• Tuberculosis and Respiratory Diseases
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• 제63권6호
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• pp.475-479
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• 2007

• Tuberculosis and Respiratory Diseases
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• 제68권5호
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• pp.273-279
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• 2010

Background: Pulmonary hypertension is considered as a poor prognosis factor in patients with chronic obstructive pulmonary disease (COPD). There has been reported brain natriuretic peptide (pro-BNP) is related with increased right ventricular (RV) workloads. However, there are few studies that evaluate the relationship between BNP and pulmonary arterial pressure (PAP), RV function and St. George Respiratory Questionnaire (SGRQ) score in patients with COPD, and the effects of angiotensin converting enzyme inhibitor (ACEI) on these parameters. Methods: Pulmonary function test, echocardiography, blood BNP, and SGRQ score were evaluated in stabilized moderate degree COPD patients ($FEV_1$/FVC< 70%, $50%{\leq}FEV_1$ < 80%) aged 45 years and over, without worsening of symptoms within recent 3 months. After treating with ramipril 10 mg for 3 months, the same evaluation was repeated. Results: Twenty-two patients were included in this study. BNP was significantly correlated with PAP (Pearson coefficient ${\rho}=0.51$, p=0.02), but not with RV ejection fraction (EF) and predicted $FEV_1%$. The values for predicted $FEV_1%$ showed significant correlation with SGRQ total score and activity score, but not with BNP or PAP. After ramipril treatment, PAP showed significant decrease ($42.8{\pm}8.1$ vs. $34.5{\pm}4.5mm$ Hg p=0.0003), tricuspid annular plane systolic excursion significant increase ($21.5{\pm}3.3$ vs. $22.7{\pm}3.1mm$ p=0.009). BNP showed a tendency to decrease without statistical significance ($40.8{\pm}59.6$ vs. $18.0{\pm}9.1pg/mL$ p=0.55). SGRQ scores showed no significant change. Conclusion: BNP showed significant correlation with resting PAP, which means BNP could be used as markers for pulmonary hypertension. Treatment with ACEI didn't show significant change in the level of BNP, while pulmonary hypertension and RV function were improved.

• Journal of Cardiovascular Imaging
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• 제31권3호
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• pp.152-154
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• 2023

• Journal of Chest Surgery
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• 제46권1호
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• pp.41-48
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• 2013

Background: We present our 12-year experience of pulmonary thromboendarterectomy in patients with chronic thromboembolic pulmonary hypertension. Materials and Methods: Between January 1999 and March 2011, 16 patients underwent pulmonary thromboendarterectomy. Eleven patients (69%) were classified as functional class III or IV based on the New York Heart Association (NYHA) classification. Seven patients had a history of inferior vena cava filter insertion, and 5 patients showed coagulation disorders. Pulmonary thromboendarterectomy was performed during total circulatory arrest with deep hypothermia in 14 patients. Results: In-hospital mortality and late death occurred in 2 patients (12.5%) and 1 patient (6.3%), respectively. Extracorporeal membrane oxygenation support was required in 4 patients who developed severe hypoxemia after surgery. Thirteen of the 14 survivors have been followed up for 54 months (range, 2 to 141 months). The pulmonary arterial systolic pressure and cardiothoracic ratio on chest radiography was significantly decreased after surgery ($76{\pm}26$ mmHg vs. $41{\pm}17$ mmHg, p=0.001; $55%{\pm}8%$ vs. $48%{\pm}3%$, p=0.003). Tricuspid regurgitation was reduced from $2.1{\pm}1.1$ to $0.7{\pm}0.6$ (p=0.007), and the NYHA functional class was also improved to I or II in 13 patients (81%). These symptomatic and hemodynamic improvements maintained during the late follow-up period. Conclusion: Pulmonary thromboendarterectomy for chronic thromboembolic pulmonary hypertension shows good clinical outcomes with acceptable early and long term mortality.

