• Journal of the Korean Society of Radiology
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• v.83 no.2
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• pp.360-371
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• 2022

Purpose This study aimed to assess the factors influencing aortic unfolding (AU) defined by aortic width on coronary artery calcium (CAC) scan and determine the normal limits for AU. Materials and Methods In this retrospective study, we measured AU in 924 asymptomatic subjects who underwent CAC scanning during routine health screening from June 2015 to June 2018. Multivariate regression analysis was used to evaluate the factors influencing AU. After the exclusion of subjects with risk factors associated with AU, 283 subjects were included in the analysis of normal values of AU. Mean AU, standard deviation, and upper normal limit were calculated. Results Sex, age, CAC score, body mass index, body surface area, hypertension, left ventricular hypertrophy, plasma creatinine, and smoking were significantly associated with AU. The mean AU was 102.2 ± 12.8 mm for men and 93.1 ± 10.7 mm for women. AU increased with advancing age (9.6 mm per decade). Conclusion AU determined from a single measurement on CAC scans was associated with cardiovascular risk factors. The normal limits of AU were defined by age, sex, and body surface area in low-risk subjects in this study.

• Journal of Chest Surgery
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• v.50 no.3
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• pp.144-152
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• 2017

Background: The ubiquitin-proteasome system (UPS) is an important pathway of proteolysis in pathologic hypertrophic cardiomyocytes. We hypothesize that MG132, a proteasome inhibitor, might prevent hypertrophic cardiomyopathy (CMP) by blocking the UPS. Nuclear factor kappa-light-chain-enhancer of activated B cells ($NF-{\kappa}B$) and androgen receptor (AR) have been reported to be mediators of CMP and heart failure. This study drew upon pathophysiologic studies and the analysis of $NF-{\kappa}B$ and AR to assess the cardioprotective effects of MG132 in a left ventricular hypertrophy (LVH) rat model. Methods: We constructed a transverse aortic constriction (TAC)-induced LVH rat model with 3 groups: sham (TAC-sham, n=10), control (TAC-cont, n=10), and MG132 administration (TAC-MG132, n=10). MG-132 (0.1 mg/kg) was injected for 4 weeks in the TAC-MG132 group. Pathophysiologic evaluations were performed and the expression of AR and $NF-{\kappa}B$ was measured in the left ventricle. Results: Fibrosis was prevalent in the pathologic examination of the TAC-cont model, and it was reduced in the TAC-MG132 group, although not significantly. Less expression of AR, but not $NF-{\kappa}B$, was found in the TAC-MG132 group than in the TAC-cont group (p<0.05). Conclusion: MG-132 was found to suppress AR in the TAC-CMP model by blocking the UPS, which reduced fibrosis. However, $NF-{\kappa}B$ expression levels were not related to UPS function.

• Annals of Occupational and Environmental Medicine
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• v.35
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• pp.34.1-34.8
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• 2023

Background: Hydrogen sulfide is a toxic substance that humans can be exposed to occupationally, and cases of hydrogen sulfide poisoning of workers in industrial sites are commonly reported. However, there have been no cases of poisoning of the public due to an unauthorized discharge of wastewater, so it is important to describe this incident. Case presentation: In a small village in Jeollanam-do, Republic of Korea, accounts of a terrible stench had been reported. A 26-year-old man who lived and worked in a foul-smelling area was taken to the emergency room with a headache, dizziness, nausea, and repeated syncope. A subsequent police and Ministry of Environment investigation determined that the cause of the stench was the unauthorized discharge of 9 tons of wastewater containing hydrogen sulfide through a stormwater pipe while the villagers were sleeping. The patient had no previous medical history or experience of symptoms. Leukocytes and cardiac markers were elevated, an electrocardiogram indicated biatrial enlargement, left ventricular hypertrophy, and corrected QT interval prolongation. Myocardial hypertrophy was detected on a chest computed tomography scan, and hypertrophic cardiomyopathy was confirmed on echocardiography. After hospitalization, cardiac marker concentrations declined, symptoms improved, and the patient was discharged after 7 days of hospitalization. There was no recurrence of symptoms after discharge. Conclusions: We suspect that previously unrecognized heart disease manifested or was aggravated in this patient due to exposure to hydrogen sulfide. Attention should be paid to the possibility of unauthorized discharge of hydrogen sulfide, etc., in occasional local incidents and damage to public health. In the event of such an accident, it is necessary to have government guidelines in place to investigate health impact and follow-up clinical management of exposed residents.

