• 제목/요약/키워드: Cardiac Injury

검색결과 305건 처리시간 0.026초

허혈후 폐 보존효과를 측정하기 위한 폐장 분리관류 모형 (An Experimental Hlodel of Isolated Lung Block for Evaluation of Pulmonary Preservation after Ischemial)

  • 성숙환;임청;김영태;박종호
    • Journal of Chest Surgery
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    • 제30권6호
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    • pp.573-579
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    • 1997
  • 지난 30년동안 장기이식분야의 괄목할만한 발전과 더불어 국내에서도 신장, 간 등은 물론 심장이식도 활 발히 이루어지고 있다. 그러나 폐 이식만은 많은 제약으로 인하여 답보상태를 면하지 못하고 있으며 그중에 서도 장기공여자의 부족과 상대적으로 허혈-재관류손상에 예민한 폐 자체의 보존시간의 문제가 가장 먼저 해결해야 할 과제로 여겨지고 있다. 일반적으로 폐는 허혈에 견딜수 있는 시간이 4-6시간으로 알려져 있으 며 많은 연구자들이 더 좋은 폐보존방법을 연구하고 평가하기 위한 실험모델을 개발하여 왔다. 그러나 많 은 실험모델의 등장으로 같은 실험도 서로 상반되는 결과를 낳고 있으며 각각의 모델이 가진 단점들로 인 하여 실험모형의 표준화와 결과분석의 기준을 정하는데 있어 완벽한 모델은 정립된 것이 없는 상태이다. 폐 보존후 기능에 영향을 미칠 수 있는 요인들 즉 허혈성 보존기간, 보존 온도, 폐관류액치 구성성분 등 을 분석하는데는 비교적 간단하고, 경비가 적게 들며 실험결과의 신뢰도가 높은 새로운 모형의 개발이 요 구 되었다. 이에 서울대학교병원 흉부외과에서는 빠르게 변화하는 폐 보존 방법의 실험 및 한국에서는 거 \ulcorner이루어지지 않고 있는 폐 보존 방법에 대한 통계 자료를 확보하여 폐 이식 수술에 이를 적용하고자, 연 구노력 끝에 토끼 폐장으로 상기 목적에 적합한 폐장 분리관류 모형을 완성하였다.

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Surgical Outcomes of Congenital Atrial Septal Defect Using da VinciTM Surgical Robot System

  • Kim, Ji Eon;Jung, Sung-Ho;Kim, Gwan Sic;Kim, Joon Bum;Choo, Suk Jung;Chung, Cheol Hyun;Lee, Jae Won
    • Journal of Chest Surgery
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    • 제46권2호
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    • pp.93-97
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    • 2013
  • Background: Minimally invasive cardiac surgery has emerged as an alternative to conventional open surgery. This report reviews our experience with atrial septal defect using the da VinciTM surgical robot system. Materials and Methods: This retrospective study included 50 consecutive patients who underwent atrial septal defect repair using the da VinciTM surgical robot system between October 2007 and May 2011. Among these, 13 patients (26%) were approached through a totally endoscopic approach and the others by mini-thoracotomy. Nineteen patients had concomitant procedures including tricuspid annuloplasty (n=10), mitral valvuloplasty (n=9), and maze procedure (n=4). The mean follow-up duration was $16.9{\pm}10.4$ months. Results: No remnant interatrial shunt was detected by intraoperative or postoperative echocardiography. The atrial septal defects were mainly repaired by Gore-Tex patch closure (80%). There was no operative mortality or serious surgical complications. The aortic cross clamping time and cardiopulmonary bypass time were $74.1{\pm}32.2$ and $157.6{\pm}49.7$ minutes, respectively. The postoperative hospital stay was $5.5{\pm}3.3$ days. Conclusion: The atrial septal defect repair with concomitant procedures like mitral valve repair or tricuspid valve repair using the da VinciTM system is a feasible method. In addition, in selected patients, complete port access can be helpful for better cosmetic results and less musculoskeletal injury.

