• Korean Circulation Journal
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• 제53권5호
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• pp.344-346
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• 2023

• Molecules and Cells
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• 제43권4호
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• pp.408-418
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• 2020

The sinus node (SN) is located at the apex of the cardiac conduction system, and SN dysfunction (SND)-characterized by electrical remodeling-is generally attributed to idiopathic fibrosis or ischemic injuries in the SN. SND is associated with increased risk of cardiovascular disorders, including syncope, heart failure, and atrial arrhythmias, particularly atrial fibrillation. One of the histological SND hallmarks is degenerative atrial remodeling that is associated with conduction abnormalities and increased right atrial refractoriness. Although SND is frequently accompanied by increased fibrosis in the right atrium (RA), its molecular basis still remains elusive. Therefore, we investigated whether SND can induce significant molecular changes that account for the structural remodeling of RA. Towards this, we employed a rabbit model of experimental SND, and then compared the genome-wide RNA expression profiles in RA between SND-induced rabbits and sham-operated controls to identify the differentially expressed transcripts. The accompanying gene enrichment analysis revealed extensive pro-fibrotic changes within 7 days after the SN ablation, including activation of transforming growth factor-β (TGF-β) signaling and alterations in the levels of extracellular matrix components and their regulators. Importantly, our findings suggest that periostin, a matricellular factor that regulates the development of cardiac tissue, might play a key role in mediating TGF-β-signaling-induced aberrant atrial remodeling. In conclusion, the present study provides valuable information regarding the molecular signatures underlying SND-induced atrial remodeling, and indicates that periostin can be potentially used in the diagnosis of fibroproliferative cardiac dysfunctions.

• Journal of Chest Surgery
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• 제54권1호
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• pp.45-52
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• 2021

Background: Atrial septal defect (ASD) is the most common congenital heart disease. However, the details of cardiac chamber remodeling after surgery are not well known, although this is an important issue that should be analyzed to understand long-term outcomes. Methods: Between November 2017 and January 2019, cardiac magnetic resonance imaging was performed preoperatively, at a 1-month postoperative follow-up, and at a 1-year postoperative follow-up. Cardiac chamber volume, valve regurgitation volume, and ejection fraction were measured as functions of time. Results: Thirteen patients (10 men and 3 women) were included. The median age at surgery was 51.4 years. The preoperative median ratio of flow in the pulmonary and systemic circulation was 2.3. The preoperative mean right ventricular (RV) end-diastolic volume index (EDVi) and RV end-systolic volume index (ESVi) had significantly decreased at the 1-month postoperative follow-up (p<0.001, p=0.001, respectively). The decrease in the RVEDVi (p=0.085) and RVESVi (p=0.023) continued until the postoperative 1-year follow-up, although the rate of decrease was slower. Tricuspid valve regurgitation had also decreased at the 1-month postoperative follow-up (p=0.022), and continued to decrease at a reduced rate (p=0.129). Although the RVEDVi and RVESVi improved after ASD closure, the RV volume parameters were still larger than the left ventricular (LV) volume parameters at the 1-year follow-up (RVEDVi vs. LVEDVi: p=0.016; RVESVi vs. LVESVi: p=0.001). Conclusion: Cardiac remodeling after ASD closure is common and mainly occurs in the early postoperative period. However, complete normalization does not occur.

• The Korean Journal of Physiology and Pharmacology
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• 제26권6호
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• pp.469-478
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• 2022

