International heart journal最新文献_第9页

LncRNA NEAT1/miR-211/IL-10 Axis Regulates Inflammation of Peripheral Blood Mononuclear Cells in Acute Myocardial Infarction LncRNA NEAT1/miR-211/IL-10 轴调控急性心肌梗死时外周血单核细胞的炎症反应

IF 1.5 4区医学

International heart journal Pub Date : 2024-05-31 DOI: 10.1536/ihj.23-368

Min-na Hou, Gang-jun Zong, Ying Sun, Jia-jia Jiang, Jun Ding

{"title":"LncRNA NEAT1/miR-211/IL-10 Axis Regulates Inflammation of Peripheral Blood Mononuclear Cells in Acute Myocardial Infarction","authors":"Min-na Hou, Gang-jun Zong, Ying Sun, Jia-jia Jiang, Jun Ding","doi":"10.1536/ihj.23-368","DOIUrl":"https://doi.org/10.1536/ihj.23-368","url":null,"abstract":"This study aimed to explore the expression of long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) in patients with acute myocardial infarction (AMI) and its inflammatory regulation mechanism through miR-211/interleukin 10 (IL-10) axis.A total of 75 participants were enrolled in this study: 25 healthy people in the control group, 25 patients with stable angina pectoris (SAP) in the SAP group, and 25 patients with AMI in the AMI group. Real-time qPCR was used to detect mRNA expression levels of NEAT1, miR-211, and IL-10. The interaction between miR-211, NEAT1, and IL-10 was confirmed by dual-luciferase reporter assay, and protein expression was detected using western blot.High expression of NEAT1 in peripheral blood mononuclear cells (PBMCs) of patients with AMI was negatively related to serum creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), IL-6, and IL-1β and was positively correlated with left ventricular ejection fraction (LVEF). In THP-1 cells, miR-211 was confirmed to target and inhibit IL-10 expression. NEAT1 knockdown and miR-211-mimic markedly decreased IL-10 protein levels, whereas anti-miR-211 markedly increased IL-10 protein levels. Importantly, miR-211 level was negatively related to NEAT1 and IL-10 levels, whereas IL-10 level was positively related to the level of NEAT1 expression in PBMCs of patients with AMI.LncRNA NEAT1 was highly expressed in PBMCs of patients with AMI, and NEAT1 suppressed inflammation via miR-211/IL-10 axis in PBMCs of patients with AMI.\u0000","PeriodicalId":13711,"journal":{"name":"International heart journal","volume":"15 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141189701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Diverse Phenotypic Manifestations in a Family with a Novel RYR2 E4107A Variant 一个家族中的新型 RYR2 E4107A 变体的多种表型表现

IF 1.5 4区医学

International heart journal Pub Date : 2024-05-31 DOI: 10.1536/ihj.23-652

Hiroshi Hasegawa, Shuntaro Tamura, Tadashi Nakajima, Reika Kawabata-Iwakawa, Takashi Kobari, Naohiro Matsumoto, Yukie Sano, Masahiko Nishiyama, Masahiko Kurabayashi, Yoshiaki Kaneko, Yosuke Nakatani, Hideki Ishii

{"title":"Diverse Phenotypic Manifestations in a Family with a Novel RYR2 E4107A Variant","authors":"Hiroshi Hasegawa, Shuntaro Tamura, Tadashi Nakajima, Reika Kawabata-Iwakawa, Takashi Kobari, Naohiro Matsumoto, Yukie Sano, Masahiko Nishiyama, Masahiko Kurabayashi, Yoshiaki Kaneko, Yosuke Nakatani, Hideki Ishii","doi":"10.1536/ihj.23-652","DOIUrl":"https://doi.org/10.1536/ihj.23-652","url":null,"abstract":"Cardiac ryanodine receptor (RyR2) gain-of-function mutations cause catecholaminergic polymorphic ventricular tachycardia (CPVT). Conversely, RyR2 loss-of-function mutations cause a new disease entity, termed calcium release deficiency syndrome (CRDS), which may include RYR2-related long QT syndrome (LQTS). Importantly, unlike CPVT, patients with CRDS do not always exhibit exercise- or epinephrine-induced ventricular arrhythmias, which precludes a diagnosis of CRDS. Here we report a boy and his father, who both experienced exercise-induced cardiac events and harbor the same RYR2 E4107A variant. In the boy, an exercise stress test (EST) and epinephrine provocation test (EPT) did not induce any ventricular arrhythmias. QTc was slightly prolonged (QTc: 474 ms), and an EPT induced QTc prolongation (QTc-baseline: 466 ms, peak: 532 ms, steady-state: 527 ms). In contrast, in his father, QTc was not prolonged (QTc: 417 ms), and neither an EST nor EPT induced QTc prolongation. However, an EST induced multifocal premature ventricular contraction (PVC) bigeminy and bidirectional PVC couplets. Thus, they exhibited distinct clinical phenotypes: the boy exhibited LQTS (or CRDS) phenotype, whereas his father exhibited CPVT phenotype. These findings suggest that, in addition to the altered RyR2 function, other unidentified factors, such as other genetic, epigenetic, and environmental factors, and aging, may be involved in the diverse phenotypic manifestations. Considering that a single RYR2 variant can cause both CPVT and LQTS (or CRDS) phenotypes, in cascade screening of patients with CPVT and CRDS, an EST and EPT are not sufficient and genetic analysis is required to identify individuals who are at increased risk for life-threatening arrhythmias.\u0000","PeriodicalId":13711,"journal":{"name":"International heart journal","volume":"25 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141197992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MiR-378 Inhibits Angiotensin II-Induced Cardiomyocyte Hypertrophy by Targeting AKT2 MiR-378 通过靶向 AKT2 抑制血管紧张素 II 诱导的心肌细胞肥大

