotein convertase subtilisin/kexin type 9 inhibitor, has been shown to reduce lipoprotein(a). However, the effect of evolocumab on lipoprotein(a) in patients with acute myocardial infarction (AMI) is poorly studied. This study aims to investigate the change in lipoprotein(a) under evolocumab therapy in patients with AMI.</p><p><strong>Methods: </strong>This retrospective cohort analysis included a total of 467 AMI patients with LDL-C level >2.6 mmol/L upon admission, among whom 132 received in-hospital evolocumab (140 mg every 2 weeks) plus statin (20 mg atorvastatin or 10 mg rosuvastatin per day) and the remaining 335 received statin only. Lipid profiles at 1-month follow-up were compared between the two groups. A propensity score matching analysis was also conducted based on age, sex, and baseline lipoprotein(a) at a 1:1 ratio using a 0.02 caliper.</p><p><strong>Results: </strong>At the 1-month follow-up, the lipoprotein(a) level decreased from 27.0 (17.5, 50.6) mg/dL to 20.9 (9.4, 52.5) mg/dL in evolocumab plus statin group, but increased from 24.5 (13.2, 41.1) mg/dL to 27.9 (14.8, 58.6) mg/dL in statin only group. The propensity score matching analysis included 262 patients (131 in each group). In subgroup analysis of the propensity score matching cohort stratified by the baseline lipoprotein(a) at cutoff values of 20 and 50 mg/dL, the absolute change in lipoprotein(a) was -4.9 (-8.5, -1.3), -5.0 (-13.9, 1.9), -0.2 (-9.9, 16.9) mg/dL in three subgroups in evolocumab plus statin group, and 0.9 (-1.7, 5.5), 10.7 (4.6, 21.9), 12.2 (2.9, 35.6) mg/dL in three subgroups in statin only group. In comparison to statin only group, evolocumab plus statin group had lower lipoprotein(a) level at 1 month in all subgroups (<i>P</i> < 0.05).</p><p><strong>Conclusions: </strong>In-hospital initiation of evolocumab on a background statin therapy reduced lipoprotein(a) level at 1-month follow-up in patients with AMI. Evolocumab plus statin therapy inhibited the increase in lipoprotein(a) in statin only therapy, regardless of the baseline lipoprotein(a) level.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"46-52"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/bd/d2/cp9-8-46.PMC10179980.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9869960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial progenitor cells and major adverse cardiovascular events in patients receiving elective coronary angiography","authors":"Chung-Te Liu, Jiun-Yu Guo, R. Chou, Ya-Wen Lu, Y. Tsai, C. Kuo, Chun-Chin Chang, Po‐Hsun Huang, Jaw-wen Chen, Shing-Jong Lin","doi":"10.1097/CP9.0000000000000041","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000041","url":null,"abstract":"Background and purpose: The association of circulating endothelial progenitor cells (EPCs) with different cardiovascular diseases and their related major adverse cardiovascular events (MACE) remained inconclusive. We aimed to clarify associations between the circulating EPC levels and the risk of MACE concerning different atherosclerosis-related diseases. Methods: This prospective cohort study was conducted from December 2009 to March 2015. Patients who underwent non-emergent coronary angiography (CAG) were included. The circulating EPC levels were measured using flow cytometry prior to the CAG procedure. The study evaluation of circulating EPC levels among patients with obstructive coronary artery disease (CAD) and other comorbidities. Patients were then assigned to tertiles by circulating EPC levels to evaluate the predictive values of the development of MACEs. Results: The study enrolled 1099 patients, of whom, 736 (67%) were men, with a mean age of 66.7 ± 12.5 years old. Overall, 637 (58%) patients were diagnosed with obstructive CAD according to CAG. MACE occurred in 268 (24.4%) patients. Circulating EPC levels were lower in patients with peripheral artery disease (PAD) but not associated with the presence of obstructive CAD, atrial fibrillation, chronic kidney disease (CKD), heart failure, and diabetes mellitus. Higher circulating EPC levels are linked with higher MACE among patients with suspected CAD, regardless of the presence or absence of obstructive CAD or CKD. The association did not present in patients with PAD. Conclusions: Higher circulating EPC levels are associated with a greater risk of MACE, regardless of the presence of obstructive CAD or CKD. This association was not apparent in the patients with PAD, suggesting impaired endothelial repair in these patients.