WNT signaling plays an important role in cardiac development, but abnormal activity is often associated with cardiac hypertrophy, myocardial infarction, remodeling, and heart failure. The effect of WNT signaling on regulation of atrial natriuretic peptide (ANP) secretion is unclear. Therefore, the purpose of this study was to investigate the effect of Wnt agonist 1 (Wnta1) on ANP secretion and mechanical dynamics in beating rat atria. Wnta1 treatment significantly increased atrial ANP secretion and pulse pressure; these effects were blocked by U73122, an antagonist of phospholipase C. U73122 also abolished the effects of Wnta1-mediated upregulation of protein kinase C (PKC) β and γ expression, and the PKC antagonist Go 6983 eliminated Wnta1-induced secretion of ANP. In addition, Wnta1 upregulated levels of phospho-transforming growth factor-β activated kinase 1 (p-TAK1), TAK1 banding 1 (TAB1) and phospho-activating transcription factor 2 (p-ATF2); these effects were blocked by both U73122 and Go 6983. Wnta1-induced ATF2 was abrogated by inhibition of TAK1. Furthermore, Wnta1 upregulated the expression of T cell factor (TCF) 3, TCF4, and lymphoid enhancer factor 1 (LEF1), and these effects were blocked by U73122 and Go 6983. Tak1 inhibition abolished the Wnta1-induced expression of TCF3, TCF4, and LEF1 and Wnta1-mediated ANP secretion and changes in mechanical dynamics. These results suggest that Wnta1 increased the secretion of ANP and mechanical dynamics in beating rat atria by activation of PKC-TAK1-ATF2-TCF3/LEF1 and TCF4/LEF1 signaling mainly via the WNT/Ca²⁺ pathway. It is also suggested that WNT-ANP signaling is implicated in cardiac physiology and pathophysiology.

• 대한영상의학회지
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• 제81권2호
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• pp.272-289
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• 2020

전산화단층촬영(이하 CT) 영상 기술의 발전으로 박동하는 심장에 대한 섬세한 영상의학적 평가가 가능해졌다. 심초음파 및 MRI에 비해 심장 CT의 강점은 대부분의 의료기관에 보급되어 있고 고품질 이미지의 빠른 생산이 가능하며 해부학적 묘사가 뛰어나다는 것이다. 좌심방과 좌심방이에서 생기는 대부분의 변이 혹은 병리적 상태들은 CT 상의 소견만으로도 추정 진단을 내릴 수 있다. 또한 CT 영상은 성공적인 카테터 기반 시술 또는 수술에 중요한 해부학적 정보들을 제공한다. 특히 좌심방과 좌심방이는 심방세동 환자들의 치료 및 관리에 중요한데, 이는 다양한 카테터 기반 시술들이 두 구조물의 기계적 혹은 전기적 차단을 목표로 하기 때문이다. 따라서 임상적으로 의미 있는 판독을 위해서는 병리적 상태의 CT 소견 기술과 함께 좌심방 및 좌심방이의 모양, 크기 및 주변 구조물과의 상대적 위치 관계 등에 대한 포괄적인 검토를 해야 한다.

• Clinical and Experimental Pediatrics
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• 제56권3호
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• pp.101-106
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• 2013

Despite developments in surgical techniques and other interventions, right ventricular (RV) failure remains an important clinical problem in several congenital heart diseases (CHD). RV function is one of the most important predictors of mortality and morbidity in patients with CHD. RV failure is a progressive disorder that begins with myocardial injury or stress, neurohormonal activation, cytokine activation, altered gene expression, and ventricular remodeling. Pressure-overload RV failure caused by RV outflow tract obstruction after total correction of tetralogy of Fallot, pulmonary stenosis, atrial switch operation for transposition of the great arteries, congenitally corrected transposition of the great arteries, and systemic RV failure after the Fontan operation. Volume-overload RV failure may be caused by atrial septal defect, pulmonary regurgitation, or tricuspid regurgitation. Although the measurement of RV function is difficult because of many reasons, the right ventricle can be evaluated using both imaging and functional modalities. In clinical practice, echocardiography is the primary mode for the evaluation of RV structure and function. Cardiac magnetic resonance imaging is increasingly used for evaluating RV structure and function. A comprehensive evaluation of RV function may lead to early and optimal management of RV failure in patients with CHD.