IF 1.5 4区医学

International heart journal Pub Date : 2024-05-31 DOI: 10.1536/ihj.23-485

Guili Wang, Linlin Feng, Chunxiang Liu, Zongqiang Han, Xia Chen

{"title":"MiR-378 Inhibits Angiotensin II-Induced Cardiomyocyte Hypertrophy by Targeting AKT2","authors":"Guili Wang, Linlin Feng, Chunxiang Liu, Zongqiang Han, Xia Chen","doi":"10.1536/ihj.23-485","DOIUrl":"https://doi.org/10.1536/ihj.23-485","url":null,"abstract":"Cardiomyocyte hypertrophy plays a crucial role in heart failure development, potentially leading to sudden cardiac arrest and death. Previous studies suggest that micro-ribonucleic acids (miRNAs) show promise for the early diagnosis and treatment of cardiomyocyte hypertrophy.To investigate the miR-378 expression in the cardiomyocyte hypertrophy model, reverse transcription-polymerase chain reaction (RT-qPCR), Western blot, and immunofluorescence tests were conducted in angiotensin II (Ang II)-induced H9c2 cells and Ang II-induced mouse model of cardiomyocyte hypertrophy. The functional interaction between miR-378 and AKT2 was studied by dual-luciferase reporter, RNA pull-down, Western blot, and RT-qPCR assays.The results of RT-qPCR analysis showed the downregulated expression of miR-378 in both the cell and animal models of cardiomyocyte hypertrophy. It was observed that the introduction of the miR-378 mimic inhibited the hypertrophy of cardiomyocytes induced by Ang II. Furthermore, the co-transfection of AKT2 expression vector partially mitigated the negative impact of miR-378 overexpression on Ang II-induced cardiomyocytes. Molecular investigations provided evidence that miR-378 negatively regulated AKT2 expression by interacting with the 3' untranslated region (UTR) of AKT2 mRNA.Decreased miR-378 expression and AKT2 activation are linked to Ang II-induced cardiomyocyte hypertrophy. Targeting miR-378/AKT2 axis offers therapeutic opportunity to alleviate cardiomyocyte hypertrophy.\u0000","PeriodicalId":13711,"journal":{"name":"International heart journal","volume":"99 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141188164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cholesterol Crystal Embolism in a Patient with Spontaneous Ruptured Aortic Plaques Identified by Non-Obstructive General Angioscopy 非阻塞性普通血管造影发现的主动脉斑块自发性破裂患者体内的胆固醇结晶栓塞

IF 1.5 4区医学

International heart journal Pub Date : 2024-05-31 DOI: 10.1536/ihj.23-559

Yutaka Koyama, Keisuke Kojima, Masanori Abe, Yasuo Okumura

引用次数: 0

LncRNA Peg13 Alleviates Myocardial Infarction/Reperfusion Injury through Regulating MiR-34a/Sirt1-Mediated Endoplasmic Reticulum Stress LncRNA Peg13 通过调节 MiR-34a/Sirt1 介导的内质网应激减轻心肌梗死/再灌注损伤

