좌심방에 발생한 원발성 미분류 방추세포 육종 1례

조정환,홍그루,송인욱,손창우,정선영,남종호,김미진 영남대학교 의과대학 2009 Yeungnam University Journal of Medicine Vol.26 No.2

급성 호산구성 심근염으로 나타난 과호산구 증후군 1예

박용호,홍그루,김민경,정항재,신동구,김영조,심봉섭 대한내과학회 2004 대한내과학회지 Vol.66 No.3

과호산구 증후군은 특별한 원인없이 호산구가 1,500/㎣ 이상의 호산구 증가증이 6개월 이상 지속되고 다양한 기관의 침범으로 인한 증상과 증후를 보이는 질환이다. 본 저자들은 흉부 불쾌감을 주소로 내원한 환자에서 과호산구 증후군의 합병증의 일종으로 다발성 뇌경색과 급성 호산구성 심근염으로 나타난 1예를 체험하여 문헌고찰과 함께 보고한다. The hypereosinophilic syndrome (HES) is a leukoproliferative disorder, marked by sustained blood eosinophilia of greater than 1,500/㎣, for longer than 6 months and predilection to damage specific oragans. Any organ system may be affected in HES, but the most severe clinicopathophysio-logical involvements are of the heart and nervous system. We report a case of a 48-year-old man with acute eosinophilic myocarditis combined with hypereosinophilic syndrome who was successfully treated with steroids.

심장내로 연장된 정맥내 평활근종증 1예 : 심장내 평활근종증 intracardiac leiomyomatosis-case report and literature review

정재헌,민필기,박소영,변영섭,홍그루,임세중,심원흠 대한내과학회 2003 대한내과학회지 Vol.65 No.2

정맥내 평활근종증은 병리학적으로는 양성 질환이나 진행 양상은 악성으로 모든 종양의 적출술이 시행되어야 하며, 자궁적출술시 병리학적으로 정맥내 평활근종증을 진단받은 경우 정기적인 검사를 통해 종양의 재발이나 하대정맥과 심장내로의 연장을 확인하여야 한다. 우측 심장내 종양이 발견된 경우는 점액종을 포함한 원발성 심내 종양 외에도 다른 원인 질환을 확인하여야 하며, 반드시 정맥내 평활근종증을 감별진단하여야 한다. Intravenous leiomyomatosis is a rare benign vascular tumor defined as the extension into venous channels of a histologically benign smooth muscle tumor arising either from a uterus or from the walls of uterine vessels, and about 10% spread to the heart. The treatment of choice is complete resection of the tumor. Hormonal therapy should be considered in cases of unresectable residual tumor. A 46-year-old woman was admitted for abdominal discomfort and pain. She was found to have intravenous leiomyomatosis of the uterus with extension into inferior vena cava and right atrium. The patient underwent surgery employing simultaneous sternotomy and laparotomy. Radical excision was achieved using cardiopulmonary bypass. We herein describe a patient in whom complete removal of intravenous leiomyomatosis with cardiac extension was successfully performed.

핵의학 의사를 위한 심초음파의 최신지견

홍그루 ( Geu Ru Hong ),신동구 ( Dong Gu Shin ) 대한핵의학회 2006 핵의학 분자영상 Vol.39 No.6

승모판 질환에 동반된 심방세동에 대한 고주파 절제술을 이?한 수술 중 폐정맥 분리술의 유용성

홍그루,신동구,박종선,김영조,심봉섭,이장훈,정태은,이동협,한승세 대한순환기학회 2002 Korean Circulation Journal Vol.32 No.7

Deficiency of iNOS Does Not Prevent Isoproterenol-induced Cardiac Hypertrophy in Mice

Cha, Hye-Na,Hong, Geu-Ru,Kim, Yong-Woon,Kim, Jong-Yeon,Dan, Jin-Myoung,Park, So-Young The Korean Society of Pharmacology 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.3

