Cardiology PlusPub Date : 2022-03-01DOI: 10.1097/CP9.0000000000000004
B. He, Panyang Xu, Qi Zhou, J. Xu, Lu Cai
{"title":"Serum N-terminal-pro-B-type natriuretic peptide is dependent on age and sex: a cross-sectional analysis in healthy adults from Northeast China","authors":"B. He, Panyang Xu, Qi Zhou, J. Xu, Lu Cai","doi":"10.1097/CP9.0000000000000004","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000004","url":null,"abstract":"Abstract Background: Previous studies suggested higher serum N-terminal-pro-B-type natriuretic peptide (NT-proBNP) level with older age and in women, but the reference intervals (RIs) recommended by assay manufacturers do not fully recognize such pattern. Aims: In this study, we aimed to establish a set of age- and sex-specific RIs for serum NT-proBNP in healthy adults from Northeast China. Methods: Healthy adult subjects (20 to ≤95 years old) were recruited from the physical examination center at a teaching hospital during a period from March 2020 to July 2020. Serum NT-proBNP concentration was measured using the VITROS 5600 Integrated System with a chemiluminescence method. RIs were calculated based on the EP28-A3c guidelines by the Clinical and Laboratory Standards Institute. A generalized linear model was performed to factors that were associated with NT-proBNP level. Results: The final analysis included 2,183 subjects (1,074 men and 1,109 women, mean age 54.2 ± 19.5 years). Serum NT-proBNP level increased with advancing age (20 to <50, 50 to <60, 60 to <75 and ≥75 years), and was significantly higher in women than in men with the exception of the ≥75 age group. Higher NT-proBNP level was associated with the female sex, older age, lower body mass index, higher urea nitrogen, higher creatinine, lower uric acid, and lower triglyceride (P < 0.05 for all). The strongest association was with the female sex, followed by age. Conclusions: Serum NT-proBNP level must be interpreted with consideration of sex and age. Higher NT-proBNP is associated with the female sex and older age.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"48 - 55"},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47379031","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}
Cardiology PlusPub Date : 2022-03-01DOI: 10.1097/CP9.0000000000000008
Shidi Hu, Ji'e Yang, Feng Zhang
{"title":"Signaling pathways of inflammation in myocardial ischemia/reperfusion injury","authors":"Shidi Hu, Ji'e Yang, Feng Zhang","doi":"10.1097/CP9.0000000000000008","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000008","url":null,"abstract":"Abstract Primary percutaneous coronary intervention is the current standard treatment for myocardial infarction, but is associated with ischemia/reperfusion injury for which inflammation is an important part. This review summaries the recent findings in the study of pro- and anti-inflammatory signaling pathways (eg, TLR4/Myd88/NF-κB, MAPKs/NF-κB, NLRP3 inflammasome, JAK2/STAT3, and Nrf2/HO-1) in myocardial ischemia/reperfusion injury, as well as relevant drug development efforts. Despite of the vast body of literature, no concrete advances have been made in translating the new knowledge into clinical practice, but we do anticipate major breakthroughs in the foreseeable future.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"29 - 38"},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44708546","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}
Cardiology PlusPub Date : 2022-03-01DOI: 10.1097/cp9.0000000000000001
Magnus Bäck, M. Hashem, A. Giani, S. Pawelzik, A. Franco-Cereceda
{"title":"Calcific aortic valve stenosis and COVID-19: clinical management, valvular damage, and pathophysiological mechanisms","authors":"Magnus Bäck, M. Hashem, A. Giani, S. Pawelzik, A. Franco-Cereceda","doi":"10.1097/cp9.0000000000000001","DOIUrl":"https://doi.org/10.1097/cp9.0000000000000001","url":null,"abstract":"","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45433050","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}
Cardiology PlusPub Date : 2021-10-01DOI: 10.4103/2470-7511.334396
W. Pan, Nan-Chao Hong, J. Ge, Da-Xin Zhou
{"title":"Coronary artery fistula: To close or not close, that is the question","authors":"W. Pan, Nan-Chao Hong, J. Ge, Da-Xin Zhou","doi":"10.4103/2470-7511.334396","DOIUrl":"https://doi.org/10.4103/2470-7511.334396","url":null,"abstract":"Prognosis in subjects with coronary artery fistula (CAF) is highly variable. CAF may remain asymptomatic throughout the entire lifetime in some; however, in others, CAF may become hemodynamically significant and complications ensue. CAF closure, either surgically or via a transcatheter approach, eliminates the underlying anatomical anomaly but is associated with a variety of complications, including but not limited to coronary thrombosis and even full-blown myocardial infarction. In this review, we summarize the evidence that argued for versus against CAF closure and attempt to provide a balanced view of the benefits versus harm of CAF closure in patients with different types of CAF.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"256 - 263"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45288638","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}