IF 1.5 4区医学

International heart journal Pub Date : 2024-05-31 DOI: 10.1536/ihj.23-453

Yonghong Wang, Jian Luo, Huiqiong Yang, Yanfei Liu

{"title":"LncRNA Peg13 Alleviates Myocardial Infarction/Reperfusion Injury through Regulating MiR-34a/Sirt1-Mediated Endoplasmic Reticulum Stress","authors":"Yonghong Wang, Jian Luo, Huiqiong Yang, Yanfei Liu","doi":"10.1536/ihj.23-453","DOIUrl":"https://doi.org/10.1536/ihj.23-453","url":null,"abstract":"Myocardial infarction/reperfusion (I/R) injury significantly impacts the health of older individuals. We confirmed that the level of lncRNA Peg13 was downregulated in I/R injury. However, the detailed function of Peg13 in myocardial I/R injury has not yet been explored.To detect the function of Peg13, in vivo model of I/R injury was constructed. RT-qPCR was employed to investigate RNA levels, and Western blotting was performed to assess levels of endoplasmic reticulum stress and apoptosis-associated proteins. EdU staining was confirmed to assess the cell proliferation.I/R therapy dramatically produced myocardial injury, increased the infarct area, and decreased the amount of Peg13 in myocardial tissues of mice. In addition, hypoxia/reoxygenation (H/R) notably induced the apoptosis and promoted the endoplasmic reticulum (ER) stress of HL-1 cells, while overexpression of Peg13 reversed these phenomena. Additionally, Peg13 may increase the level of Sirt1 through binding to miR-34a. Upregulation of Peg13 reversed H/R-induced ER stress via regulation of miR-34a/Sirt1 axis.LncRNA Peg13 reduces ER stress in myocardial infarction/reperfusion injury through mediation of miR-34a/Sirt1 axis. Hence, our research might shed new lights on developing new strategies for the treatment of myocardial I/R injury.\u0000","PeriodicalId":13711,"journal":{"name":"International heart journal","volume":"37 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141189700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sirtuin 6 Deacetylates Apoptosis-Associated Speck-Like Protein (ASC) to Inhibit Endothelial Cell Pyroptosis in Atherosclerosis Sirtuin 6 可使凋亡相关斑点样蛋白 (ASC) 去乙酰化，从而抑制动脉粥样硬化中的内皮细胞猝死现象

IF 1.5 4区医学

International heart journal Pub Date : 2024-05-15 DOI: 10.1536/ihj.23-334

Jian Huang, Shuilin Dong, Yanhui Wu, Huiming Yi, Wei Zhang, Xi Ai

{"title":"Sirtuin 6 Deacetylates Apoptosis-Associated Speck-Like Protein (ASC) to Inhibit Endothelial Cell Pyroptosis in Atherosclerosis","authors":"Jian Huang, Shuilin Dong, Yanhui Wu, Huiming Yi, Wei Zhang, Xi Ai","doi":"10.1536/ihj.23-334","DOIUrl":"https://doi.org/10.1536/ihj.23-334","url":null,"abstract":"Endothelial cell dysfunction is the main pathology of atherosclerosis (AS). Sirtuin 6 (SIRT6), a deacetylase, is involved in AS progression. This study aimed to investigate the impacts of SIRT6 on the pyroptosis of endothelial cells and its underlying mechanisms. ApoE−/− mice were fed a high-fat diet (HFD) to establish the AS mouse model, atherosclerotic lesions were evaluated using oil red O staining, and blood lipids and inflammatory factors were measured using corresponding kits. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) to establish the cell model, and pyroptosis was evaluated by flow cytometry, ELISA, and western blot. Immunoprecipitation (IP), co-IP, western blot, and immunofluorescence were used to detect the molecular mechanisms. The results showed that SIRT6 expression was downregulated in the blood of HFD-induced mice and ox-LDL-induced HUVECs. Overexpression of SIRT6 reduced atherosclerotic lesions, blood lipids, and inflammation in vivo and suppressed pyroptosis of HUVECs in vitro. Moreover, SIRT6 interacted with ASC to inhibit the acetylation of ASC, thus, reducing the interaction between ASC and NLRP3. Moreover, SIRT6 inhibits endothelial cell pyroptosis in the aortic roots of mice by deacetylating ASC. In conclusion, SIRT6 deacetylated ASC to inhibit its interaction with NLRP3 and then suppressed pyroptosis of endothelial cells, thus, decelerating the progression of AS. The findings provide new insights into the function of SIRT6 in AS.\u0000","PeriodicalId":13711,"journal":{"name":"International heart journal","volume":"30 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140941203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Surviving Case of Myocardial Infarction with Ventricular Septal Rupture and Ventricular Aneurysm following Gastrointestinal Bleeding 胃肠道出血后心肌梗死伴室间隔破裂和心室动脉瘤的存活病例

IF 1.5 4区医学

International heart journal Pub Date : 2024-05-15 DOI: 10.1536/ihj.23-586

Misa Kusumoto, Jumpei Yamamoto, Sakura Kaneda, Takuya Matsushiro, Masaya Yamamoto, Hisao Hara, Nobuyuki Inoue, Yukio Hiroi

