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The Inflammatory Response and Cardiac Repair After Myocardial Infarction
나득영,이무용 대한심장학회 2009 Korean Circulation Journal Vol.39 No.10
One of the most important therapeutic targets of current cardiology practice is to determine optimal strategies for the minimization of myocardial necrosis and optimization of cardiac repair following an acute myocardial infarction. Myocardial necrosis after acute myocardial infarction induces complement activation and free radical generation, triggering a cytokine cascade initiated by tumor necrosis factor-alpha (TNF-α) release. When reperfusion of the infarcted area is initiated, intense inflammation follows. Chemokines, cytokines and the complement system play an important role in recruiting neutrophils in the ischemic and reperfused myocardium. Cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. The recruited neutrophils have potent cytotoxic effects through the release of proteolytic enzymes, and they interact with adhesion molecules on cardiomyocytes. In spite of the potential injury, reperfusion enhances cardiac repair; this may be related to the inflammatory response. Monocyte chemoattractant protein (MCP)-1 is upregulated in reperfused myocardium and can induce monocyte recruitment in the infarcted area. Monocyte subsets play a role in phagocytosis of dead cardiomyocytes and in granulation tissue formation. In addition, the transforming growth factor (TGF)-β plays a crucial role in cardiac repair by suppressing inflammation. Resolution of inflammatory infiltration, containment of inflammation and the reparative response affecting the infarcted area are essential for optimal infarct healing. Here, we review the current literature on the inflammatory response and cardiac repair after myocardial infarction. One of the most important therapeutic targets of current cardiology practice is to determine optimal strategies for the minimization of myocardial necrosis and optimization of cardiac repair following an acute myocardial infarction. Myocardial necrosis after acute myocardial infarction induces complement activation and free radical generation, triggering a cytokine cascade initiated by tumor necrosis factor-alpha (TNF-α) release. When reperfusion of the infarcted area is initiated, intense inflammation follows. Chemokines, cytokines and the complement system play an important role in recruiting neutrophils in the ischemic and reperfused myocardium. Cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. The recruited neutrophils have potent cytotoxic effects through the release of proteolytic enzymes, and they interact with adhesion molecules on cardiomyocytes. In spite of the potential injury, reperfusion enhances cardiac repair; this may be related to the inflammatory response. Monocyte chemoattractant protein (MCP)-1 is upregulated in reperfused myocardium and can induce monocyte recruitment in the infarcted area. Monocyte subsets play a role in phagocytosis of dead cardiomyocytes and in granulation tissue formation. In addition, the transforming growth factor (TGF)-β plays a crucial role in cardiac repair by suppressing inflammation. Resolution of inflammatory infiltration, containment of inflammation and the reparative response affecting the infarcted area are essential for optimal infarct healing. Here, we review the current literature on the inflammatory response and cardiac repair after myocardial infarction.
ST절 상승 심전도 소견을 동반한 급성 근위부 대동맥 박리증
나득영,박건욱,김성호 대한심장학회 2004 Korean Circulation Journal Vol.34 No.8
Inappropriate administration of thrombolytic agents to acute type A aortic dissection patients with acute myocardial infarction could result in catastrophic outcomes. A 38-year-old female patient without any previous cardiac history visited the emergency room due to a severe acute onset of retrosternal chest pain. The ECG showed a complete heart block with a junctional escape rhythm at 33 beats/min and more than 2 mm of ST elevation in the inferior and anterior precordial leads. Because of an acute myocardial infarction, prompt thrombolytic agent (tPA) was administered. The patient had cardiogenic shock and persistent chest pain after the thrombolytic therapy. We performed the transthoracic echocardiography (TTE). The TTE showed a dissection flap just above the aortic valve and akinesia of the inferior wall of the left ventricle. She underwent an emergency surgical correction. However, the patient died due to the failure of weaning from the cardiopulmonary bypass machine. 38세의 과거 순환기 질환의 과거 병력이 없는 여자가 갑자기 시작된 흉통을 주소로 내원하였다, 심전도상 Ⅱ, Ⅲ, AVF 및 전흉부유도 V1, V2, V3에 ST절의 상승을 보여 급성 심근 경색증으로 진단 하였고 혈전용해제를 투약받았다. 중환자실에서 치료중 심인성 쇽 소견을 보여 경흉부 심장 초음파를 시행하였고 심초음파도 결과 상행 대동맥에 내막박리가 관찰된 급성 A형 대동맥 박리증에 동반된 하벽부 심근경색증으로 진단하였다. 환자는 응급 수술을 받았지만 과다한 심실의 손상으로 심폐기의 이탈에서 실패하여 사망 하였다. 저자들은 아주 드문 ST분절 상승을 보인 급성 하벽부 심근 경색증으로 표현된 급성 A형 대동맥 박리증 1예를 경험 하였기에 문헌고찰과 함께 보고하는 바이다.
나득영,김지현,이명묵,김용석,김영권,이무용,이창근,배준호,정진욱 대한심장학회 2013 Korean Circulation Journal Vol.43 No.4
Background and Objectives: Microalbuminuria (MAU) and decreased estimated glomerular filtration rate (eGFR) are risk factors for car-diovascular disease (CVD) in patients with hypertension. However, in hypertensive patients with normal or minimally reduced eGFR (≥60 mL/min/1.73 m 2 ) and with normo- or MAU, the value of combined estimation of eGFR and urine microalbumin for the risk assessment has not been widely reported. We evaluated the association between arterial stiffness and the combined estimation of eGFR and urine microalbumin. Subjects and Methods: Subjects with never treated hypertension and normal or minimally reduced eGFR were evaluated (n=491, 50.1±10.4 years). eGFR was calculated by the simplified Modification of Diet in Renal Disease formula. Urinary albumin-to-creatinine ratio (UACR)was assessed with spot urine. Arterial stiffness was assessed with heart-femoral pulse wave velocity (hfPWV). All subjects were divided into four groups; group 1, eGFR ≥90 mL/min/1.73 m 2 (normal eGFR) and normo-albuminuria (NAU); group 2, eGFR 89.9-60 mL/min/1.73 m 2 (mini-mally reduced eGFR) and NAU; group 3, normal eGFR and MAU; group 4, minimally reduced eGFR and MAU. Results: Group 1 had the lowest hfPWV (964.6±145.4; group 2, 1013.5±168.9; group 3, 1058.2±238.0; group 4, 1065.8±162.9 cm/sec). Analysis adjusting age, sex, body mass index, heart rate and mean arterial pressure showed significantly lower hfPWV of group 1 compared to group 2 (p=0.032) and 3 (p=0.007). Multiple regression analysis showed a significant association of hfPWV with logUACR {beta=0.096,95% confidence interval (CI) 8.974-60.610, p=0.008 } and eGFR (beta=-0.069, 95% CI -1.194 - -0.005, p=0.048). Conclusion: Minimally reduced eGFR or MAU is independently associated with increased arterial stiffness, indicating greater CVD risk.
정진욱,나득영,배준호 대한심장학회 2013 Korean Circulation Journal Vol.43 No.4
Peripheral arterial disease represents a significant problem, particularly among the elderly population. There has been great progress made in the treatment of peripheral arterial disease in recent years. Percutaneous transluminal angioplasty (PTA) has been employed as a meth-od of treatment for patients with a variety of peripheral arterial disease. We report our experience with PTA of contralateral common iliac and superficial femoral arteries via graft vessel in a patient with femorofemoral bypass due to ipsilateral iliac artery occlusion.