Pub Date : 2023-04-01DOI: 10.1097/CP9.0000000000000048
P. Du, Kailai Lu, Can-Jing Zhang, Ting Liu, Jianlin Hu, Tiantian Li
Background and purpose: Acute myocardial infarction (AMI) is a manifestation of coronary artery disease. Fine particulate matter (PM2.5) has been regarded as a risk factor for AMI-related mortality and hospitalizations. Agricultural activities contribute greatly to PM2.5 formation, indicating potential health risks of PM2.5 in agricultural areas. Health effect studies on agricultural source remain scarce, and currently available evidence is controversial. This study investigated the health effects of short-term exposure to PM2.5 from agricultural sources on AMI onset using a nationwide analysis in China. Methods: We reviewed case records from the China Cardiovascular Association Database and extracted the data of 355,815 patients with AMI onset from 1,653 hospitals for the period 2015 to 2018. We obtained daily concentrations of PM2.5 from agricultural sources using the source-oriented Community Multiscale Air Quality model. Moreover, we proposed a time-stratified case-crossover study to examine associations between exposure to PM2.5 from agricultural sources and AMI onset and determined lag effects with a maximum of 3 days. Additionally, we conducted multiple subgroup and sensitivity analyses. Results: Exposure to PM2.5 from agricultural sources caused a significantly increased risk of the onset of AMI and its subtypes. Short-term exposure to PM2.5 from agricultural sources on the current day (lag 0) was positively associated with a 4.4% (95% confidence interval [95% CI]: 3.3%–5.5%), 4.9% (95% CI: 3.5%–6.3%), and 3.4% (95% CI: 1.5%–5.4%) increase in the odds of AMI, ST-elevation myocardial infarction (STEMI), and non-STEMI (NSTEMI), for each 10 μg/m3 increase. Meanwhile, higher risk estimations were pronounced in individuals who were aged above 65 years, who lived in southern China, and who resided in the rural area setting, and significant differences were mostly found in NSTEMI onsets. Conclusions: Short-term exposure to PM2.5 from agricultural sources may trigger the onset of AMI and its two subtypes. Improving agriculture management through ammonia emission abatement can help in achieving PM2.5 reduction and protecting public health.
{"title":"Association of PM2.5 from agriculture sources and acute myocardial infarction onset: results from 2015 to 2018 in China","authors":"P. Du, Kailai Lu, Can-Jing Zhang, Ting Liu, Jianlin Hu, Tiantian Li","doi":"10.1097/CP9.0000000000000048","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000048","url":null,"abstract":"Background and purpose: Acute myocardial infarction (AMI) is a manifestation of coronary artery disease. Fine particulate matter (PM2.5) has been regarded as a risk factor for AMI-related mortality and hospitalizations. Agricultural activities contribute greatly to PM2.5 formation, indicating potential health risks of PM2.5 in agricultural areas. Health effect studies on agricultural source remain scarce, and currently available evidence is controversial. This study investigated the health effects of short-term exposure to PM2.5 from agricultural sources on AMI onset using a nationwide analysis in China. Methods: We reviewed case records from the China Cardiovascular Association Database and extracted the data of 355,815 patients with AMI onset from 1,653 hospitals for the period 2015 to 2018. We obtained daily concentrations of PM2.5 from agricultural sources using the source-oriented Community Multiscale Air Quality model. Moreover, we proposed a time-stratified case-crossover study to examine associations between exposure to PM2.5 from agricultural sources and AMI onset and determined lag effects with a maximum