{"title":"A Surviving Case of Myocardial Infarction with Ventricular Septal Rupture and Ventricular Aneurysm following Gastrointestinal Bleeding","authors":"Misa Kusumoto, Jumpei Yamamoto, Sakura Kaneda, Takuya Matsushiro, Masaya Yamamoto, Hisao Hara, Nobuyuki Inoue, Yukio Hiroi","doi":"10.1536/ihj.23-586","DOIUrl":"https://doi.org/10.1536/ihj.23-586","url":null,"abstract":"A 55-year-old man presented to the emergency department with worsening shortness of breath 1 month after a gastrointestinal bleed. He had congestive heart failure, and an electrocardiogram suggested ischemic heart disease involvement. Echocardiography revealed a ventricular septal defect complicated by a left ventricular aneurysm in the inferior-posterior wall. Conservative treatment was started, but hemodynamic collapse occurred on the third day of admission and coronary angiography revealed a revascularizing lesion in the right fourth posterior descending coronary artery. Subsequently, his hemodynamic status continued to deteriorate, even with an Impella CP® heart pump, so ventricular septal defect patch closure and left ventricular aneurysm suture were performed. His condition improved and he was discharged on day 23 of admission and was not readmitted within 6 months after the procedure. Hemodynamic management of ventricular septal defects requires devices that reduce afterload, and clinicians should be aware of the risk of myocardial infarction after gastrointestinal bleeding.\u0000","PeriodicalId":13711,"journal":{"name":"International heart journal","volume":"2 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140941209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Impact of Cancer History on Temporal Changes in the Cardiopulmonary Exercise Test of Patients with Cardiovascular Disease 癌症史对心血管疾病患者心肺运动测试时间变化的影响

IF 1.5 4区医学

International heart journal Pub Date : 2024-05-15 DOI: 10.1536/ihj.24-037

Keisuke Satogami, Junko Morimoto, Takaya Naraoka, Motoki Taniguchi, Takahiro Nishi, Yoshinori Asae, Akira Taruya, Atsushi Tanaka

{"title":"Impact of Cancer History on Temporal Changes in the Cardiopulmonary Exercise Test of Patients with Cardiovascular Disease","authors":"Keisuke Satogami, Junko Morimoto, Takaya Naraoka, Motoki Taniguchi, Takahiro Nishi, Yoshinori Asae, Akira Taruya, Atsushi Tanaka","doi":"10.1536/ihj.24-037","DOIUrl":"https://doi.org/10.1536/ihj.24-037","url":null,"abstract":"The elevated risk of cardiovascular disease (CVD) in cancer patients and survivors is likely the result of normal age-related pathologies coupled with the direct and indirect effects of cancer therapy that extend across multiple systems. The purpose of this study was to investigate the impact of cardiac rehabilitation (CR) on CVD patients with a history of cancer.In this study, patients who had participated in the outpatient CR program were enrolled and were divided into 2 groups (cancer survivor group and no-cancer group) based on their history of cancer. The cardiopulmonary exercise test (CPET) was performed at the beginning (baseline) and at the end of the CR program (follow-up). The results of CPET at baseline and those at follow-up were analyzed retrospectively.A total of 105 patients were analyzed in this study. The cancer survivor group had 25 patients, and the non-cancer group 80. At baseline, peak oxygen uptake (peak VO2) (14.7 [11.9 to 17.6] mL/kg/minute versus 11.3 [9.7 to 14.7] mL/kg/minute; P = 0.003) was significantly lower in cancer survivors. The percent changes in peak VO2 between baseline and follow-up were not significantly different between the 2 groups (7.9 % [−11.5 to 24.5] versus 9.4 % [−7.5 to 27.3] P = 0.520).The percent changes in peak VO2 of CR participants were not significantly different despite their cancer history.\u0000","PeriodicalId":13711,"journal":{"name":"International heart journal","volume":"15 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140941318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Potential Effects of Ischemic Postconditioning and Changes in Heat Shock Protein 72 in Patients with Acute Myocardial Infarction without Prodromal Angina 缺血后条件和热休克蛋白 72 变化对无心绞痛前兆的急性心肌梗死患者的潜在影响

IF 1.5 4区医学

International heart journal Pub Date : 2024-05-15 DOI: 10.1536/ihj.23-651

Toshiharu Takeuchi, Yuya Kitani, Akiho Minoshima, Hisanobu Ota, Naoki Nakagawa, Kazuhiro Sumitomo, Yoshinao Ishii, Naoyuki Hasebe