동맥경화도와 생리학적 변수들 간의 상관관계 (Correlation between Arterial Stiffness and Physiological Parameters)

  • 신재욱;석성자;이길현;최석철;현경예
    • 보건의료산업학회지
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    • 제7권3호
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    • pp.71-82
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    • 2013
  • Arterial stiffness(AS) is an important pathologic state of vascular injury. This study was carried out to elucidate the effect of physiological variables on brachial-ankle pulse wave velocity(BAPWV), index of AS. Four hundred adults(volunteers) participated in this study. Body indices, biochemical, cardiac and inflammatory markers, and right(Rt)- and left(Lt)-BAPWV were measured. Body mass index(BMI), Rt- and Lt-BAPWV, glucose, triglyceride, alkaline phosphatase(ALP), gamma-glutamyl transferase(GGT), creatinine, uric acid, troponin-I(TNI), NT-proBNP and high sensitivity C-reactive protein(hs-CRP) levels were higher than the reference value of each variable. Rt- and Lt-BAPWV were directly correlated with age, body weight, BMI, glucose, ketone, aspartate aminotransferase, alanine aminotransferase, ALP, GGT, total cholesterol, low density lipoprotein, lipoprotein(a), apolipoprotein-B, blood urea nitrogen, heart rate, TNI, creatine kinase, CK-MB, lactic dehydrogenase, myoglobin, hs-CRP, lipase, reumatoid factor, fibrinogen and D-dimer (P<0.05, P<0.01, P<0.001 or P<0.000, respectively), but inversely associated with total bilirubin, uric acid, apolipoprotein-A1 and GFR (P<0.05). These observations suggest that a variety of physiological variables may influence BAPWV, resulting in increased risk or prevention of cardiovascular and/or cerebrovascular attacks. Therefore, physiological variables affecting BAPWV should be regularly controlled.

인공 대동맥판막 기능부전을 일으킨 특발성 과호산구 증후군 -1예 보고- (Dysfunction of the Prosthetic Aortic Valve in Idiopathic Hypereosinophilic Syndrome -A case report -)

  • 유동곤;성규완;정상식;강길현;김종욱;박종빈
    • Journal of Chest Surgery
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    • 제40권4호
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    • pp.297-300
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    • 2007
  • 특발성 과호산구 증후군은 호산구 매개에 의한 조직 손상으로 인해 다발성 장기부전, 특히 심장을 침범하는 드문 전신성, 백혈구증식성 질환이다. 심장침범은 특발성 과호산구 증후군 환자의 75% 이상에서 일어난다. 심장증상은 심내막 하 섬유증, 제한성 심근병증, 판막부전, 그리고 말초동맥 혈전증을 유발하는 혈전이다. 이 질환은 남자에서 여자보다 9 : 1로 호발하고, $20{\sim}50$대에서 주로 발현하는 경향이 있으며 소아에서는 매우 드물다. 인공 대동맥판막부전을 나타낸 특발성 과호산구 증후군 환자(58세, 남자)를 인공판막 재치환 수술 후 부신피질호르몬제와 hydroxyurea 투여로 성공적으로 치료하였기에 보고하는 바이다.

대동맥 축착증 및 심한 대동맥 협착을 가진 저체중 신생아(2.4 kg)의 수술 전후 발생한 심실 기능 부전의 치료에 대한 양심실 보조 장치 적용 치험 예 (The Application of a Bi-ventricular Assist Device for a Low Weight (2.4 kg) Neonate with Coarctation of the Aorta and Critical Aortic Stenosis)

  • 곽재건;박천수;이창하;이철
    • Journal of Chest Surgery
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    • 제43권3호
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    • pp.304-307
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    • 2010
  • 대동맥 축착증 및 심한 대동맥 협착을 가진 생후 5일의 환자가 대동맥 협착을 해결하려는 중재적 시술 도중 유도 카테터에 의한 우측 경동맥 손상으로 인한 출혈 및 심낭 내 탐폰으로 인한 심정지가 발생하여 심폐소생술 후 체외막성산화기 보조를 받았다. 환자의 체중은 2.4 kg이었다. 1일 후 수술적 완전 교정술을 시행하였으나, 수술 직후 심한 심기능 저하로 인하여 양심실 보조 장치로 순환 보조를 하였고, 3일 후 양심실 보조 장치 이탈에 성공하였다. 이후 환자는 일반적인 치료 후 특별한 문제없이 퇴원하였다.

