Pub Date : 2021-07-01DOI: 10.4103/2470-7511.327242
Yi Zhang, Qiuyue Li, Tianqing Li
Background and Objectives: Cardiovascular diseases (CVDs) are associated with a heavy health burden globally. Although there are several studies and reviews with a focus on the effects of ambient particulate matter on CVDs, presently, review of the association between particulate matter components and cardiovascular biomarkers has not been reported. Therefore, in this study, we reviewed the effects of particulate matter exposure on the levels of cardiovascular biomarkers. Methods: PubMed, Embase, and Web of Science databases were searched for related studies published between January 1, 2010, and May 30, 2021, using keywords, including particle, particulate, constituent, component, composition, cardiovascular biomarker, inflammation, oxidative stress, coagulation vasoactivity, and lipid metabolism. Results: Ten studies, which met the inclusion criteria, highlighted the existence of significant associations between particulate matter components and the levels of cardiovascular biomarkers, including lipid, inflammation and coagulation biomarkers, etc. However, multicenter studies evidence regarding the effects of long-term exposure to particulate matter components on cardiovascular biomarkers is still lacking. Further, studies with a focus on proteomics, and metabolomics of cardiovascular biomarkers owing to particulate matter exposure are also scarce. Conclusions: Exposure to particulate matter components was found to be significantly associated with cardiovascular biomarkers. However, in future, it would be necessary to conduct multicenter studies on the effects of long-term exposure to particulate components on the levels of cardiovascular biomarkers.
背景和目的:心血管疾病(cvd)在全球范围内与沉重的健康负担相关。虽然有一些研究和综述关注环境颗粒物对心血管疾病的影响，但目前，关于颗粒物成分与心血管生物标志物之间关系的综述尚未见报道。因此，在本研究中，我们回顾了颗粒物暴露对心血管生物标志物水平的影响。方法:检索PubMed、Embase和Web of Science数据库，检索2010年1月1日至2021年5月30日期间发表的相关研究，检索关键词包括颗粒、颗粒、成分、成分、组成、心血管生物标志物、炎症、氧化应激、凝血血管活性和脂质代谢。结果:符合纳入标准的10项研究强调了颗粒物组分与心血管生物标志物水平之间存在显著相关性，包括脂质、炎症和凝血生物标志物等。然而，关于长期暴露于颗粒物组分对心血管生物标志物的影响的多中心研究证据仍然缺乏。此外，由于颗粒物暴露，关注心血管生物标志物的蛋白质组学和代谢组学的研究也很少。结论:暴露于颗粒物成分与心血管生物标志物显著相关。然而，在未来，有必要开展多中心研究，研究长期暴露于颗粒成分对心血管生物标志物水平的影响。
{"title":"Epidemiological evidence in the effects of ambient particulate matter components on cardiovascular biomarkers: A systematic review","authors":"Yi Zhang, Qiuyue Li, Tianqing Li","doi":"10.4103/2470-7511.327242","DOIUrl":"https://doi.org/10.4103/2470-7511.327242","url":null,"abstract":"Background and Objectives: Cardiovascular diseases (CVDs) are associated with a heavy health burden globally. Although there are several studies and reviews with a focus on the effects of ambient particulate matter on CVDs, presently, review of the association between particulate matter components and cardiovascular biomarkers has not been reported. Therefore, in this study, we reviewed the effects of particulate matter exposure on the levels of cardiovascular biomarkers. Methods: PubMed, Embase, and Web of Science databases were searched for related studies published between January 1, 2010, and May 30, 2021, using keywords, including particle, particulate, constituent, component, composition, cardiovascular biomarker, inflammation, oxidative stress, coagulation vasoactivity, and lipid metabolism. Results: Ten studies, which met the inclusion criteria, highlighted the existence of significant associations between particulate matter components and the levels of cardiovascular biomarkers, including lipid, inflammation and coagulation biomarkers, etc. However, multicenter studies evidence regarding the effects of long-term exposure to particulate matter components on cardiovascular biomarkers is still lacking. Further, studies with a focus on proteomics, and metabolomics of cardiovascular biomarkers owing to particulate matter exposure are also scarce. Conclusions: Exposure to particulate matter components was found to be significantly associated with cardiovascular biomarkers. However, in future, it would be necessary to conduct multicenter studies on the effects of long-term exposure to particulate components on the levels of cardiovascular biomarkers.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"149 - 155"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41753264","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}