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"37 - 45"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48457163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to Stretococcus <i>gallolyticus</i> infective endocarditis, a different presentation-a case report.","authors":"","doi":"10.1097/CP9.0000000000000045","DOIUrl":"10.1097/CP9.0000000000000045","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1097/CP9.0000000000000020.].</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"67"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c6/1e/cp9-8-67.PMC10180010.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9471441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Injury mechanism, risk factors and outcomes associated with blunt cardiac injury: a systematic review and meta-analysis","authors":"Yongjing Jiang, Gaoliang Zhou, Jun Feng, Likun Ma, Jianyuan Pan","doi":"10.1097/CP9.0000000000000044","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000044","url":null,"abstract":"Background and purpose: Risk factors that could be used to assess early and further improve the positive predictive value of blunt cardiac injury (BCI) are still inconclusive. We conducted a meta-analysis to quantitatively analyze the injury mechanism, risk factors, and outcomes associated with BCI in trauma patients. Methods: This systematic review and meta-analysis were performed to gather data on trauma patients with blunt cardiac injury. PubMed, Web of Science, and EMBASE databases were searched for studies until 20th November 2021. A pooled meta-analysis of injury mechanisms, risk factors, and outcomes concerning BCI was conducted. Results: We screened 256 records from which 11 studies published from 2000 to 2019 reporting 68,039 patients with trauma were included. Motor vehicle crash was the main injury mechanism, accounting for 65.2% of the attributed mechanisms for BCI [pool proportion = 0.652 (0.595–0.709)]. The pooled relative risks (RRs) revealed that patients with sternal fracture, shock on arrival, and history of cardiac disease were associated with increased risk of BCI (for sternal fracture: RR = 7.21 [95% confidence interval (CI) = 3.99–13.05]; for the shock on arrival: RR = 2.45, 95% CI = 2.12–2.84; for the history of cardiac disease: RR = 1.87, 95% CI = 1.11–3.16). A significant difference was observed in the length of stay between the BCI group compared to the no BCI group, 11.68 (95% CI = 8.79–14.58 days) vs. 20.46 (95% CI = 16.78–24.14 days). The risk of mortality was significantly higher in trauma patients with BCI as compared to those without BCI (RR = 1.70, 95% CI = 1.53–1.90). Conclusions: BCI was associated with increased mortality in our study. Patients also tended towards a longer length of stay. In addition to electrocardiogram and TnI, we recommend screening for BCI when trauma patients are in the presence of sternal fracture, shock, and a history of cardiac disease.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"53 - 62"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47638817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammation macrophages contribute to cardiac homeostasis","authors":"Yu Zhang, Junchu Tu, Yujie Li, Yanli Wang, Lin Lu, Chengjie Wu, Xi-Yong Yu, Yangxin Li","doi":"10.1097/CP9.0000000000000035","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000035","url":null,"abstract":"Cardiovascular diseases (CVDs) have high morbidity. Many endogenous and exogenous factors provoke the innate immune response causing tissue damage and accelerating the progression of the diseases. The macrophages are the major cells mediating the inflammatory response. Inflammasomes are multi-protein complexes that recognize danger signals, activate cytokines, and participate in the inflammatory response. Both macrophages and inflammasomes play a critical role in the development and progression of CVDs, such as myocardial infarction, hypertension, and atherosclerosis. This review will summarize the studies on macrophages and inflammasomes and discuss potential therapeutic interventions. Moreover, macrophages and inflammasomes play distinct role in the inflammation process, but closely linked. The inflammasome system occur in macrophages, and macrophage pyroptosis may be provoked by inflammasome activation. The cytokines secreted by macrophages may be related to the activation of inflammasomes, and further activate macrophages in the heart and cause the interconversion of M1 phenotype and M2 phenotype. The mechanism of inflammasomes regulating macrophage polarization remains to be further investigated.