• Title/Summary/Keyword: myocardial infarct

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In Vivo Protein Transduction: Delivery of PEP-1-SOD1 Fusion Protein into Myocardium Efficiently Protects against Ischemic Insult

  • Zhang, You-en;Wang, Jia-ning;Tang, Jun-ming;Guo, Ling-yun;Yang, Jian-ye;Huang, Yong-zhang;Tan, Yan;Fu, Shou-zhi;Kong, Xia;Zheng, Fei
    • Molecules and Cells
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    • v.27 no.2
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    • pp.159-166
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    • 2009
  • Myocardial ischemia-reperfusion injury is a medical problem occurring as damage to the myocardium following blood flow restoration after a critical period of coronary occlusion. Oxygen free radicals (OFR) are implicated in reperfusion injury after myocardial ischemia. The antioxidant enzyme, Cu, Zn-superoxide dismutase (Cu, Zn-SOD, also called SOD1) is one of the major means by which cells counteract the deleterious effects of OFR after ischemia. Recently, we reported that a PEP-1-SOD1 fusion protein was efficiently delivered into cultured cells and isolated rat hearts with ischemia-reperfusion injury. In the present study, we investigated the protective effects of the PEP-1-SOD1 fusion protein after ischemic insult. Immunofluorescecnce analysis revealed that the expressed and purified PEP-1-SOD1 fusion protein injected into rat tail veins was efficiently transduced into the myocardium with its native protein structure intact. When injected into Sprague-Dawley rat tail veins, the PEP-1-SOD1 fusion protein significantly attenuated myocardial ischemia-reperfusion damage; characterized by improving cardiac function of the left ventricle, decreasing infarct size, reducing the level of malondialdehyde (MDA), decreasing the release of creatine kinase (CK) and lactate dehydrogenase (LDH), and relieving cardiomyocyte apoptosis. These results suggest that the biologically active intact forms of PEP-1-SOD1 fusion protein will provide an efficient strategy for therapeutic delivery in various diseases related to SOD1 or to OFR.

Complete Versus Culprit-Only Revascularization for ST-Segment Elevation Myocardial Infarction and Multivessel Disease in the 2nd Generation Drug-Eluting Stent Era: Data from the INTERSTELLAR Registry

  • Kwon, Sung Woo;Park, Sang-Don;Moon, Jeonggeun;Oh, Pyung Chun;Jang, Ho-Jun;Park, Hyun Woo;Kim, Tae-Hoon;Lee, Kyounghoon;Suh, Jon;Kang, WoongChol
    • Korean Circulation Journal
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    • v.48 no.11
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    • pp.989-999
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    • 2018
  • Background and Objectives: We aimed to compare outcomes of complete revascularization (CR) versus culprit-only revascularization for ST-segment elevation myocardial infarction (STEMI) and multivessel disease (MVD) in the $2^{nd}$ generation drug-eluting stent (DES) era. Methods: From 2009 to 2014, patients with STEMI and MVD, who underwent primary percutaneous coronary intervention (PCI) using a $2^{nd}$ generation DES for culprit lesions were enrolled. CR was defined as PCI for a non-infarct-related artery during the index admission. Major adverse cardiovascular event (MACE) was defined as cardiovascular (CV) death, non-fatal myocardial infarction, target lesion revascularization, or heart failure during the follow-up year. Results: In total, 705 MVD patients were suitable for the analysis, of whom 286 (41%) underwent culprit-only PCI and 419 (59%) underwent CR during the index admission. The incidence of MACE was 11.5% in the CR group versus 18.5% in the culprit-only group (hazard ratio [HR], 0.56; 95% confidence interval [CI], 0.37-0.86; p<0.01; adjusted HR, 0.64; 95% CI, 0.40-0.99; p=0.04). The CR group revealed a significantly lower incidence of CV death (7.2% vs. 12.9%; HR, 0.51; 95% CI, 0.31-0.86; p=0.01 and adjusted HR, 0.57; 95% CI; 0.32-0.97; p=0.03, respectively). Conclusions: CR was associated with better outcomes including reductions in MACE and CV death at 1 year of follow-up compared with culprit-only PCI in the $2^{nd}$ generation DES era.