Pub Date : 2021-07-01DOI: 10.4103/2470-7511.327239
Ding-cheng Xiang, Yinghui Jin, W. Fang, X. Su, Bo Yu, Yan Wang, Wei-min Wang, Lefeng Wang, Hong-Bing Yan, Xianghua Fu, Zhijie Zheng, K. Labresh, Y. Huo, J. Ge
Background: The National Chest Pain Centers Program (NCPCP) is the largest nationwide, hospital-based, multifaceted, continuous quality improvement initiative, which aims to monitor and improve the quality of care for patients with acute chest pain. The accreditation of the standardized chest pain center is central to the project. The purpose of establishing chest pain centers is to develop a mechanism for “sending acute chest pain patients to a hospital with capabilities for the best treatment in the shortest time possible.” Objectives: This study aims to evaluate the effectiveness and implementation of the chest pain center accreditation and to identify factors that may influence its implementation in local settings. Study Design and Methods: Hospitals that have been accredited between January 2016 and September 2020 will be recruited in this study. We will conduct a self-controlled retrospective cohort study by comparing the care performance before, during, and after the accreditation. Measures for care performance will be selected based on the American College of Cardiology/American Heart Association clinical practice guidelines, which will be divided into prehospital processes, in-hospital processes, and in-hospital outcomes. For the implementation of the chest pain center accreditation, we will use a modified reach, effectiveness, adoption, implementation, maintenance (RE-AIM) framework to investigate the implementation process, and the consolidated framework for implementation research will be used to identify factors that emerge within the local context and influence the implementation fidelity and feasibility. Progress to Date: As of September 2020, there were 4,621 hospitals that registered the NCPCP, of which 1,507 hospitals were accredited. A total of 5,228,973 patients with a primary diagnosis on admission were enrolled from the registered hospitals, among which 34.6% were acute coronary syndromes. Conclusions: In this study, we proposed recommendations for improving the implementation of chest pain center accreditation, which will improve the quality of care for patients with acute chest pain and promote the sustainable development of chest pain center.
{"title":"The national chest pain centers program: Monitoring and improving quality of care for patients with acute chest pain in China","authors":"Ding-cheng Xiang, Yinghui Jin, W. Fang, X. Su, Bo Yu, Yan Wang, Wei-min Wang, Lefeng Wang, Hong-Bing Yan, Xianghua Fu, Zhijie Zheng, K. Labresh, Y. Huo, J. Ge","doi":"10.4103/2470-7511.327239","DOIUrl":"https://doi.org/10.4103/2470-7511.327239","url":null,"abstract":"Background: The National Chest Pain Centers Program (NCPCP) is the largest nationwide, hospital-based, multifaceted, continuous quality improvement initiative, which aims to monitor and improve the quality of care for patients with acute chest pain. The accreditation of the standardized chest pain center is central to the project. The purpose of establishing chest pain centers is to develop a mechanism for “sending acute chest pain patients to a hospital with capabilities for the best treatment in the shortest time possible.” Objectives: This study aims to evaluate the effectiveness and implementation of the chest pain center accreditation and to identify factors that may influence its implementation in local settings. Study Design and Methods: Hospitals that have been accredited between January 2016 and September 2020 will be recruited in this study. We will conduct a self-controlled retrospective cohort study by comparing the care performance before, during, and after the accreditation. Measures for care performance will be selected based on the American College of Cardiology/American Heart Association clinical practice guidelines, which will be divided into prehospital processes, in-hospital processes, and in-hospital outcomes. For the implementation of the chest pain center accreditation, we will use a modified reach, effectiveness, adoption, implementation, maintenance (RE-AIM) framework to investigate