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"6 - 17"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44936686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of the metabolic state of surviving cardiomyocytes in the human infarcted heart by spatial single-cell transcriptomics.","authors":"Yan Shen,&nbsp;Il-Man Kim,&nbsp;Neal L Weintraub,&nbsp;Yaoliang Tang","doi":"10.1097/CP9.0000000000000038","DOIUrl":"10.1097/CP9.0000000000000038","url":null,"abstract":"<p><p>The metabolic status of surviving cardiomyocytes (CM) in the myocardial tissues of patients who sustained myocardial infarction (MI) is largely unknown. Spatial single-cell RNA-sequencing (scRNA-seq) is a novel tool that enables the unbiased analysis of RNA signatures within intact tissues. We employed this tool to assess the metabolic profiles of surviving CM in the myocardial tissues of patients post-MI.</p><p><strong>Methods: </strong>A spatial scRNA-seq dataset was used to compare the genetic profiles of CM from patients with MI and control patients; we analyzed the metabolic adaptations of surviving CM within the ischemic niche. A standard pipeline in Seurat was used for data analysis, including normalization, feature selection, and identification of highly variable genes using principal component analysis (PCA). Harmony was used to remove batch effects and integrate the CM samples based on annotations. Uniform manifold approximation and projection (UMAP) was used for dimensional reduction. The Seurat \"FindMarkers\" function was used to identify differentially expressed genes (DEGs), which were analyzed by the Gene Ontology (GO) enrichment pathway. Finally, the scMetabolism R tool pipeline with parameters method = VISION (Vision is a flexible system that utilizes a high-throughput pipeline and an interactive web-based report to annotate and explore scRNA-seq datasets in a dynamic manner) and metabolism.type = Kyoto Encyclopedia of Genes and Genomes (KEGG) was used to quantify the metabolic activity of each CM.</p><p><strong>Results: </strong>Analysis of spatial scRNA-seq data showed fewer surviving CM in infarcted hearts than in control hearts. GO analysis revealed repressed pathways in oxidative phosphorylation, cardiac cell development, and activated pathways in response to stimuli and macromolecular metabolic processes. Metabolic analysis showed downregulated energy and amino acid pathways and increased purine, pyrimidine, and one-carbon pool by folate pathways in surviving CM.</p><p><strong>Conclusions: </strong>Surviving CM within the infarcted myocardium exhibited metabolic adaptations, as evidenced by the downregulation of most pathways linked to oxidative phosphorylation, glucose, fatty acid, and amino acid metabolism. In contrast, pathways linked to purine and pyrimidine metabolism, fatty acid biosynthesis, and one-carbon metabolism were upregulated in surviving CM. These novel findings have implications for the development of effective strategies to improve the survival of hibernating CM within the infarcted heart.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"18-26"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7d/ed/cp9-8-18.PMC10180026.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10301091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Scimitar syndrome and distal tracheoesophageal fistula with esophageal atresia (type III b): a case report of diagnostic and therapeutic approach","authors":"Ida Nađ, Dorotea Šijak, A. Miculinić, D. Bartoniček, Maja Hrabak Paar, I. Malcic","doi":"10.1097/CP9.0000000000000042","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000042","url":null,"abstract":"Scimitar syndrome is a rare congenital heart defect (CHD) manifested by a partial abnormal inflow of pulmonary veins of the right lung into the suprahepatic segment of the inferior vena cava (VCI), making an angiographic image with the right heart edge similar to a Turkish saber (“scimitar”). It is found in only 1 to 3 per 100,000 births. Here we are presenting a patient who, in addition to the basic finding and presentation of a special partial anomalous inflow of pulmonary veins, also had other features of the Scimitar syndrome; dextroposition of the heart, without signs of heterotaxy, hypoplasia of the right lung, aberrant arterial supply of the right lung from the descending aorta (lung