• Journal of Chest Surgery
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• v.39 no.10 s.267
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• pp.775-778
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• 2006

Hypertrophic cardiomyopathy is characterized by inappropriate hypertrophy of the myocardium and is associated with various clinical presentations ranging from complete absence of symptoms to sudden, unexpected death. These are caused by dynamic obstruction of the left ventricular outflow tract and surgical approaches were initiated. But, the complete resection of hypertrophied midventricular septum is impossible by standard, transaortic approach, because of narrow vision and limited approach. And it leads to inadequate excision, will leave residual left ventricular out-flow tract obstruction or systolic anterior motion of mitral leaflet, and limit symptomatic improvement and patient's survival. We report a case of extended septal myectomy for hypertrophic cardiomyopathy of mid-septum in a child. The extended septal myectomy was performed by aortotomy and left ventricular apical incision, and made possible the complete resection of mid-ventricular septum, abnormal papillary muscles and chordae. The patient's symptom was improved and the postoperative course was uneventful.

• Clinical and Experimental Pediatrics
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• v.55 no.9
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• pp.350-353
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• 2012

An 18-year-old boy was admitted with chest discomfort, nausea, and dyspnea at rest. At the age of 3 years, he underwent muscle biopsy and dystrophin gene analysis owing to an enlarged calf muscle and elevated serum kinase level (6,378 U/L) without overt weakness; based on the results, Becker muscular dystrophy (BMD) was diagnosed. The dystrophin gene showed deletion of exons 45 to 49. He remained ambulant and could step upstairs without significant difficulties. A chest roentgenogram showed cardiomegaly (cardiothoracic ratio, 54%), and his electrocardiogram (ECG) showed abnormal ST-T wave, biatrial enlargement, and left ventricular hypertrophy. The 2-dimensional and M-mode ECGs showed a severely dilated left ventricular cavity with diffuse hypokinesis. The systolic indices were reduced, including fractional shortening (9%) and ejection fraction (19%). Despite receiving intensive medical treatment, he died from congestive heart failure 5 months after the initial cardiac symptoms. We report a case of BMD with early-onset dilated cardiomyopathy associated with deletion of exons 45 to 49. Early cardiomyopathy can occur in BMD patients with certain genotypes; therefore, careful follow-up is required even in patients with mild phenotypes of BMD.

• Korean Journal of Veterinary Service
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• v.40 no.1
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• pp.67-70
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• 2017

A 4 months old, intact male Shih-tzu was referred to the Veterinary Medical Teaching Hospital of Chungnam National University for evaluation of the cause of cardiac murmur and syncope. Thoracic radiography revealed right-sided cardiomegaly. Echocardiography showed marked hypertrophy of right ventricular free wall and obstruction of right ventricular outflow tract, indicating double chambered right ventricle (DCRV). The dog was medicated with atenolol and sildenafil for DCRV, however, clinical signs did not control by medication. Balloon dilation for DCRV was performed to ameliorate patient's clinical signs. The peak systolic pressure gradient across the obstruction region was decreased and clinical signs was improved by balloon dilation procedure. This is the first case report of balloon dilation for the treatment of canine DCRV in South Korea.

• Journal of Chest Surgery
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• v.23 no.5
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• pp.962-967
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• 1990

The anomalous pulmonary venous return of the entire left lung was an extremely rare congenital anomaly. The reported surgical experience with correction of this disorder was limited. The 3-year-old female patient underwent an operation upon the unilateral total anomalous pulmonary venous return from the left lung, in which the left superior pulmonary vein drained into innominate vein and the left inferior pulmonary vein into the coronary sinus, in Yeungnam University Hospital. The symptoms were nonspecific except frequent upper respiratory infection. Cyanosis was not seen. On auscultatory findings, a grade 2/6 systolic ejection murmur was audible over left second intercostal space of left sternal border and second heart sound had an increased pulmonary component which was widely splitted. The electrocardiogram demonstrated a right ventricular hypertrophy and right axis deviation and chest X-ray showed slightly increased pulmonary vascularity and bulged pulmonary conus. The echocardiogram demonstrated increased right atrial, ventricular, and pulmonary arterial dimension, and also secundum atrial septal defect and enlarged coronary sinus. The cardiac catheterization confirmed the left-to-right with a Qp/Qs of 2.0: 1 and oxygen step-up was seen in pulmonary artery, right ventricle, right atrium, and left innominate vein, and the catheter was not been introduced into the left pulmonary vein. A median sternotomy incision was done. Left superior pulmonary vein was drained to the innominate vein through anomalous vertical vein and the left inferior pulmonary vein drained to right atrium through the coronary sinus. The diversion of the left inferior pulmonary vein to posterior wall of left atrium was done after division in the proximity of coronary sinus. The anomalous vertical vein was diverted to base of left atrial auricle and then a atrial septal defect was sutured directly. The postoperative course was uneventful and she was discharged on the eleventh postoperative day. In the postoperative follow-up-2 months, she has been well without specific problems.