the implementation process, and the consolidated framework for implementation research will be used to identify factors that emerge within the local context and influence the implementation fidelity and feasibility. Progress to Date: As of September 2020, there were 4,621 hospitals that registered the NCPCP, of which 1,507 hospitals were accredited. A total of 5,228,973 patients with a primary diagnosis on admission were enrolled from the registered hospitals, among which 34.6% were acute coronary syndromes. Conclusions: In this study, we proposed recommendations for improving the implementation of chest pain center accreditation, which will improve the quality of care for patients with acute chest pain and promote the sustainable development of chest pain center.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"187 - 197"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48836232","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}
Pub Date : 2021-07-01DOI: 10.4103/2470-7511.327243
S. Liao, Rongrong Gao, I. Cheang, Xinyi Lu, Yan-li Zhou, Hai-Feng Zhang, W. Yao, Xinli Li
Background and Objective: Clinical studies have suggested that low tri-iodothyronine (T3) syndrome negatively affects the clinical outcomes of patients with acute heart failure (AHF). The aim of this prospective cohort study was to evaluate the effect of low T3 syndrome in terms of prognosis and risk-predictive potential in AHF. Methods: A prospective observational cohort study was conducted from April 2012 to August 2016 in Nanjing, China. All clinical baseline characteristics were retrieved from electronic medical records. Low T3 syndrome was defined by a low free T3 level (<3.1 pM) accompanied by a normal thyroid-stimulating hormone level. The association between the free T3 level and mortality and the incremental risk prediction were estimated in Cox regression adjusted models. Results: In total, 312 patients with AHF for whom detailed thyroid hormone profiles were available were prospectively enrolled. Seventy-two patients exhibited low T3 syndrome. Over a median follow-up period of 35 months, 121 cumulative deaths occurred. Cardiovascular death was observed in 94 patients. After extensive adjustment for confounders, the low T3 syndrome-associated hazard ratios (95% confidence intervals) were 1.74 (1.16–2.61, P = 0.007) for all-cause mortality and 1.90 (1.21–2.98, P = 0.005) for cardiovascular mortality. The restricted cubic splines suggested a negative linear relationship between the free T3 level and mortality risk. Considering reclassification, adding low T3 syndrome to the fully adjusted model improved the risk prediction for all-cause mortality (integrated discrimination improvement [IDI]: 2.0%, P = 0.030; net reclassification improvement [NRI]: 8.9%, P = 0.232) and cardiovascular mortality (IDI: 2.5%, P = 0.030; NRI: 21.3%, P = 0.013). Conclusions: Low T3 syndrome reclassified risk prediction for mortality beyond traditional risk factors for patients with AHF.
{"title":"Low tri-iodothyronine syndrome improves the risk prediction for mortality in patients with acute heart failure: A prospective observational cohort study","authors":"S. Liao, Rongrong Gao, I. Cheang, Xinyi Lu, Yan-li Zhou, Hai-Feng Zhang, W. Yao, Xinli Li","doi":"10.4103/2470-7511.327243","DOIUrl":"https://doi.org/10.4103/2470-7511.327243","url":null,"abstract":"Background and Objective: Clinical studies have suggested that low tri-iodothyronine (T3) syndrome negatively affects the clinical outcomes of patients with acute heart failure (AHF). The aim of this prospective cohort study was to evaluate the effect of low T3 syndrome in terms of prognosis and risk-predictive potential in AHF. Methods: A prospective observational cohort study was conducted from April 2012 to August 2016 in Nanjing, China. All clinical baseline characteristics were retrieved from electronic medical records. Low T3 syndrome was defined by a low free T3 level (<3.1 pM) accompanied by a normal thyroid-stimulating hormone level. The association between the free T3 level and mortality and the incremental risk prediction were estimated in Cox regression adjusted models. Results: In total, 312 patients with AHF for whom detailed thyroid hormone profiles were available were prospectively enrolled. Seventy-two patients