of 3 days. Additionally, we conducted multiple subgroup and sensitivity analyses. Results: Exposure to PM2.5 from agricultural sources caused a significantly increased risk of the onset of AMI and its subtypes. Short-term exposure to PM2.5 from agricultural sources on the current day (lag 0) was positively associated with a 4.4% (95% confidence interval [95% CI]: 3.3%–5.5%), 4.9% (95% CI: 3.5%–6.3%), and 3.4% (95% CI: 1.5%–5.4%) increase in the odds of AMI, ST-elevation myocardial infarction (STEMI), and non-STEMI (NSTEMI), for each 10 μg/m3 increase. Meanwhile, higher risk estimations were pronounced in individuals who were aged above 65 years, who lived in southern China, and who resided in the rural area setting, and significant differences were mostly found in NSTEMI onsets. Conclusions: Short-term exposure to PM2.5 from agricultural sources may trigger the onset of AMI and its two subtypes. Improving agriculture management through ammonia emission abatement can help in achieving PM2.5 reduction and protecting public health.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"118 - 125"},"PeriodicalIF":0.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49574316","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 : 2023-04-01Epub Date: 2023-07-20DOI: 10.1097/CP9.0000000000000043
Feng Bai, Jun Pu, Wenliang Che, Jiyan Chen, Mao Chen, Wei Chen, Xiaoping Chen, Yundai Chen, Xianwu Cheng, Xiang Cheng, Hongliang Cong, Cuilian Dai, Dali Fan, Guosheng Fu, Lei Gao, Chuanyu Gao, Wei Gao, Junbo Ge, Ben He, Tao Hu, Congxin Huang, Jing Huang, Yong Huo, Shaobin Jia, Jun Jiang, Zhicheng Jing, Xiangqing Kong, Lang Li, Yan Li, Yigang Li, Zhijuan Li, Chun Liang, Xianhe Lin, Xianxia Liu, Xuebo Liu, Chengzhi Lu, Genshan Ma, Yitong Ma, Wei Mao, Xia Mei, Zhongping Ning, Jiafu Ou, Shaderdin Slaj, Chengxing Shen, Haiming Shi, Hong Shi, Bei Shi, Xi Su, Ningling Sun, Qizhu Tang, Fang Wang, Changqian Wang, Jin Wang, Yanqing Wu, Yongjian Wu, Yunlong Xia, Dingcheng Xiang, Pingxi Xiao, Ping Xie, Dingding Xiong, Yawei Xu, Jiefu Yang, Lixia Yang, Zaixin Yu, Zuyi Yuan, Haitao Yuan, Guogang Zhang, Heng Zhang, Jian Zhang, Li Zhang, Ruiyan Zhang, Shuning Zhang, Shuyang Zhang, Zheng Zhang, Guoan Zhao, Xianxian Zhao, Jingang Zheng, Haoyi Zheng, Daxin Zhou, Shenghua Zhou, Yujie Zhou
The primary site of infection in COVID-19 exhibit is the respiratory system, but multiple organ systems could be affected. The virus could directly invade cardiomyocytes. Alternatively, cytokine storm could lead to myocardial injury. More importantly, the management of existing cardiovascular diseases must be re-examined in COVID-19 due to, for example, interaction between antiviral agents and with a wide variety of pharmacological agents. The Branch of Cardiovascular Physicians of Chinese Medical Doctor Association organized a panel of experts in cardiovascular and related fields to discuss this important issue, and formulated the "2023 Chinese Expert Consensus on the Impact of COVID-19 on the Management of Cardiovascular Diseases." The Consensus was drafted on the basis of systematic review of existing evidence and diagnosis and treatment experience, and covers three major aspects: myocardial injury caused by COVID-10 and COVID-19 vaccine, the impact of COVID-19 on patients with cardiovascular disease, and the impact of COVID-19 on the cardiovascular system of healthy people, and rehabilitation guidance recommendations. The Consensus involves 11 core clinical issues, including incidence, pathogenesis, clinical manifestations, treatment strategies, prognosis, and rehabilitation. It is our hope that this Consensus will provide a practical guidance to cardiologists in the management of cardiovascular diseases in the new era of COVID-19 pandemic.