Comparison of Emergency Tc-99m Sestamibi Myocardial Perfusion SPECT and ECG in the Diagnosis of Acute Myocardial Infarction (급성심근경색증 환자에서 응급으로 시행한 Tc-99m Sestamibi 심근관류 SPECT와 심전도의 비교)

  • Cho, Ihn-Ho;Lee, Hyoung-Woo;Park, Jong-Sun;Won, Kyu-Chang;Do, Jun-Young;Sin, Dong-Gu;Yoon, Kyung-Woo;Kim, Young-Jo;Shim, Bong-Sup;Lee, Hyun-Woo
    • The Korean Journal of Nuclear Medicine
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    • v.30 no.1
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    • pp.104-111
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    • 1996
  • We did Tc-99m sestamibi myocardial perfusion SPECT in 36 patients with acute myocardial infarction when they arrived at the emergency room. And we compared myocardial perfusion images with ECG findings. Then we obtained the follows. The myocardial infarction by the obstruction of left coronary descending artery and right coronary artery showed a good concordance in the diagnosis and infarction site between myocardial perfusion images and ECG findings. The 7 patients with myocardial infarction by a left circumflex coronary artery showed a perfusion defect in the lateral wall in myocardial perfusion SPECT images. But 4 patients of them showed ST segment elevation, 2 patients showed ST depression and 1 patient showed normal ECG findings. The diagnostic sensitivity of Tc-99m sestamibi myocardial perfusion SPECT was 100% by a qualified analysis. The perfusion defect site in the myocardial perfusion SPECT were corresponded with the infarct related coronary artery in 31 patients which was diagnosed by coronary angiograpy. The size of perfusion defect in the po1ar map was $31{\pm}18%(M{\pm}SD)$, in the myocardial infarction with left anterior descending coronary arery obstruction, $31{\pm}13% (M{\pm}SD)$ in the myocardial infarction with right coronary artery obstruction and $25{\pm}5.9%(M{\pm}SD)$ in the myocardial infarction with left circumflex coronary artery obstruction. We concluded that emergency myocardial perfusion SPECT images are useful in the diagnose of myocardial infarction and it's very useful when we are difficult to diagnose with ECG like as lateral wall infarction or left bundle branch block.

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Expression of Bcl-2 Protein in Ischemia-Reperfused Myocardium of Rabbit (가토 허혈-재관류 심근에서의 Bcl-2 단백의 발현)

  • 류재욱;김삼현;서필원;박성식;최창휴;류경민;김영권;박이태;김성숙
    • Journal of Chest Surgery
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    • v.31 no.10
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    • pp.924-927
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    • 1998
  • Background: Myocardial cell death after myocardial infarction or reperfusion is classified into necrosis and apoptosis. Bcl-2 protein is a cytoplasmic protein, which inhibits apoptosis and is expressed in acute stage of myocardial infarction but not in normal heart. This study was performed to investigate whether Bcl-2 protein was expressed respectively to the reperfusion time. Materials and methods: Thirty nine New Zealand white rabbits weighing 1.5-4.8 kg (mean, 2.9kg) were alloted into 7 groups (n=5 in each group) which underwent left anterior descending coronary artery(LAD) occlusion for 30 minutes, followed by reperfusion. The animals were sacrificed at 1, 4, 8, 12, 24 hours, and 3, 7 days after occlusion. Ventricle was excised immediately after intervention. Tissues were fixed in 10% buffured formalin and embedded in paraffin. Bcl-2 protein was detected by immunohistochemical stain with using monoclonal antibody against Bcl-2 protein. Results: The positive immunohistochemical reactivity for Bcl-2 protein was observed in 12, 24 hours, and 3 days reperfusion groups. Bcl-2 protein was detected in salvaged myocytes surrounding the infarcted area. Conclusions: Bcl-2 protein is expressed at the late acute stage of infarct. Therefore, the expression of Bcl-2 protein may not protect acute cell death, but may play a role in the prevention of late cell death after myocardial is chemia-reperfusion.

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A Study on Optimal Myocardium Perfusion SPECT According to Possible Myocardial Infarct Sites (8) 예측성 경색 부위별 최적의 심근관류 단층촬영술 시행에 관한 연구)

  • Song Jae Beom;Lee Wan Kyu;Shu Myung Duk;Jang Sang Sup
    • Journal of The Korean Radiological Technologist Association
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    • v.25 no.1
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    • pp.234-252
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    • 1999
  • Purpose : Physical properties of radiophamaceuticals of technetium($^{99m}Tc$) and thallium($^{201}Tl$) have early been used for clinical diagnostics. The studies of those radiophamaceuticals have been contributed to the efficient to

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Protective effect of KR-32000 against hypoxia- and oxidative stress-induced cardiac cell death