exhibited low T3 syndrome. Over a median follow-up period of 35 months, 121 cumulative deaths occurred. Cardiovascular death was observed in 94 patients. After extensive adjustment for confounders, the low T3 syndrome-associated hazard ratios (95% confidence intervals) were 1.74 (1.16–2.61, P = 0.007) for all-cause mortality and 1.90 (1.21–2.98, P = 0.005) for cardiovascular mortality. The restricted cubic splines suggested a negative linear relationship between the free T3 level and mortality risk. Considering reclassification, adding low T3 syndrome to the fully adjusted model improved the risk prediction for all-cause mortality (integrated discrimination improvement [IDI]: 2.0%, P = 0.030; net reclassification improvement [NRI]: 8.9%, P = 0.232) and cardiovascular mortality (IDI: 2.5%, P = 0.030; NRI: 21.3%, P = 0.013). Conclusions: Low T3 syndrome reclassified risk prediction for mortality beyond traditional risk factors for patients with AHF.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"174 - 180"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46501155","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}
Pub Date : 2021-04-01DOI: 10.4103/2470-7511.320321
Yan-xiang Zang, Wei-min Li, Qi Lou, H. Wang, Yu Duan
At present, guideline-directed medical therapy of heart failure (HF) has achieved certain results, but the evidence mostly focuses on HF with reduced ejection fraction, and there are some problems in the research on HF with preserved ejection fraction (HFpEF), such as inconsistent inclusion criteria and unconvincing results. Therefore, it may be more individualized and targeted to perform classification, typing, and treatment of HF from aspects such as pathogenesis, etiology, or pathophysiology, but not ejection fraction, especially HFpEF with strong heterogeneity. Ge's phenotyping of HFpEF is based on etiology and pathology, aiming at improving the outcome of HFpEF and exploring new approaches for the prognosis of HF.
{"title":"Viewing the future research directions of heart failure from ge's phenotyping of heart failure with preserved ejection fraction","authors":"Yan-xiang Zang, Wei-min Li, Qi Lou, H. Wang, Yu Duan","doi":"10.4103/2470-7511.320321","DOIUrl":"https://doi.org/10.4103/2470-7511.320321","url":null,"abstract":"At present, guideline-directed medical therapy of heart failure (HF) has achieved certain results, but the evidence mostly focuses on HF with reduced ejection fraction, and there are some problems in the research on HF with preserved ejection fraction (HFpEF), such as inconsistent inclusion criteria and unconvincing results. Therefore, it may be more individualized and targeted to perform classification, typing, and treatment of HF from aspects such as pathogenesis, etiology, or pathophysiology, but not ejection fraction, especially HFpEF with strong heterogeneity. Ge's phenotyping of HFpEF is based on etiology and pathology, aiming at improving the outcome of HFpEF and exploring new approaches for the prognosis of HF.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"88 - 91"},"PeriodicalIF":0.0,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43173526","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}
Pub Date : 2021-04-01DOI: 10.4103/2470-7511.320324
Amir Ajoolabady, J. Tuomilehto, Gregory H. Lip, D. Klionsky, Jun Ren
Heart failure (HF) refers to a progressive pathological condition when cardiac muscles fail to pump adequate blood supply (cardiac output) to meet the metabolic demand of the body. Among various cellular and molecular mechanisms identified for the onset and progression of HF, autophagy dysregulation is increasingly getting recognized. Autophagy is a natural cellular process that is observed in almost all eukaryotic cells. Autophagy removes damaged/long-lived organelles, protein aggregates, and unwanted cellular compomemts via forming autophagosomes then fusing with lysosomes. Although mild-to-moderate induction of autophagy is deemed cytoprotective and adaptive, excessive or unchecked induction of autophagy can be detrimental and maladaptive. Both adaptive and maladaptive autophagy play a vital role in the pathophysiology of HF. In the current review, we provide an overview of autophagy regulation in HF and possible strategies targeting autophagy for the management of HF.