We investigated whether deficiency of inducible nitric oxide synthase (iNOS) could prevent isoproterenol-induced cardiac hypertrophy in iNOS knockout (KO) mice. Isoproterenol was continuously infused subcutaneously (15 mg/kg/day) using an osmotic minipump. Isoproterenol reduced body weight and fat mass in both iNOS KO and wild-type mice compared with saline-infused wild-type mice. Isoproterenol increased the heart weight in both iNOS KO and wild-type mice but there was no difference between iNOS KO and wild-type mice. Posterior wall thickness of left ventricle showed the same tendency with heart weight. Protein level of iNOS in the left ventricle was increased in isoproterenol-infused wild-type mice. The gene expression of interleukin-6 (IL-6) and transforming growth factor-${\beta}$ (TGF-${\beta}$) in isoproterenol-infused wild-type was measured at 2, 4, 24, and 48-hour and isoproterenol increased both IL-6 (2, 4, 24, and 48-hour) and TGF-${\beta}$ (4 and 24-hour). Isoproterenol infusion for 7 days increased the mRNA level of IL-6 and TGF-${\beta}$ in iNOS KO mice, whereas the gene expression in wild-type mice was not increased. Phosphorylated form of extracellular signal-regulated kinases (pERK) was also increased by isoproterenol at 2 and 4-hour but was not increased at 7 days after infusion in wild-type mice. However, the increased pERK level in iNOS KO mice was maintained even at 7 days after isoproterenol infusion. These results suggest that deficiency of iNOS does not prevent isoproterenol-induced cardiac hypertrophy and may have potentially harmful effects on cardiac hypertrophy.

Deficiency of iNOS Does Not Prevent Isoproterenol-induced Cardiac Hypertrophy in Mice

Hye-Na Cha,Geu-Ru Hong,Yong-Woon Kim,Jong-Yeon Kim,Jin-Myoung Dan,So-Young Park 대한생리학회-대한약리학회 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.3

We investigated whether deficiency of inducible nitric oxide synthase (iNOS) could prevent isoproterenol-induced cardiac hypertrophy in iNOS knockout (KO) mice. Isoproterenol was continuously infused subcutaneously (15 mg/kg/day) using an osmotic minipump. Isoproterenol reduced body weight and fat mass in both iNOS KO and wild-type mice compared with saline-infused wild-type mice. Isoproterenol increased the heart weight in both iNOS KO and wild-type mice but there was no difference between iNOS KO and wild-type mice. Posterior wall thickness of left ventricle showed the same tendency with heart weight. Protein level of iNOS in the left ventricle was increased in isoproterenol-infused wild-type mice. The gene expression of interleukin-6 (IL-6) and transforming growth factor-Ղ (TGF-Ղ) in isoproterenol-infused wild-type was measured at 2, 4, 24, and 48-hour and isoproterenol increased both IL-6 (2, 4, 24, and 48-hour) and TGF-Ղ (4 and 24-hour). Isoproterenol infusion for 7 days increased the mRNA level of IL-6 and TGF-Ղ in iNOS KO mice, whereas the gene expression in wild-type mice was not increased. Phosphorylated form of extracellular signal-regulated kinases (pERK) was also increased by isoproterenol at 2 and 4-hour but was not increased at 7 days after infusion in wild-type mice. However, the increased pERK level in iNOS KO mice was maintained even at 7 days after isoproterenol infusion. These results suggest that deficiency of iNOS does not prevent isoproterenol- induced cardiac hypertrophy and may have potentially harmful effects on cardiac hypertrophy.

Impact of central haemodynamics on left ventricular function in individuals with an exaggerated blood pressure response to exercise

Shim, Chi Young,Hong, Geu-Ru,Park, Sungha,Yang, Woo-In,Choi, Donghoon,Chung, Namsik,Ha, Jong-Won Wolters Kluwer Health, Inc. All rights reserved. 2015 Journal of Hypertension Vol.33 No.3

OBJECTIVE:: The impact of exaggerated blood pressure response (EBPR) to exercise on left ventricular function and the mechanism of its association are poorly understood. This study investigated the impact of arterial stiffening on left ventricular function in individuals with an EBPR to exercise. We hypothesized that individuals with low pulse pressure (PP) amplification during exercise would have worse left ventricular function than those with high PP amplification in individuals with an EBPR to exercise. METHODS:: Fifty-nine individuals with an EBPR to exercise (18 men, age 57 ± 12 years) and 59 age and sex-matched controls were studied. Radial artery tonometry was performed at rest and immediately after exercise during supine bicycle exercise echocardiography. RESULTS:: There were no differences in left ventricular structure or function between individuals with an EBPR to exercise and controls. When individuals with an EBPR to exercise were divided into two groups on the basis of PP amplification after exercise [Group 1 (n = 30), high PP amplification after exercise; Group 2 (n = 29), low PP amplification after exercise], group 2 showed larger left atrial volume and lower early diastolic (e’) and systolic (S’) mitral annular velocities. Left ventricular apical rotation was also exaggerated in group 2. In multiple regression, PP amplification after exercise was an independent determinant of e’ (&bgr; = 0.16, P = 0.019) and S’ (&bgr; = 0.25, P = 0.009) in individuals with an EBPR to exercise. CONCLUSION:: In individuals with an EBPR to exercise, the degree of left ventricular dysfunction is variable. EBPR to exercise in the presence of arterial stiffening contributes to the deterioration of left ventricular function.