  • Kim, Mi-Jeong;Yoo, Sung-Eun;Yi, Kiu-Yang;Lee, Sun-Kyung;Lee, Soo-Hwan;Baik, Eun-Joo;Moon, Chang-Hyun;Jung, Yi-Sook
    • Proceedings of the PSK Conference
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    • 2002.10a
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    • pp.297.3-298
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    • 2002
  • A benzopyranyl derivative. KR32000. synthesized as a plausible KATP opener. has been shown to exert cardioprotective effect in vivo myocardial infarct model. In this study. we investigated whether KR32000 can produce cardioprotective effect against hypoxia- and reactive oxygen species(ROS)-induced injury in heart-derived H9c2 cells. Hypoxic injury was induced by incubating cells in anaerobic chamber (glucose-free. serum-free DMEM. 85% N2. 5% CO2. 10% H2) and oxidative stress was induced by buthionine sulfoximine(BSO). (omitted)

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Puerarin pretreatment attenuates cardiomyocyte apoptosis induced by coronary microembolization in rats by activating the PI3K/Akt/GSK-3β signaling pathway

  • Chen, Zhi-Qing;Zhou, You;Huang, Jun-Wen;Chen, Feng;Zheng, Jing;Li, Hao-Liang;Li, Tao;Li, Lang
    • The Korean Journal of Physiology and Pharmacology
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    • v.25 no.2
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    • pp.147-157
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    • 2021
  • Coronary microembolization (CME) is associated with cardiomyocyte apoptosis and cardiac dysfunction. Puerarin confers protection against multiple cardiovascular diseases, but its effects and specific mechanisms on CME are not fully known. Hence, our study investigated whether puerarin pretreatment could alleviate cardiomyocyte apoptosis and improve cardiac function following CME. The molecular mechanism associated was also explored. A total of 48 Sprague-Dawley rats were randomly divided into CME, CME + Puerarin (CME + Pue), sham, and sham + Puerarin (sham + Pue) groups (with 12 rats per group). A CME model was established in CME and CME + Pue groups by injecting 42 ㎛ microspheres into the left ventricle of rats. Rats in the CME + Pue and sham + Pue groups were intraperitoneally injected with puerarin at 120 mg/kg daily for 7 days before operation. Cardiac function, myocardial histopathology, and cardiomyocyte apoptosis index were determined via cardiac ultrasound, hematoxylin-eosin (H&E) and hematoxylin-basic fuchsin-picric acid (HBFP) stainings, and TdT-mediated dUTP nick-end labeling (TUNEL) staining, respectively. Western blotting was used to measure protein expression related to the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3β (GSK-3β) pathway. We found that, puerarin significantly ameliorated cardiac dysfunction after CME, attenuated myocardial infarct size, and reduced myocardial apoptotic index. Besides, puerarin inhibited cardiomyocyte apoptosis, as revealed by decreased Bax and cleaved caspase-3, and up-regulated Bcl-2 and PI3K/Akt/GSK-3β pathway related proteins. Collectively, puerarin can inhibit cardiomyocyte apoptosis and thus attenuate myocardial injury caused by CME. Mechanistically, these effects may be achieved through activation of the PI3K/Akt/GSK-3β pathway.

Cardioprotective effect of ginsenoside Rb1 via regulating metabolomics profiling and AMP-activated protein kinase-dependent mitophagy

  • Hu, Jingui;Zhang, Ling;Fu, Fei;Lai, Qiong;Zhang, Lu;Liu, Tao;Yu, Boyang;Kou, Junping;Li, Fang
    • Journal of Ginseng Research
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    • v.46 no.2
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    • pp.255-265
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    • 2022
  • Background: Ginsenoside Rb1, a bioactive component isolated from the Panax ginseng, acts as a remedy to prevent myocardial injury. However, it is obscure whether the cardioprotective functions of Rb1 are related to the regulation of endogenous metabolites, and its potential molecular mechanism still needs further clarification, especially from a comprehensive metabolomics profiling perspective. Methods: The mice model of acute myocardial ischemia (AMI) and oxygen glucose deprivation (OGD)-induced cardiomyocytes injury were applied to explore the protective effect and mechanism of Rb1. Meanwhile, the comprehensive metabolomics profiling was conducted by high-performance liquid chromatography and quadrupole time-of-flight mass spectrometry (HPLC-Q/TOF-MS) and a tandem liquid chromatography and mass spectrometry (LC-MS). Results: Rb1 treatment profoundly reduced the infarct size and attenuated myocardial injury. The metabolic network map of 65 differential endogenous metabolites was constructed and provided a new inspiration for the treatment of AMI by Rb1, which was mainly associated with mitophagy. In vivo and in vitro experiments, Rb1 was found to improve mitochondrial morphology, mitochondrial function and promote mitophagy. Interestingly, the mitophagy inhibitor partly attenuated the cardioprotective effect of Rb1. Additionally, Rb1 markedly facilitated the phosphorylation of AMP-activated protein kinase α (AMPKα), and AMPK inhibition partially weakened the role of Rb1 in promoting mitophagy. Conclusions: Ginsenoside Rb1 protects acute myocardial ischemia injury through promoting mitophagy via AMPKα phosphorylation, which might lay the foundation for the further application of Rb1 in cardiovascular diseases.