{"title":"Deciphering the role of autophagy in heart failure","authors":"Amir Ajoolabady, J. Tuomilehto, Gregory H. Lip, D. Klionsky, Jun Ren","doi":"10.4103/2470-7511.320324","DOIUrl":"https://doi.org/10.4103/2470-7511.320324","url":null,"abstract":"Heart failure (HF) refers to a progressive pathological condition when cardiac muscles fail to pump adequate blood supply (cardiac output) to meet the metabolic demand of the body. Among various cellular and molecular mechanisms identified for the onset and progression of HF, autophagy dysregulation is increasingly getting recognized. Autophagy is a natural cellular process that is observed in almost all eukaryotic cells. Autophagy removes damaged/long-lived organelles, protein aggregates, and unwanted cellular compomemts via forming autophagosomes then fusing with lysosomes. Although mild-to-moderate induction of autophagy is deemed cytoprotective and adaptive, excessive or unchecked induction of autophagy can be detrimental and maladaptive. Both adaptive and maladaptive autophagy play a vital role in the pathophysiology of HF. In the current review, we provide an overview of autophagy regulation in HF and possible strategies targeting autophagy for the management of HF.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"92 - 101"},"PeriodicalIF":0.0,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43937007","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}
Pub Date : 2021-04-01DOI: 10.4103/2470-7511.320322
Q. Jin, W. Pan, Shasha Chen, Lei Zhang, Daxin Zhou, J. Ge
Background and Objectives: The anatomical characteristics of patients with mitral valve prolapse (MVP) and mitral regurgitation (MR) have rarely been investigated demographically to determine the applicability of transcatheter intervention. Therefore, the study objective was to analyze potential candidates and their prognosis. Predictors determining the prognosis were also investigated. Methods: Patients diagnosed with MVP and MR severity of ≥2+ were screened from our echocardiography database from 2010 to 2012. All clinical and echocardiogram information was retrieved from electronic medical records. The endpoint was all-cause mortality analyzed by a proportional hazards model. Results: A total of 1268 patients (mean age 57.50 ± 14.88 years, 47.16% female) with MVP and MR severity of ≥ 2+ were included. Isolated P2 (n = 239, 18.85%) appeared as the most common site of leaflet prolapse. The incidence of MR jet solely from middle scallop (A2 and/or P2) was 31.07% (n = 394). If a nonsignificant jet from other locations was also accepted, the incidence of MR jet derived from mainly the middle scallop (A2 and/or P2) was 52.10% (n = 659). For MVP patients with MR R + 3, the conservative therapy group had higher mortality than the early surgery group (31.45% vs. 5.25%, P < 0.001) after 4.5 ± 1.0 years of follow-up, multiple analysis showed that surgical treatment (hazard ratio [HR]: 0.202, P < 0.001), systolic pulmonary artery pressure of o60 mmHg (HR: 6.816, P < 0.001), age of ≥ 60 years (HR: 3.838, P < 0.001), and pericardial effusion (HR: 1.915, P = 0.003) were independent predictors of all-cause mortality. Conclusions: In patients with MVP, one-fifth leaflet prolapse located solely in P2 and one-half of MR jet derived from the middle scallop were anatomically eligible for transcatheter chordal repair and edge-to-edge repair therapy, respectively. Initial conservative therapy, pericardial effusion, pulmonary hypertension, and advanced age were independent predictors of a higher mortality rate in MVP patients with MR severity of ≥ 3+.