{"title":"2023 Chinese expert consensus on the impact of COVID-19 on the management of cardiovascular diseases.","authors":"Feng Bai, Jun Pu, Wenliang Che, Jiyan Chen, Mao Chen, Wei Chen, Xiaoping Chen, Yundai Chen, Xianwu Cheng, Xiang Cheng, Hongliang Cong, Cuilian Dai, Dali Fan, Guosheng Fu, Lei Gao, Chuanyu Gao, Wei Gao, Junbo Ge, Ben He, Tao Hu, Congxin Huang, Jing Huang, Yong Huo, Shaobin Jia, Jun Jiang, Zhicheng Jing, Xiangqing Kong, Lang Li, Yan Li, Yigang Li, Zhijuan Li, Chun Liang, Xianhe Lin, Xianxia Liu, Xuebo Liu, Chengzhi Lu, Genshan Ma, Yitong Ma, Wei Mao, Xia Mei, Zhongping Ning, Jiafu Ou, Shaderdin Slaj, Chengxing Shen, Haiming Shi, Hong Shi, Bei Shi, Xi Su, Ningling Sun, Qizhu Tang, Fang Wang, Changqian Wang, Jin Wang, Yanqing Wu, Yongjian Wu, Yunlong Xia, Dingcheng Xiang, Pingxi Xiao, Ping Xie, Dingding Xiong, Yawei Xu, Jiefu Yang, Lixia Yang, Zaixin Yu, Zuyi Yuan, Haitao Yuan, Guogang Zhang, Heng Zhang, Jian Zhang, Li Zhang, Ruiyan Zhang, Shuning Zhang, Shuyang Zhang, Zheng Zhang, Guoan Zhao, Xianxian Zhao, Jingang Zheng, Haoyi Zheng, Daxin Zhou, Shenghua Zhou, Yujie Zhou","doi":"10.1097/CP9.0000000000000043","DOIUrl":"10.1097/CP9.0000000000000043","url":null,"abstract":"<p><p>The primary site of infection in COVID-19 exhibit is the respiratory system, but multiple organ systems could be affected. The virus could directly invade cardiomyocytes. Alternatively, cytokine storm could lead to myocardial injury. More importantly, the management of existing cardiovascular diseases must be re-examined in COVID-19 due to, for example, interaction between antiviral agents and with a wide variety of pharmacological agents. The Branch of Cardiovascular Physicians of Chinese Medical Doctor Association organized a panel of experts in cardiovascular and related fields to discuss this important issue, and formulated the \"2023 Chinese Expert Consensus on the Impact of COVID-19 on the Management of Cardiovascular Diseases.\" The Consensus was drafted on the basis of systematic review of existing evidence and diagnosis and treatment experience, and covers three major aspects: myocardial injury caused by COVID-10 and COVID-19 vaccine, the impact of COVID-19 on patients with cardiovascular disease, and the impact of COVID-19 on the cardiovascular system of healthy people, and rehabilitation guidance recommendations. The Consensus involves 11 core clinical issues, including incidence, pathogenesis, clinical manifestations, treatment strategies, prognosis, and rehabilitation. It is our hope that this Consensus will provide a practical guidance to cardiologists in the management of cardiovascular diseases in the new era of COVID-19 pandemic.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 2","pages":"82-102"},"PeriodicalIF":0.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0b/59/cp9-8-082.PMC10358441.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9856057","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}
Pub Date : 2023-01-01Epub Date: 2023-03-27DOI: 10.1097/CP9.0000000000000037
Zihang Huang, Aijun Sun
{"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}
Pub Date : 2023-01-01Epub Date: 2023-04-27DOI: 10.1097/CP9.0000000000000036
Ge Gao, Tao Zheng, Beidi Lan, Weiying Hui, Shi Chen, Zuyi Yuan, Yue Wu, John Y L Chiang, Tao Chen
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.
Methods: 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.
Results: 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 (P < 0.05).
Conclusions: 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.
{"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, Tao Zheng, Beidi Lan, Weiying Hui, Shi Chen, Zuyi Yuan, Yue Wu, John Y L Chiang, 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}
Pub Date : 2023-01-01DOI: 10.1097/CP9.0000000000000041
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
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.
{"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}
Pub Date : 2023-01-01Epub Date: 2023-04-04DOI: 10.1097/CP9.0000000000000045
[This corrects the article DOI: 10.1097/CP9.0000000000000020.].
[这更正了文章DOI:10.1097/CP90000000000000020.]。
{"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}
Pub Date : 2023-01-01DOI: 10.1097/CP9.0000000000000044
Yongjing Jiang, Gaoliang Zhou, Jun Feng, Likun Ma, Jianyuan Pan
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.