Cardiology PlusPub Date : 2021-10-01DOI: 10.4103/2470-7511.334401
Rachel Parise, S. Ramesh, Manoj Govindarajulu, Amir Ajoolabady, Timothy Moore, M. Dhanasekaran
{"title":"COVID-19-induced cardiovascular damage differs from other prevalent viruses","authors":"Rachel Parise, S. Ramesh, Manoj Govindarajulu, Amir Ajoolabady, Timothy Moore, M. Dhanasekaran","doi":"10.4103/2470-7511.334401","DOIUrl":"https://doi.org/10.4103/2470-7511.334401","url":null,"abstract":"Viral infections persist globally, among all ages, gender, and ethnicity. Of particular importance is COVID-19, associated with asymptomatic to severe symptoms, including complications/mortality. Cardiovascular disease (CVD) involves heart and blood vessel disorders including coronary heart disease, cerebrovascular disease, peripheral artery disease, thrombosis, and more. CVD associated with severe COVID-19 includes heart failure, coronary artery disease, cardiomyopathy, hypertension, and cerebrovascular disease/stroke. Data were acquired from PubMed, Google Scholar, Centers for Disease Prevention and Control, and Lexi-Comp using the search terms “COVID-19 and cardiovascular pathology;” “COVID-19 induced CVD;” “Viral infection induced CVD;” and “Viral infection induced heart damage.” COVID-19-induced CVD mechanisms include direct viral entry, inflammation, cytokine storm, hypoxia, interferon-mediated immune response, plaque destabilization, stress, and drug-induced causes. Other viral pathologies causing CVD include atherosclerosis, inflammation, cytokine storm, and plaque destabilization. Individual parameters, such as old age, males, and higher body mass index (BMI), are more likely to experience viral-associated complications, possibly explained by patient risk factors or comorbidities. Populations at higher risk include older males with an elevated BMI. Viral mechanisms associated with CVD are similar but differ in disease severity, potentially explained by diverse cytokine profiles where COVID-19 activates different types at higher quantities.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"231 - 245"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42766914","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":"Cardiac protective effects of proinflammatory cytokines during ischemia-reperfusion","authors":"Li-Sha Li, Hong Wu, Shu-Xia Wang, Sui-xin Liu, Le-Qing Lin, Da-Ke Qi","doi":"10.4103/2470-7511.334402","DOIUrl":"https://doi.org/10.4103/2470-7511.334402","url":null,"abstract":"Myocardial ischemia and reperfusion (I/R) lead to an inflammatory response that causes cardiac injury and remodeling. However, increasing evidence suggests this is an over-simplified view. Several proinflammatory cytokines, including tumor necrosis factor-α, interleukin-1α, interleukin-6, macrophage migration inhibitory factor and D-dopachrome tautomerase have been shown to improve cell survival and compensate energy deprivation during I/R. This review summarizes the recent findings that support protective role of proinflammatory cytokines against cardiac injury during acute I/R, as well as therapeutic ramifications of these findings.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"246 - 255"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43302434","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}
Cardiology PlusPub Date : 2021-10-01DOI: 10.4103/2470-7511.334403
Donghui Zhao, Sidney Smith Jr
{"title":"Quality of Care for Patients with Acute Coronary Syndrome","authors":"Donghui Zhao, Sidney Smith Jr","doi":"10.4103/2470-7511.334403","DOIUrl":"https://doi.org/10.4103/2470-7511.334403","url":null,"abstract":"Acute coronary syndrome (ACS) is a severe clinical manifestation of ischemic heart disease with a high risk of death. The quality of care provided by the health system and medical providers to patients with ACS in daily clinical practice determines the likelihood of desired health outcomes or prognosis. This review provides an overview of several key issues in the quality of care for ACS, including how to measure the quality of care for ACS and the main strategies to improve the quality of care for ACS patients in both the acute and chronic phases. Efforts to improve the quality of care for ACS through specific programs in Western countries and in China are also described.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"202 - 209"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46928291","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}