sequestration) with all hemodynamic signs of left-right flow (dilated right heart cavity and pulmonary artery), but without pulmonary hypertension. In addition, the patient had esophageal atresia with distal tracheoesophageal fistula (TEF). Treatment included operative occlusion of TEF with termino-terminal esophageal anastomosis. In the further course, esophagography revealed circular esophageal stenosis at the anastomosis site, but without the need for dilatation, which resolved spontaneously. Tracheotomy was needed due to the inability to separate from mechanical ventilation. Considering cardiopulmonary stability and the absence of pulmonary hypertension, a complete cardiosurgical correction was postponed to after the first year of life. The review is exceptional due to the concomitant occurrence of a TEF Vogt type IIIb, because the unusual combination of Scimitar syndrome with such type of TEF has not been described in the literature so far. To our knowledge, there is only one described case report with an H-type of TEF.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"63 - 66"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43660676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-322 inhibition of calcification of arterial smooth muscle cells by regulation of galactosyltransferase 1-associating protein UBE2Q1 and Runx2","authors":"Shanshan Gao, Song Gao, Zhen Sun, Mikael Åkesson, H. Shelat, Yongjian Geng","doi":"10.1097/CP9.0000000000000039","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000039","url":null,"abstract":"Background and purpose: Vascular smooth muscle cell (SMC) calcification represents a prominent phenotypic alteration in atherosclerosis. MicroRNA-322 (miR-322) is crucially involved in myogenic stem cell growth and differentiation. The galactosyltransferase 1-associated protein (GTAP) is a ubiquitin-conjugating enzyme E2Q1 (UBE2Q1) that serves as a critical mediator of post-translational regulation of certain cellular enzymes and transcription factors. Runt-related transcription factor 2 (Runx2) plays a critical role in arterial calcification. However, the interplay between miR-322, UBE2Q1, and Runx2 during cardiovascular calcification remain largely unknown. Therefore, the purpose of this study is to delineate the molecular mechanisms by which miR-322 regulates vascular calcification. Methods: Here we examined miR-322 expression in murine SMC, and determined whether miR-322 regulates SMC calcification via modulating expression of UBE2Q1 and calcifying proteins. Murine SMC cultures or aortic segments were exposed to inorganic phosphate (Pi) for induction of calcification. Expressions of calcification-related genes in SMC with lentivirus-mediated knockdown of UBE2Q1 were determined with Western blot analysis and quantitative real-time polymerase chain reaction (qRT-PCR). Luciferase reporter assay was performed to validate miR-322 target binding and SMC were transfected with anti-miR-322 oligonucleotides to inhibit miR-322 function. Results: Aortic rings derived from UBE2Q1−/− mice exhibited much higher calcium content compared to aortic rings from wildtype (WT) animals, following calcification induction. Knockdown of UBE2Q1 by lentiviral short hairpin RNA (shRNA) significantly enhanced the calcium deposition and expression of osteogenic gene Runx2 in SMC. Enhanced UBE2Q1 expression dramatically reduced calcification while promoting expression of contractile proteins SM22α and α-SMA. Treatment with anti-miR-322 diminished the luciferase activity in SMC transfected with the reporter gene driven by the 3′-untranslated region of UBE2Q1 mRNA. Anti-miR-322 treatment also inhibited calcification significantly. Conclusions: Our study identified miR-322 regulates vascular calcification by targeting UBE2Q1. The miR-322–dependent regulation of UBE2Q1 and calcification represents a novel regulatory mechanism that controls vascular SMC function during the pathogenesis of vascular calcification.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"27 - 36"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46731118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Implications of updated epidemiological characteristics from heart diseases in China","authors":"Dong Zhao","doi":"10.1097/cp9.0000000000000025","DOIUrl":"https://doi.org/10.1097/cp9.0000000000000025","url":null,"abstract":"","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48919045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}