背景和目的：可用于早期评估并进一步提高钝性心脏损伤（BCI）阳性预测价值的风险因素尚不确定。我们进行了一项荟萃分析，以定量分析创伤患者脑机接口的损伤机制、危险因素和结果。方法：本系统综述和荟萃分析旨在收集外伤性心脏钝性损伤患者的数据。PubMed、Web of Science和EMBASE数据库在2021年11月20日之前一直在搜索研究。对脑机接口损伤机制、危险因素和结果进行了汇总荟萃分析。结果：我们筛选了256份记录，其中包括2000年至2019年发表的11项研究，报告了68039名创伤患者。机动车碰撞是主要的损伤机制，占脑机接口归因机制的65.2%[综合比例=0.652（0.595–0.709）]。综合相对风险（RR）显示，胸骨骨折、到达时休克、，心脏病史与脑机接口风险增加相关（胸骨骨折：RR=7.21[95%置信区间（CI）=3.99-13.05]；对于到达时的冲击：RR=2.45，95%CI=2.12-2.84；心脏病史：RR=1.87，95%CI=1.11–3.16）。与无脑机接口组相比，脑机接口治疗组的住院时间有显著差异，分别为11.68（95%CI=8.79–14.58天）和20.46（95%CI=16.78–24.14天）。有脑机接口的创伤患者的死亡率明显高于无脑机接口患者（RR=1.70，95%CI=1.53-1.90）。结论：在我们的研究中，脑机接口与死亡率增加有关。患者也倾向于延长住院时间。除了心电图和TnI外，当创伤患者存在胸骨骨折、休克和心脏病史时，我们建议对脑机接口进行筛查。
{"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}
Pub Date : 2023-01-01DOI: 10.1097/CP9.0000000000000035
Yu Zhang, Junchu Tu, Yujie Li, Yanli Wang, Lin Lu, Chengjie Wu, Xi-Yong Yu, Yangxin Li
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.
{"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}
Pub Date : 2023-01-01Epub Date: 2023-04-04DOI: 10.1097/CP9.0000000000000038
Yan Shen, Il-Man Kim, Neal L Weintraub, Yaoliang Tang
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.
Methods: 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.
Results: 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.
Conclusions: 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.
心肌梗死（MI）患者心肌组织中存活心肌细胞（CM）的代谢状况在很大程度上是未知的。空间单细胞RNA测序（scRNA-seq）是一种新的工具，能够对完整组织内的RNA特征进行无偏分析。我们使用该工具评估MI后患者心肌组织中存活CM的代谢谱。方法：使用空间scRNA-seq数据集比较MI患者和对照患者CM的遗传谱；我们分析了存活的CM在缺血生态位内的代谢适应。Seurat中的标准管道用于数据分析，包括归一化、特征选择和使用主成分分析（PCA）识别高度可变基因。Harmony用于消除批量效应，并基于注释集成CM样本。统一流形近似和投影（UMAP）用于降维。Seurat“FindMarkers”功能用于鉴定差异表达基因（DEG），通过基因本体论（GO）富集途径对其进行分析。最后scMetabolism R工具管道的参数方法=VISION（VISION是一个灵活的系统，它利用高通量管道和交互式网络报告以动态方式注释和探索scRNA-seq数据集）和metabolism.type=Kyoto Encyclopedia of Genes and Genomes（KEGG）来量化每个CM的代谢活性数据显示梗死心脏中存活的CM少于对照心脏。GO分析揭示了氧化磷酸化、心脏细胞发育中被抑制的途径，以及刺激和大分子代谢过程中被激活的途径。代谢分析显示，在存活的CM中，能量和氨基酸途径下调，嘌呤、嘧啶和一个碳库被叶酸途径增加。结论：梗死心肌中存活的CM表现出代谢适应，与氧化磷酸化、葡萄糖、脂肪酸和氨基酸代谢相关的大多数途径下调就是明证。相反，在存活的CM中，与嘌呤和嘧啶代谢、脂肪酸生物合成和单碳代谢相关的途径被上调。这些新发现对开发有效策略以提高梗死心脏内冬眠CM的存活率具有启示意义。
{"title":"Identification of the metabolic state of surviving cardiomyocytes in the human infarcted heart by spatial single-cell transcriptomics.","authors":"Yan Shen, Il-Man Kim, Neal L Weintraub, 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}
Pub Date : 2023-01-01DOI: 10.1097/CP9.0000000000000042
Ida Nađ, Dorotea Šijak, A. Miculinić, D. Bartoniček, Maja Hrabak Paar, I. Malcic
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.
{"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}
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