• Journal of Chest Surgery
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• 제21권5호
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• pp.911-917
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• 1988

Pulmonary thromboembolism originated most commonly from the venous thrombus, especially deep vein thrombus in the leg, which migrated to and occluded the pulmonary vasculatures. The failure of clot lysis and repeated embolic episodes resulted in the hemodynamic compromise -that is- in the increasing in the pulmonary vascular resistance, which would cause the right ventricle failure[Car Pulmonale]. Under the cardiopulmonary bypass, 20 year old male patient was treated successfully by thromboembolectomy of pulmonary thromboembolism with pulmonary hypertension, which originated from the deep vein thrombus in the leg. The results of radiologic studies and clinical evaluations were excellent in that the postoperative lung perfusion scan showed the newly increased perfusion of post-embolectomy territories and in the arterial blood gas finding of 76 from 66[mmHg] in PaO2. The patient was uneventful and discharged on postop. $ 14 days with anticoagulant continued.

• Journal of Chest Surgery
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• 제31권7호
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• pp.718-721
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• 1998

심한 폐동맥고혈압증을 동반한 심실중격결손증을 교정하는 수술은 술후 높은 사망률 때문에 외과의에게 많은 어려움이 있다.. 최근에 술후 급성 우심부전이 발생시 우좌혈류단락이 가능하여 심혈류역학을 개선하는 일방성 판막 팻취를 이용한 수술이 안전한 수술법으로 보고되고 있다. 환자는 20 년 전에 선천성심질환을 진단을 받은 바 있으며, 내원 3 개월 전부터 운동성 호흡곤란이 발생하였고, 정밀검사상 심한 폐동맥 고혈압증을 동반한 심실중격결손증으로 진단되었다. 저자등은 심실중격결손을 첨포를 이용하여 폐쇄하는 대신에 술 후 우심실부전을 예방하는 일방성 판막 팻취를 이용하여 결손을 교정하였다. 환자는 건강한 상태로 술 후 14 일째 퇴원하였으며, 일방성 판막 개구부는 술 후 9 개월에 자연 폐쇄되었고, 12 개월 양호한 상태를 유지하고 있다.

• 한국임상수의학회지
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• 제34권1호
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• pp.1-6
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• 2017

Heartworm disease (HWD) in dogs is a life-threatening mosquito-borne disease resulting in right-sided congestive heart failure and inflammatory pulmonary disease. Due to complications from adulticidal therapy with melarsomine, slow kill protocol either with preventive dose of ivermectin or combined with doxycycline has been proposed for an alternative adultcidal therapy in dogs with HWD. Therefore, this study evaluated the clinical outcome of adultcidal therapy in dogs with class II stage of HWD after treating either American Heartworm Society (AHS) or slow kill protocol for 10 months. Clinical outcome after therapy was evaluated by clinical, radiographic and echocardiographic examination along with hematology before (D0) and after therapy (D300). Although clinical signs associated with HWD were all resolved after therapy in both groups, the infection was not cleared out 67% of dogs treated by slow kill protocol at the end of therapy. Furthermore, pulmonary arterial flow of acceleration time to ejection time ratio (AT/ET) and the right pulmonary artery distensibility index (RPADI) have been firstly used for detecting pulmonary hypertension in this study group. The pulmonary hypertension was more common in dogs with mild clinical signs, although tricuspid and pulmonary regurgitation were not detectable in most dogs in this study. Our study findings suggested that the slow kill protocol might not be efficacious enough to clear out HWD in dogs and more attention on the presence of pulmonary hypertension might be necessary for effective management of HWD in dogs.