Implication of microRNA as a potential biomarker of myocarditis

  • Oh, Jin-Hee;Kim, Gi Beom;Seok, Heeyoung
    • Clinical and Experimental Pediatrics
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    • 제65권5호
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    • pp.230-238
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    • 2022
  • Myocarditis was previously attributed to an epidemic viral infection. Additional harmful reagents, in addition to viruses, play a role in its etiology. Coronavirus disease 2019 (COVID-19) vaccine-induced myocarditis has recently been described, drawing attention to vaccine-induced myocarditis in children and adolescents. Its pathology is based on a series of complex immune responses, including initial innate immune responses in response to viral entry, adaptive immune responses leading to the development of antigen-specific antibodies, and autoimmune responses to cellular injury caused by cardiomyocyte rupture that releases antigens. Chronic inflammation and fibrosis in the myocardium eventually result in cardiac failure. Recent advancements in molecular biology have remarkably increased our understanding of myocarditis. In particular, microRNAs (miRNAs) are a hot topic in terms of the role of new biomarkers and the pathophysiology of myocarditis. Myocarditis has been linked with microRNA-221/222 (miR-221/222), miR-155, miR-10a*, and miR-590. Despite the lack of clinical trials of miRNA intervention in myocarditis yet, multiple clinical trials of miRNAs in other cardiac diseases have been aggressively conducted to help pave the way for future research, which is bolstered by the success of recently U.S. Food and Drug Administration-approved small-RNA medications. This review presents basic information and recent research that focuses on myocarditis and related miRNAs as a potential novel biomarker and the therapeutics.

Historical Review and Future of Cardiac Xenotransplantation

  • Jiwon Koh;Hyun Keun Chee;Kyung-Hee Kim;In-Seok Jeong;Jung-Sun Kim;Chang-Ha Lee;Jeong-Wook Seo
    • Korean Circulation Journal
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    • 제53권6호
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    • pp.351-366
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    • 2023
  • Along with the development of immunosuppressive drugs, major advances on xenotransplantation were achieved by understanding the immunobiology of xenograft rejection. Most importantly, three predominant carbohydrate antigens on porcine endothelial cells were key elements provoking hyperacute rejection: α1,3-galactose, SDa blood group antigen, and N-glycolylneuraminic acid. Preformed antibodies binding to the porcine major xenoantigen causes complement activation and endothelial cell activation, leading to xenograft injury and intravascular thrombosis. Recent advances in genetic engineering enabled knock-outs of these major xenoantigens, thus producing xenografts with less hyperacute rejection rates. Another milestone in the history of xenotransplantation was the development of co-stimulation blockaded strategy. Unlike allotransplantation, xenotransplantation requires blockade of CD40-CD40L pathway to prevent T-cell dependent B-cell activation and antibody production. In 2010s, advanced genetic engineering of xenograft by inducing the expression of multiple human transgenes became available. So-called 'multi-gene' xenografts expressing human transgenes such as thrombomodulin and endothelial protein C receptor were introduced, which resulted in the reduction of thrombotic events and improvement of xenograft survival. Still, there are many limitations to clinical translation of cardiac xenotransplantation. Along with technical challenges, zoonotic infection and physiological discordances are major obstacles. Social barriers including healthcare costs also need to be addressed. Although there are several remaining obstacles to overcome, xenotransplantation would surely become the novel option for millions of patients with end-stage heart failure who have limited options to traditional therapeutics.

Histological Validation of Cardiovascular Magnetic Resonance T1 Mapping for Assessing the Evolution of Myocardial Injury in Myocardial Infarction: An Experimental Study

  • Lu Zhang;Zhi-gang Yang;Huayan Xu;Meng-xi Yang;Rong Xu;Lin Chen;Ran Sun;Tianyu Miao;Jichun Zhao;Xiaoyue Zhou;Chuan Fu;Yingkun Guo
    • Korean Journal of Radiology
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    • 제21권12호
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    • pp.1294-1304
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    • 2020
  • Objective: To determine whether T1 mapping could monitor the dynamic changes of injury in myocardial infarction (MI) and be histologically validated. Materials and Methods: In 22 pigs, MI was induced by ligating the left anterior descending artery and they underwent serial cardiovascular magnetic resonance examinations with modified Look-Locker inversion T1 mapping and extracellular volume (ECV) computation in acute (within 24 hours, n = 22), subacute (7 days, n = 13), and chronic (3 months, n = 7) phases of MI. Masson's trichrome staining was performed for histological ECV calculation. Myocardial native T1 and ECV were obtained by region of interest measurement in infarcted, peri-infarct, and remote myocardium. Results: Native T1 and ECV in peri-infarct myocardium differed from remote myocardium in acute (1181 ± 62 ms vs. 1113 ± 64 ms, p = 0.002; 24 ± 4% vs. 19 ± 4%, p = 0.031) and subacute phases (1264 ± 41 ms vs. 1171 ± 56 ms, p < 0.001; 27 ± 4% vs. 22 ± 2%, p = 0.009) but not in chronic phase (1157 ± 57 ms vs. 1120 ± 54 ms, p = 0.934; 23 ± 2% vs. 20 ± 1%, p = 0.109). From acute to chronic MI, infarcted native T1 peaked in subacute phase (1275 ± 63 ms vs. 1637 ± 123 ms vs. 1471 ± 98 ms, p < 0.001), while ECV progressively increased with time (35 ± 7% vs. 46 ± 6% vs. 52 ± 4%, p < 0.001). Native T1 correlated well with histological findings (R2 = 0.65 to 0.89, all p < 0.001) so did ECV (R2 = 0.73 to 0.94, all p < 0.001). Conclusion: T1 mapping allows the quantitative assessment of injury in MI and the noninvasive monitoring of tissue injury evolution, which correlates well with histological findings.