Socioeconomic Differentials in Stroke and Cardiovascular Disease Mortality in Korea (소득계층에 따른 뇌심혈관질환 사망률 차이)

  • Im Jeong-Soo;Choi Dae-Kyung;Yim Jun;Hong Du-Ho;Kim Jong-Kyun;Park Sang-Hyun;Youn Sung-Tae
    • Korean Journal of Health Education and Promotion
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    • v.23 no.2
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    • pp.109-119
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    • 2006
  • Objectives: A number of studies in economically developed countries have shown occurrence of stroke and cardiovascular disease to be inversely related to socioeconomic class. The purpose of this study is to investigate socioeconomic differentials in stroke and cardiovascular disease mortality in Korea. Methods: Two data from two sources, registry data from National Health Insurance Corporation and death certification data from National Statistics Office, were used to calculate mortality rate for five socioeconomic classes. Poisson regression analysis was used to calculate relative indices of inequality as a measure of mortality differentials between socioeconomic classes. Results: For males, graded socioeconomic differentials in mortality were observed with higher mortality rates related to lower socioeconomic class for intracerebral hemorrhage, cerebral infarct, hypertension, ischemic heart disease, myocardial infarct, and arrhythmia. The relative index of inequality for stroke and cardiovascular disease was 1.61(95% CI=1.54-1.68). For females, these differentials were observed for arrhythmia and intracerebral hemorrhage. The relative index of inequality was 1.06(95% CI=1.02-1.11). Conclusions: This socioeconomic differential in mortality, consistent with the results of other studies performed in economically developed countries suggest that Socioeconomic class can influence mortality regardless of the developmental stage of the country.

Post-Infarction Ventricular Septal Rupture : 10 Years of Experience (급성 심근경색증 후 심실중격 결손: 10년 경험)

  • Jung, Yo-Chun;Cho, Kwang-Ree;Kim, Ki-Bong
    • Journal of Chest Surgery
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    • v.40 no.5 s.274
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    • pp.351-355
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    • 2007
  • Background: Postinfarction ventricular septal rupture is associated with mortality as high as $85\sim90%$, if it is treated medically. This report documents our experience with postinfarction ventricular septal rupture that was treated surgically, Material and Method: We retrospectively reviewed the medical records of 11 patients who were operated on due to postinfarction ventricular septal rupture between August 1996 and August 2006. There were 4 men and 7 women, with a mean age of $70{\pm}11$ years (age range: $50\sim84$ years). The location of the rupture was anterior in 7 cases and posterior in 4 cases. The interval between the onset of acute myocardial infarction and the occurrence of the ventricular septal rupture was $2.0{\pm}1.3$ days (range: $1\sim5$ days). Operation was performed at an average of $2.4{\pm}2.7$ days (range: $0\sim8$ days) after the diagnosis of septal rupture. Preoperative intraaortic balloon pump therapy was performed in 10 patients. Result: The infarct exclusion technique was used in all cases. Coronary artery bypass grafting was done in 8 cases, with the mean number of distal anastomosis being $1.0{\pm}0.8$. There was one operative death. In 2 patients, reoperation was performed due to a residual septal defect. The postoperative morbidities were transient atrial fibrillation (n=7), paroxysmal supraventricular tachycardia (n=1), low cardiac output syndrome (n=3), bleeding reoperation (n=2), delayed sternal closure (n=2), acute renal failure (n=2), pneumonia (n=1), intraaortic balloon pump-related thromboembolism (n=1), and transient delirium (n=2). Nine patients have been followed up for a mean of $38{\pm}40$ months except for one follow-up loss. There have been 3 late deaths. At the latest follow-up, all 6 survivors were in a good functional class. Conclusion: We demonstrated satisfactory operative and midterm results with our strategy of preoperative intraaortic balloon pump therapy, early repair of septal rupture by infarct exclusion and combined coronary revascularization.