• Clinical and Experimental Pediatrics
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• 제55권8호
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• pp.297-300
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• 2012

Symptomatic pulmonary arterial hypertension (PAH) in patients with isolated atrial septal defect (ASD) is rare during infancy. We report a case of isolated ASD with severe PAH in an infant who developed airway obstruction as cardiomegaly progressed. The patient presented with recurrent severe respiratory insufficiency and failure to thrive before the repair of the ASD. Echocardiography confirmed volume overload on the right side of heart and severe PAH (tricuspid regurgitation [TR] with a peak pressure gradient of 55 to 60 mmHg). The chest radiographs demonstrated severe collapse of both lung fields, and a computed tomography scan showed narrowing of the main bronchus because of an intrinsic cause, as well as a dilated pulmonary artery compressing the main bronchus on the left and the intermediate bronchus on the right. ASD patch closure was performed when the infant was 8 months old. After the repair of the ASD, echocardiography showed improvement of PAH (TR with a peak pressure gradient of 22 to 26 mmHg), and the patient has not developed recurrent respiratory infections while showing successful catch-up growth. In infants with symptomatic isolated ASD, especially in those with respiratory insufficiency associated with severe PAH, extrinsic airway compression should be considered. Correcting any congenital heart diseases in these patients may improve their symptoms.

• BMB Reports
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• 제55권11호
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• pp.565-570
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• 2022

Pulmonary arterial hypertension (PAH) is a progressive and devastating disease whose pathogenesis is associated with a phenotypic switch of pulmonary arterial vascular smooth muscle cells (PASMCs). Bone morphogenetic protein (BMP) signaling and potassium two pore domain channel subfamily K member 3 (KCNK3) play crucial roles in PAH pathogenesis. However, the relationship between BMP signaling and KCNK3 expression in the PASMC phenotypic switching process has not been studied. In this study, we explored the effect of BMPs on KCNK3 expression and the role of KCNK3 in the BMP-mediated PASMC phenotypic switch. Expression levels of BMP receptor 2 (BMPR2) and KCNK3 were downregulated in PASMCs of rats with PAH compared to those in normal controls, implying a possible association between BMP/BMPR2 signaling and KCNK3 expression in the pulmonary vasculature. Treatment with BMP2, BMP4, and BMP7 significantly increased KCNK3 expression in primary human PASMCs (HPASMCs). BMPR2 knockdown and treatment with Smad1/5 signaling inhibitor substantially abrogated the BMP-induced increase in KCNK3 expression, suggesting that KCNK3 expression in HPASMCs is regulated by the canonical BMP-BMPR2-Smad1/5 signaling pathway. Furthermore, KCNK3 knockdown and treatment with a KCNK3 channel blocker completely blocked BMP-mediated anti-proliferation and expression of contractile marker genes in HPAMSCs, suggesting that the expression and functional activity of KCNK3 are required for BMP-mediated acquisition of the quiescent PASMC phenotype. Overall, our findings show a crosstalk between BMP signaling and KCNK3 in regulating the PASMC phenotype, wherein BMPs upregulate KCNK3 expression and KCNK3 then mediates BMP-induced phenotypic switching of PASMCs. Our results indicate that the dysfunction and/or downregulation of BMPR2 and KCNK3 observed in PAH work together to induce aberrant changes in the PASMC phenotype, providing insights into the complex molecular pathogenesis of PAH.

• 대한의생명과학회지
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• 제27권1호
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• pp.12-18
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• 2021

Hypertension (HTN) is one of the cardiovascular disease risk factors. Peroxisome proliferator-activated receptor γ coactivator 1 alpha (PPARGC1A) is involved in a master modulator of mitochondrial biogenesis, and pulmonary arterial hypertension. In this study, we report results of PPARGC1A were associated with hypertension and its intermediate phenotype of systolic (SBP) and diastolic blood pressure (DBP) in the Korean population. In detail, identifying a susceptibility locus, 3 SNPs for HTN, 2 SNPs for SBP, 3 SNPs for DBP at P<0.05. Among them, rs1472095 in PPARGC1A gene statistically demonstrated one of the significant correlations with Hypertension (P-value=0.00359, OR=0.8, 95% CI=0.68~0.93). The minor allele (T) of PPARGC1A was statistically associated with the increased value of DBP, SBP, and the increase risk of hypertension. We aim to manifest a significant association between genetic variant in PPARGC1A and hypertension. This finding suggested that association of PPARGC1A genetic polymorphism and HTN accelerates our understanding of blood pressure control and underlines potential drug targets for treatment of hypertension.