{"title":"Anatomical analysis and prognostic assessment of degenerative mitral regurgitation based on a large echocardiography database: Implications for transcatheter edge-to-edge and chordal repair","authors":"Q. Jin, W. Pan, Shasha Chen, Lei Zhang, Daxin Zhou, J. Ge","doi":"10.4103/2470-7511.320322","DOIUrl":"https://doi.org/10.4103/2470-7511.320322","url":null,"abstract":"Background and Objectives: The anatomical characteristics of patients with mitral valve prolapse (MVP) and mitral regurgitation (MR) have rarely been investigated demographically to determine the applicability of transcatheter intervention. Therefore, the study objective was to analyze potential candidates and their prognosis. Predictors determining the prognosis were also investigated. Methods: Patients diagnosed with MVP and MR severity of ≥2+ were screened from our echocardiography database from 2010 to 2012. All clinical and echocardiogram information was retrieved from electronic medical records. The endpoint was all-cause mortality analyzed by a proportional hazards model. Results: A total of 1268 patients (mean age 57.50 ± 14.88 years, 47.16% female) with MVP and MR severity of ≥ 2+ were included. Isolated P2 (n = 239, 18.85%) appeared as the most common site of leaflet prolapse. The incidence of MR jet solely from middle scallop (A2 and/or P2) was 31.07% (n = 394). If a nonsignificant jet from other locations was also accepted, the incidence of MR jet derived from mainly the middle scallop (A2 and/or P2) was 52.10% (n = 659). For MVP patients with MR R + 3, the conservative therapy group had higher mortality than the early surgery group (31.45% vs. 5.25%, P < 0.001) after 4.5 ± 1.0 years of follow-up, multiple analysis showed that surgical treatment (hazard ratio [HR]: 0.202, P < 0.001), systolic pulmonary artery pressure of o60 mmHg (HR: 6.816, P < 0.001), age of ≥ 60 years (HR: 3.838, P < 0.001), and pericardial effusion (HR: 1.915, P = 0.003) were independent predictors of all-cause mortality. Conclusions: In patients with MVP, one-fifth leaflet prolapse located solely in P2 and one-half of MR jet derived from the middle scallop were anatomically eligible for transcatheter chordal repair and edge-to-edge repair therapy, respectively. Initial conservative therapy, pericardial effusion, pulmonary hypertension, and advanced age were independent predictors of a higher mortality rate in MVP patients with MR severity of ≥ 3+.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"102 - 108"},"PeriodicalIF":0.0,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46747175","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}
Pub Date : 2021-04-01DOI: 10.4103/2470-7511.320318
L. Bao, Rongchen Liu, Fangying Yan, Huizhi Fan, Guomin Huang, Xiu-fang Gao, Kun Xie, Yong Li, Hai-ming Shi
Objectives: We aimed to examine the protective effects of dapagliflozin (dapa) on thoracic aortic constriction (TAC)-induced heart failure in a nondiabetic mouse model. More specifically, we determined the effects of dapa on uncoupling protein 3 (UCP3) activation and subsequent metabolic remodeling. Methods: Sixty C57BL/6J mice were divided into six groups for TAC surgery and received different doses of dapa via gavage for 4 weeks. Echocardiography was performed to evaluate cardiac structure and function. Histological and molecular markers of cardiac remodeling and metabolic changes were assessed through staining assays, RT-PCR, western blot, and ELISA. HL-1 cells were used to explore the role of UCP3 in metabolic remodeling through transfection with UCP3 siRNA. Results: Mice that received TAC exhibited elevated heart weight/body weight ratios (HW/BW), left ventricular (LV) hypertrophy, impaired LV ejection fraction, and increased rates of fibrosis and apoptosis, unlike mice that received sham operation. Treatment with dapa after TAC restored HW/BW, improved LV parameters, and reduced fibrosis and apoptosis. dapa changed the expression levels of enzymes involved in glucose and fatty acid (FA) metabolism, such as pyruvate dehydrogenase lipoamide kinase isozyme 4, glucose transporter 4, carnitine palmitoyltransferase-1α, carnitine O-acetyltransferase, carnitine O-octanoyltransferase, acyl-CoA thioesterase 1, acyl-CoA thioesterase 2, peroxisome proliferator-activated receptors α and β, proliferator-activated receptor-gamma coactivator-1α, and UCP3, relative to the levels in mice in the TAC group. UCP3 siRNA reduced the expression of AMP-activated protein kinase and of factors involved in FA oxidation in vitro. Conclusions: Dapa exhibits cardioprotective effects in the model and augments expression of UCP3, which may be involved in metabolic remodeling in the failing heart.