Severe chest pain with mid-ventricular obstruction in a patient with hyperthyroidism

Nam, Jong-Ho,Son, Jang Won,Hong, Geu-Ru Yeungnam University College of Medicine 2017 Yeungnam University Journal of Medicine Vol.34 No.1

Mid-ventricular obstruction (MVO) rarely occurs in patients without hypertrophic cardiomyopathy. Increased cardiac contractility may play an important role in causing MVO. We experienced a case of severe chest pain and MVO in a 50-year-old female patient. She had hypertension, diabetes, stroke and peripheral artery disease. Her blood pressure was very high (222/122 mmHg) with severe fluctuation. The transthoracic echocardiography revealed MVO accompanied by hyper-dynamic left ventricular systolic function. We regarded her chest pain and MVO as secondary findings related to other diseases. Coronary angiography and several tests for uncontrolled hypertension were performed, and those evaluations revealed that she had coronary artery disease and hyperthyroidism. We considered that the increase in the myocardial oxygen demand in response to the increase in cardiac contractility and workload associated with hyperthyroidism aggravated her symptoms and MVO. She was treated with methimazole and beta blockers and her symptoms dramatically improved.

S-190 Venous Thromboembolism in the Modern Era: Predisposing Factors, Treatments and Clinical Outcomes

( Kyu Kim ),( Chi Young Shim ),( Geu-ru Hong ),( Darae Kim ),( Jong-won Ha ),( Namsik ) 대한내과학회 2016 대한내과학회 추계학술대회 Vol.2016 No.1

Background: Venous thromboembolism (VTE) that includes deep vein thrombosis (DVT) and pulmonary embolism (PE) is a commonly encountered cardiovascular problem in patients with various medical or surgical comorbidities. Because of recent advances in diagnostic imaging for early detection of VTE and use of novel oral anticoagulants (NOACs), it is needed to explore current epidemiology, prescription patterns and clinical outcomes in patients with VTE. Methods: From January 2015 to December 2015, 380 consecutive patients (49.5% men, mean age 64.1±14.2), who were newly diagnosed with VTE by any diagnostic imaging modalities, were identified retrospectively in a single tertiary hospital. The baseline characteristics, predisposing factors, treatments and clinical outcomes were investigated. Clinical outcomes included admission rates, median hospital stay, in-hospital mortality and 1-year mortality. Result: About one third of overall VTE patients (262, 69.7%) had active cancer. 104 (27.4%) patients had other risk factors including marked immobilization, prior surgery and trauma. However, 40 (10.5%) patients presented unprovoked VTE. 332 (76.7%) patients presented with PE and 149 (39.2%) had DVT. Among patients with PE, minimal PE was more prevalent especially in cancer patients (201, 94.8%) than in non-cancer unprovoked (22/40, 59.5%) or in non-cancer provoked (56/104, 53.8%) PE. In terms of initial treatment strategies, 176 (46.3%) patients were treated with NOACs, while 86 (22.6%) patients with unfractionated heparin, 73 (19.2%) patients with low molecular weight heparin, 8 (2.1%) patients with warfarin and 27 (7.1%) patients were treated by an inferior vena cava placement. Patients with active cancer showed significantly poorer clinical outcomes than other groups (2.5% of unprovoked VTE vs. 6.7% of non-cancer provoked vs. 32.6% of cancer, p<0.001) Conclusions: With advances of diagnostic imaging techniques and developments of novel anticoagulants, the incidence of minimal PE is high, especially in cancer patients. A half of VTE patients were initially treated with NOACs. One-year clinical outcomes are favorable in non-cancer patients but not in cancer patients.