• The Korean Journal of Physiology and Pharmacology
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• 제26권5호
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• pp.313-323
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• 2022

Atrial fibrillation (AF) is the most common supraventricular arrhythmia, and it corresponds highly with exercise intensity. Here, we induced AF in mice using acetylcholine (ACh)-CaCl₂ for 7 days and aimed to determine the appropriate exercise intensity (no, low, moderate, high) to protect against AF by running the mice at different intensities for 4 weeks before the AF induction by ACh-CaCl₂. We examined the AF-induced atrial remodeling using electrocardiogram, patch-clamp, and immunohistochemistry. After the AF induction, heart rate, % increase of heart rate, and heart weight/body weight ratio were significantly higher in all the four AF groups than in the normal control; highest in the high-ex AF and lowest in the low-ex (lower than the no-ex AF), which indicates that low-ex treated the AF. Consistent with these changes, G protein-gated inwardly rectifying K⁺ currents, which were induced by ACh, increased in an exercise intensity-dependent manner and were lower in the low-ex AF than the no-ex AF. The peak level of Ca²⁺ current (at 0 mV) increased also in an exercise intensity-dependent manner and the inactivation time constants were shorter in all AF groups except for the low-ex AF group, in which the time constant was similar to that of the control. Finally, action potential duration was shorter in all the four AF groups than in the normal control; shortest in the high-ex AF and longest in the low-ex AF. Taken together, we conclude that low-intensity exercise protects the heart from AF, whereas high-intensity exercise might exacerbate AF.

• Journal of Chest Surgery
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• 제37권9호
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• pp.755-761
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• 2004

말기 허혈성 심근질환에서 좌심실내 원형패취 성형술(Dor 술식)이 심근 기능의 개선에 미치는 영향을 알아보고자 서울대학교병원 흉부외과에서 시행한 Dor 술식의 결과를 분석해 보았다. 대상 및 방법： 1998년 4월부터 2002년 12월 사이에 좌심박출계수 35% 이하의 허혈성 심근질환으로 관상동맥우회술과 함께 Dor 술식을 시행한 45례의 환자를 대상으로 수술 전, 수술 직후 및 술 후 1년째에 심초음파, 심근 SPECT, 심도자 및 조영술을 시행하여 좌심실 박출계수 및 용적 등의 변화를 비교 분석하였다. 결과: 심폐바이패스 및 대동맥 차단시간은 각각 평균 141$\pm$64, 69$\pm$24분이었다. 7례에서 수술전에 대동맥내풍선펌프를 사용하였으며 수술 중 및 수술 후 저심박출 증후군을 보인 9례와 3례에서 대동맥내 풍선펌프를 삽입하였다. 수술 사망은 1례(2.2%)가 있었으며, 합병증으로는 저심박출 증후군(12례), 심방세동(5례), 급성신부전(4례), 출혈에 의한 재수술(4례) 등이 있었다. 술 후 1개월째 환자의 NYHA 기능지수는 평균 2.8에서 1.1로 유의하게 향상되었다(p < 0.01). 수술 직후 시행한 좌심실조영술상 박출계수는 수술 전과 비교해서 32 $\pm$ 9%에서 52$\pm$11%로, asynergy 분획은 57 $\pm$ 12%에서 22 $\pm$ 9%로, 좌심실확장기말, 수축기말 용적 계수들도 각각 125$\pm$39 mL/$m^2$, 85 $\pm$30 mL/$m^2$에서 66$\pm$23 mL/$m^2$, 32$\pm$16 mL/$m^2$으로 통계적으로 유의한 개선을 보였다(p<0.01). 술 후 1년째에 시행한 심초음파검사, 심근 SPECT, 심도자 및 조영술상 수술 직후와 비교해서 좌심박출계수, 좌심실 확장기말용적, 좌심실 수축기말용적은 큰 차이는 없었으나, 좌심실 용적들은 조금씩 늘어나는 양상을 보였다. 결론: 허혈성심근질환에서 좌심실내 패취 성형술은 현저하게 좌심박출계수의 향상과 좌심실용적의 감소를 가져오며 술 후 1년까지도 지속되었으나, 좌심실용적은 다소 증가하는 양상을 보여 술 후에도 좌심실의 재확장을 막기 위한 적극적인 약물치료가 필요함을 시사하였다.