{"title":"Dapagliflozin Regulates Cardiac Metabolic Remodeling Partially via Uncoupling Protein 3 in a Nondiabetic Thoracic Aortic Constriction-Induced Mouse Model","authors":"L. Bao, Rongchen Liu, Fangying Yan, Huizhi Fan, Guomin Huang, Xiu-fang Gao, Kun Xie, Yong Li, Hai-ming Shi","doi":"10.4103/2470-7511.320318","DOIUrl":"https://doi.org/10.4103/2470-7511.320318","url":null,"abstract":"Objectives: We aimed to examine the protective effects of dapagliflozin (dapa) on thoracic aortic constriction (TAC)-induced heart failure in a nondiabetic mouse model. More specifically, we determined the effects of dapa on uncoupling protein 3 (UCP3) activation and subsequent metabolic remodeling. Methods: Sixty C57BL/6J mice were divided into six groups for TAC surgery and received different doses of dapa via gavage for 4 weeks. Echocardiography was performed to evaluate cardiac structure and function. Histological and molecular markers of cardiac remodeling and metabolic changes were assessed through staining assays, RT-PCR, western blot, and ELISA. HL-1 cells were used to explore the role of UCP3 in metabolic remodeling through transfection with UCP3 siRNA. Results: Mice that received TAC exhibited elevated heart weight/body weight ratios (HW/BW), left ventricular (LV) hypertrophy, impaired LV ejection fraction, and increased rates of fibrosis and apoptosis, unlike mice that received sham operation. Treatment with dapa after TAC restored HW/BW, improved LV parameters, and reduced fibrosis and apoptosis. dapa changed the expression levels of enzymes involved in glucose and fatty acid (FA) metabolism, such as pyruvate dehydrogenase lipoamide kinase isozyme 4, glucose transporter 4, carnitine palmitoyltransferase-1α, carnitine O-acetyltransferase, carnitine O-octanoyltransferase, acyl-CoA thioesterase 1, acyl-CoA thioesterase 2, peroxisome proliferator-activated receptors α and β, proliferator-activated receptor-gamma coactivator-1α, and UCP3, relative to the levels in mice in the TAC group. UCP3 siRNA reduced the expression of AMP-activated protein kinase and of factors involved in FA oxidation in vitro. Conclusions: Dapa exhibits cardioprotective effects in the model and augments expression of UCP3, which may be involved in metabolic remodeling in the failing heart.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"109 - 120"},"PeriodicalIF":0.0,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45504774","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}
Pub Date : 2021-04-01DOI: 10.4103/2470-7511.320319
Xuejie Li, Nianwei Zhou, Huiyuan Xie, Wen Liu, C. Pan, Xianghong Shu
Objectives: This study aimed to diversify the spectrum of PRKAG2 variants and explore its clinical features in a Chinese Han population with hypertrophic cardiomyopathy (HCM). Methods: Whole-exome sequencing was performed on 200 patients diagnosed with HCM, and four causative PRKAG2 variants were identified in the probands and their relatives using Sanger sequencing. Their clinical manifestations, laboratory examinations, therapeutic methods, and outcomes were documented and analyzed. Results: Four variants were identified in six probands and seven of their relatives. Left ventricular hypertrophy was present in all probands. Five probands had sinus bradycardia, three had implanted pacemakers (PM), one developed heart failure, two had ventricular preexcitation, and one had atrial fibrillation. Conclusions: PRKAG2 cardiac syndrome (PCS) is a rare autosomal dominant disease characterized by ventricular hypertrophy, preexcitation, and progressive conduction defects, resulting in a high incidence of PM implantation. Genetic testing provides robust information for distinguishing PCS from sarcomeric HCM, which will be beneficial in guiding therapy and improving prognosis.