Vanadate-Induced Renal cAMP and Malondialdehyde Accumulation Suppresses Alpha 1 Sodium Potassium Adenosine Triphosphatase Protein Levels

  • Eiam-Ong, Somchit;Nakchui, Yuyen;Chaipipat, Mookda;Eiam-Ong, Somchai
    • Toxicological Research
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    • 제34권2호
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    • pp.143-150
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    • 2018
  • It has been demonstrated that vanadate causes nephrotoxicity. Vanadate inhibits renal sodium potassium adenosine triphosphatase (Na, K-ATPase) activity and this is more pronounced in injured renal tissues. Cardiac cyclic adenosine monophosphate (cAMP) is enhanced by vanadate, while increased cAMP suppresses Na, K-ATPase action in renal tubular cells. There are no in vivo data collectively demonstrating the effect of vanadate on renal cAMP levels; on the abundance of the alpha 1 isoform (${\alpha}_1$) of the Na, K-ATPase protein or its cellular localization; or on renal tissue injury. In this study, rats received a normal saline solution or vanadate (5 mg/kg BW) by intraperitoneal injection for 10 days. Levels of vanadium, cAMP, and malondialdehyde (MDA), a marker of lipid peroxidation were measured in renal tissues. Protein abundance and the localization of renal ${\alpha}_1-Na$, K-ATPase was determined by Western blot and immunohistochemistry, respectively. Renal tissue injury was examined by histological evaluation and renal function was assessed by blood biochemical parameters. Rats treated with vanadate had markedly increased vanadium levels in their plasma, urine, and renal tissues. Vanadate significantly induced renal cAMP and MDA accumulation, whereas the protein level of ${\alpha}_1-Na$, K-ATPase was suppressed. Vanadate caused renal damage, azotemia, hypokalemia, and hypophosphatemia. Fractional excretions of all studied electrolytes were increased with vanadate administration. These in vivo findings demonstrate that vanadate might suppress renal ${\alpha}_1-Na$, K-ATPase protein functionally by enhancing cAMP and structurally by augmenting lipid peroxidation.

Angiotensin II $AT_1$ 수용체 길항제인 SK-1080의 적출심장에 대한 허혈후 재관류시의 작용 및 혈소판응집과 혈액응고에 대한 효과 (Effects of the AngiotensinII $AT_1$ Receptor Antagonist SK-1080 on Ischemia/reperfusion in Isolated Rat Hearts and on Platelet Aggregation and Coagulation in Human Blood)

  • 우수경;최상수;이병호;권광일
    • 약학회지
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    • 제44권6호
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    • pp.558-565
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    • 2000
  • SK-1080 is one of the newly developed orally active nonpeptide angiotensinII $AT_1-receptor$ antagonist that selectively acts at $AT_1$ receptor with high affinity. The cardiac effect on ischemia/reperfusion injury of SK-1080 was compared with those of losartan, a prototype of this class, in isolated rat hearts. Isolated perfused rat heart was pretreated with drug for 10 min and then subjected to global ischemia for 30 min followed by reperfusion with- or without drug for 30 min. The possible additive effect of SK-1080 on the platelet aggregation and coagulation in human blood was also studied. We investigated whether SK-1080 effects the platelet aggregation induced by ADP, a platelet agonist partially dependent on $thromboxaneA_2$. The clotting times in the prothrombin time (PT) and activated partial thromboplastin time (APTT) were also examined in human plasma in vitro as coagulation screening test. SK-1080 improved reperfusion function (LVDP, left ventricular developed pressure; PRP, rate-pressure product) in a dose-dependent manner. SK-1080 reduced ADP-induced platelet aggregation compared with vehicle but less than losartan, and did not affect clotting times.

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