Cardiology PlusPub Date : 2021-10-01DOI: 10.4103/2470-7511.334399
D. Yan, Yongming Zhang, Yu-hua Ji, Tao Wang, Xiao-Xing Xiong, Heng Zhao
{"title":"Re-visit the concept of M1 versus M2 phenotypes of BV2 microglia and test their effects on stroke outcome in mice","authors":"D. Yan, Yongming Zhang, Yu-hua Ji, Tao Wang, Xiao-Xing Xiong, Heng Zhao","doi":"10.4103/2470-7511.334399","DOIUrl":"https://doi.org/10.4103/2470-7511.334399","url":null,"abstract":"Backgrounds: Whether there are distinctive macrophage functional phenotypes of M1 versus M2 has been debated. We re-examined them by studying M1/M2 gene and protein expressions in cultured BV2 microglial cells and their effects on stroke outcomes in vivo. Methods: BV2 microglia cells were cultured and polarized with lipopolysaccharide (LPS) and interleukin-4 (IL-4) to produce M (LPS) and M (IL-4) phenotypes, which were originally defined as M1 and M2 phenotypes, respectively. Typical M1 and M2 gene or protein expression patterns were analyzed in M (LPS) and M (IL-4) phenotypes and their distinctive effects on stroke outcomes were compared. Results: M (LPS) and M (IL-4) had distinctive morphologies. M (IL-4) had significantly higher gene expressions of the typical M2 markers and other anti-inflammatory genes, while M (LPS) had higher gene expression of typical M1 markers and other pro-inflammatory genes. Nevertheless, M2 gene expressions were also enhanced in M (LPS), and M1 gene expressions were increased in M (IL-4), although with relatively lower levels. Adoptive transfer of M (IL-4) reduced infarction and improved neurological scores, while M (LPS) macrophages generated the opposite effect. Fluorescence activated cell sorting (FACS) and confocal studies suggest that M (IL-4) inhibited, while M (LPS) promoted the infiltration of monocyte-derived macrophages and iNOS-positive cells. Conclusions: M (LPS) and M (IL-4) from cultured BV2 cells indeed are distinctive functional phenotypes, but it is inaccurate to simply classify them into M1 and M2 phenotypes based on a few typical gene and protein markers.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"264 - 273"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47752503","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}
Cardiology PlusPub Date : 2021-10-01DOI: 10.4103/2470-7511.334400
C. Tam, C. Siu, H. Tse
{"title":"Challenges in management of ST elevation myocardial infarction during COVID-19 pandemic","authors":"C. Tam, C. Siu, H. Tse","doi":"10.4103/2470-7511.334400","DOIUrl":"https://doi.org/10.4103/2470-7511.334400","url":null,"abstract":"The coronavirus disease-2019 (COVID-19) pandemic has brought unprecedented changes to our world and health-care system. Its high virulence and infectiousness directly infect people's respiratory system and indirectly disrupt our health-care infrastructure. In particular, ST elevation myocardial infarction (STEMI) is a clinical emergency emphasizes on the establishment of care system to minimize delay to reperfusion. As such, the impact of COVID-19 on STEMI care, ranging from disease severity, patient delay, diagnostic difficulty, triage to selection of reperfusion strategy and postoperative care, is immense. Importantly, not only we have to save our patients, but we must also need to protect all health-care workers and prevent environmental contamination. Otherwise, in-hospital transmission can quickly evolve into nosocomial outbreak with staff infection and quarantine which lead to health-care system collapse. In this article, we will discuss the challenges in various aspects of STEMI management during COVID-19, as well as the mitigation measures we can take to optimize outcome and our future.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"218 - 230"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47272021","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}
Cardiology PlusPub Date : 2021-10-01Epub Date: 2021-12-30DOI: 10.4103/2470-7511.334404
Jun Ren
{"title":"Cardiovascular medicine in the era of COVID-19 pandemics.","authors":"Jun Ren","doi":"10.4103/2470-7511.334404","DOIUrl":"10.4103/2470-7511.334404","url":null,"abstract":"","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"199-201"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8951666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46144437","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}