{"title":"Differential diagnosis of PRKAG2 Cardiac syndrome in hypertrophic cardiomyopathy patients of han nationality","authors":"Xuejie Li, Nianwei Zhou, Huiyuan Xie, Wen Liu, C. Pan, Xianghong Shu","doi":"10.4103/2470-7511.320319","DOIUrl":"https://doi.org/10.4103/2470-7511.320319","url":null,"abstract":"Objectives: This study aimed to diversify the spectrum of PRKAG2 variants and explore its clinical features in a Chinese Han population with hypertrophic cardiomyopathy (HCM). Methods: Whole-exome sequencing was performed on 200 patients diagnosed with HCM, and four causative PRKAG2 variants were identified in the probands and their relatives using Sanger sequencing. Their clinical manifestations, laboratory examinations, therapeutic methods, and outcomes were documented and analyzed. Results: Four variants were identified in six probands and seven of their relatives. Left ventricular hypertrophy was present in all probands. Five probands had sinus bradycardia, three had implanted pacemakers (PM), one developed heart failure, two had ventricular preexcitation, and one had atrial fibrillation. Conclusions: PRKAG2 cardiac syndrome (PCS) is a rare autosomal dominant disease characterized by ventricular hypertrophy, preexcitation, and progressive conduction defects, resulting in a high incidence of PM implantation. Genetic testing provides robust information for distinguishing PCS from sarcomeric HCM, which will be beneficial in guiding therapy and improving prognosis.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"132 - 140"},"PeriodicalIF":0.0,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44022035","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}
Pub Date : 2021-04-01DOI: 10.4103/2470-7511.320323
Siew Ho
Congenitally malformed hearts are often perceived as too complex for the general practitioner. By using a descriptive method, each malformed heart can be analyzed systematically without reference to presumptions of what went wrong during cardiac embryogenesis. The basis of this method, systemic segmental approach, is reviewed followed by examples of the common malformations.
{"title":"Congenital heart defects: A morphological approach","authors":"Siew Ho","doi":"10.4103/2470-7511.320323","DOIUrl":"https://doi.org/10.4103/2470-7511.320323","url":null,"abstract":"Congenitally malformed hearts are often perceived as too complex for the general practitioner. By using a descriptive method, each malformed heart can be analyzed systematically without reference to presumptions of what went wrong during cardiac embryogenesis. The basis of this method, systemic segmental approach, is reviewed followed by examples of the common malformations.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"141 - 147"},"PeriodicalIF":0.0,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41673470","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}
Pub Date : 2021-04-01DOI: 10.4103/2470-7511.320320
J. Ge, L. Ge, Y. Huo, Ji-yan Chen, Wei-min Wang, On Behalf of Chronic Total Occlusion Club
In 2018, the Chronic Total Occlusion Club China (CTOCC) presented a new CTO percutaneous coronary intervention (CTO PCI) algorithm. At the end of 2020, an updated CTOCC algorithm was proposed by this group after the adoption of innovative concepts and novel techniques in CTO PCI. The updated CTOCC algorithm summarizes the contemporary CTO PCI practices in China, in which simultaneous contralateral injection and careful angiographic review, along with strategic changes, are emphasized. Additionally, we provide some new recommendations for techniques such as the “move the cap” and “active greeting” techniques and investment procedures.
{"title":"Updated algorithm of chronic total occlusion percutaneous coronary intervention from chronic total occlusion club China","authors":"J. Ge, L. Ge, Y. Huo, Ji-yan Chen, Wei-min Wang, On Behalf of Chronic Total Occlusion Club","doi":"10.4103/2470-7511.320320","DOIUrl":"https://doi.org/10.4103/2470-7511.320320","url":null,"abstract":"In 2018, the Chronic Total Occlusion Club China (CTOCC) presented a new CTO percutaneous coronary intervention (CTO PCI) algorithm. At the end of 2020, an updated CTOCC algorithm was proposed by this group after the adoption of innovative concepts and novel techniques in CTO PCI. The updated CTOCC algorithm summarizes the contemporary CTO PCI practices in China, in which simultaneous contralateral injection and careful angiographic review, along with strategic changes, are emphasized. Additionally, we provide some new recommendations for techniques such as the “move the cap” and “active greeting” techniques and investment procedures.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"81 - 87"},"PeriodicalIF":0.0,"publicationDate":"2021-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47649300","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}
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