{"title":"Potential Effects of Ischemic Postconditioning and Changes in Heat Shock Protein 72 in Patients with Acute Myocardial Infarction without Prodromal Angina","authors":"Toshiharu Takeuchi, Yuya Kitani, Akiho Minoshima, Hisanobu Ota, Naoki Nakagawa, Kazuhiro Sumitomo, Yoshinao Ishii, Naoyuki Hasebe","doi":"10.1536/ihj.23-651","DOIUrl":"https://doi.org/10.1536/ihj.23-651","url":null,"abstract":"The effectiveness of ischemic postconditioning (iPoC) in patients with ST-elevation myocardial infarction (STEMI) without ischemic preconditioning has not been determined. Therefore, we investigated the impact of iPoC and its potential mechanism related to heat shock protein 72 (HSP72) induction on myocardial salvage in patients with STEMI without prodromal angina (PA).We retrospectively analyzed data from 102 patients with STEMI with successful reperfusion among 323 consecutive patients with acute coronary syndrome. Among these, 55 patients with iPoC (iPoC (+) ) underwent 4 cycles of 60-second inflation and 30-second deflation of the angioplasty balloon. Both the iPoC (+) and iPoC (-) groups were divided into 2 further subgroups: patients with PA (PA (+) ) and those without (PA (-) ). We analyzed HSP72 levels in neutrophils, which were measured until 48 hours after reperfusion. I-123 β-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) scintigraphy was performed within a week of reperfusion therapy. In 64% of patients, thallium-201 (TL) scintigraphy was performed 6-8 months after STEMI onset.Using BMIPP and TL, in the PA (-) subgroups, the iPoC (+) group had a significantly greater myocardial salvage ratio than the iPoC (-) group. iPoC was identified as an independent predictor of the myocardial salvage ratio. The HSP72 increase ratio was significantly elevated in the iPoC (+) PA (-) group. Importantly, the myocardial salvage effect in patients without PA was significantly correlated with the HSP72 increase ratio, which was greater in patients with iPoC.These results suggest the potential impact of iPoC via HSP72 induction on myocardial salvage; however, the effects may be limited to patients with STEMI without PA.\u0000","PeriodicalId":13711,"journal":{"name":"International heart journal","volume":"2 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140941205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Case of Coronary Artery Perforation Caused by Manual Cardiopulmonary Resuscitation in the Catheterization Laboratory 导管室人工心肺复苏术导致冠状动脉穿孔一例

IF 1.5 4区医学

International heart journal Pub Date : 2024-05-15 DOI: 10.1536/ihj.23-549

Kei Morishita, Takatoshi Unno, Takahiko Murakami, Kensuke Okada, Hiroshi Matsunaga, Kazuo Asada, Yasutoshi Omori, Akiko Ishihara, Yoshiro Kamoi, Takahiro Tanaka

{"title":"A Case of Coronary Artery Perforation Caused by Manual Cardiopulmonary Resuscitation in the Catheterization Laboratory","authors":"Kei Morishita, Takatoshi Unno, Takahiko Murakami, Kensuke Okada, Hiroshi Matsunaga, Kazuo Asada, Yasutoshi Omori, Akiko Ishihara, Yoshiro Kamoi, Takahiro Tanaka","doi":"10.1536/ihj.23-549","DOIUrl":"https://doi.org/10.1536/ihj.23-549","url":null,"abstract":"Cardiopulmonary resuscitation (CPR) is essential for the survival of cardiac arrest patients, but it can cause severe traumatic complications. In the catheterization laboratory, various physical constraints complicate the appropriate performance of CPR. However, we are not aware of reports of CPR complications in this setting. Here, we report a case of coronary artery perforation (CAP) caused by manual CPR in the catheterization laboratory. The patient, a 68-year-old woman, initially underwent successful percutaneous coronary intervention (PCI) for unstable angina. Back in the ward, the patient experienced acute stent thrombosis, which resulted in cardiac arrest, and another PCI was performed under ongoing manual CPR. Although revascularization was successful, sudden CAP occurred, leading to cardiac tamponade. Despite extensive treatment efforts, the patient died 18 hours later.Initially, the compression site of CPR was on the midline of the sternum; however, the compression site shifted to the left, to just above the left anterior descending artery, by the time that CAP was detected via angiography. This corresponded to the area where rib fractures were observed upon computed tomography, suggesting the possibility of traumatic CAP due to manual CPR. The physical constraints in the catheterization laboratory can lead to an inappropriate CPR technique and severe traumatic complications.\u0000","PeriodicalId":13711,"journal":{"name":"International heart journal","volume":"7 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140941316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0