• Journal of Chest Surgery
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• v.34 no.1
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• pp.57-63
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• 2001

배경: 대동맥판막협착증 환자는 판막질환으로 인한 만성적인 후부하의 증가에 대한 보상성 좌심실 심근비후가 일어나게 된다. 대동맥 판막 치환 후 좌심실 심근 비후의 감소가 이루어지는 것으로 알려져 있으나 21mm이하의 작은 인공판막으로 치환시 좌심실 심근 변화에 대해 논란이 있다. 대상 및 방법: 1994년 9월부터 1998년 7월까지 한림대학교 강동성심병원 흉부외과에서 대동맥판막협착증으로 진단받고 판막치환술을 시행한 20명을 대상으로 하였다. 환자는 남녀 각각 13명, 7명이며 평균나이 61$\pm$13.8세 체표면적은 평균 1.57$\pm$0.14m$m^2$이었다. 환자의 추적관찰은 수술 전, 수술 후 초기(평균 10.4일) 및 수술 후 만기(평균 29.9개월)에 심초음파로 시행하였다. 환자들은 사용된 판막에 따라 2개의 군(1군;21mm 이하, 2군;23mm이상)으로 나누었다. 결과: 모든 군에서 NYHA Functional class의 유의한 감소가 있었다. 좌심실 구추률은 수술 전후 1군은 유의한 차이가 없었으나 2군에서는 유의한 차이가 있었다. 그러나 수술 전 좌심실 구출률이 2군에서 1군에 비해 유의하게 감소되어 있었다(p=0.044). 좌심실근량지수는 1군은 수술후 초기에 유의한 감소가 없었으나 수술후 만기에는 유의한 감소를 보여주었다. 그러나 2군은 수술후 초기와 만기에 모두 유의한 감소를 보여주었다. 결론: 21 mm이하 군과 23 mm이상 군 모두 임상적 호전이 있었다. 그러나 19 mm판막군이 2례로 적어 19 mm 판막의 사용시 환자의 나이와 체표면적, 운동량을 고려하여 신중한 판막선택이 고려된다.

• Clinical and Experimental Pediatrics
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• v.60 no.11
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• pp.365-372
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• 2017

Purpose: The mechanism for the pathogenesis of adriamycin (ADR)-induced cardiomyopathy is not yet known. Different hypotheses include the production of free radicals, an interaction between ADR and nuclear components, and a disruption in cardiac-specific gene expression. Apoptosis has also been proposed as being involved in cardiac dysfunction. The purpose of this study was to determine if apoptosis might play a role in ADR-induced cardiomyopathy. Methods: Male Sprague-Dawley rats were separated into 2 groups: the control group (C group) and the experimental group (ADR 5 mg/wk for 3 weeks through intraperitoneal injections; A group). Echocardiographic images were obtained at week 3. Changes in caspase-3, B-cell leukemia/lymphoma (Bcl)-2, Bcl-2-associated X (Bax), interleukin (IL)-6, tumor necrosis $factor-{\alpha}$, brain natriuretic peptide (BNP), troponin I, collagen 1, and collagen 3 protein expression from the left ventricle tissues of C and A group rats were determined by Western blot. Results: Ascites and heart failure as well as left ventricular hypertrophy were noted in the A group. Ejection fraction and shortening fraction were significantly lower in the A group by echocardiography. The expression of caspase-3, Bax, IL-6, BNP, collagen 1, and collagen 3 were significantly higher in the A group as compared with the C group. Protein expression of Bcl-2 decreased significantly in the A group compared with the C group. Conclusion: ADR induced an upregulation of caspase-3, Bax, IL-6, and collagen, as well as a depression in Bcl-2. Thus, apoptosis and fibrosis may play an important role in ADR-induced cardiomyopathy.

• Journal of Ginseng Research
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• v.40 no.3
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• pp.285-291
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• 2016

Background: Ginsenosides have been shown to exert beneficial pharmacological effects on the central nervous, cardiovascular, and endocrine systems. We sought to determine whether total ginsenosides (TG) inhibit monocrotaline (MCT)-induced pulmonary hypertension and to elucidate the underlying mechanism. Methods: MCT-intoxicated rats were treated with gradient doses of TG, with or without $N^G$-nitro-$\small{L}$-arginine methyl ester. The levels of molecules involving the regulation of nitric oxide and mitogen-activated protein kinase pathways were determined. Results: TG ameliorated MCT-induced pulmonary hypertension in a dose-dependent manner, as assessed by the right ventricular systolic pressure, the right ventricular hypertrophy index, and pulmonary arterial remodeling. Furthermore, TG increased the levels of pulmonary nitric oxide, endothelial nitric oxide synthase, and cyclic guanosine monophosphate. Lastly, TG increased mitogen-activated protein kinase phosphatase-1 expression and promoted the dephosphorylation of extracellular signal-regulated protein kinases 1/2, p38 mitogen-activated protein kinase, and c-Jun NH2-terminal kinase 1/2. Conclusion: TG attenuates MCT-induced pulmonary hypertension, which may involve in part the regulation of nitric oxide and mitogen-activated protein kinase pathways.