• Korean Circulation Journal
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• v.53 no.5
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• pp.344-346
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• 2023

• Molecules and Cells
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• v.43 no.4
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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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• v.54 no.1
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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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• v.26 no.6
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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.

• Journal of the Korean Society of Radiology
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• v.81 no.2
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• pp.272-289
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• 2020

Current advances in CT techniques allow thorough evaluation of the beating heart. The strengths of cardiac CT relative to echocardiography and magnetic resonance imaging are its high availability in most institutions, rapid production of high-quality images, and outstanding delineation of the anatomy. For many normal variants and pathologic conditions, such as thrombi, masses, and congenital abnormalities of the left atrium, CT findings are sufficient to make a presumptive diagnosis. Assessments of the left atrium and left atrial appendage are particularly important for the management of atrial fibrillation, as various catheter-based procedures are aimed at the mechanical and electrical isolation of these structures. CT offers information crucial to a successful catheter-based procedure or surgery. Therefore, a comprehensive review of the geometry (shape, size, and relative position), along with various CT imaging features of pathologic states, should be provided in radiology reports to be of clinical value.

• Clinical and Experimental Pediatrics
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• v.56 no.3
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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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• v.26 no.5
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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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• v.37 no.9
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• pp.755-761
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• 2004

We evaluated the efficacy of Dor procedure in patients with ischemic left ventricular dysfunction. Material and Method: Between April 1998 and December 2002, 45 patients underwent the Dor procedure con-comitant with coronary artery bypass grafting (CABG). Left ventricular ejection fraction (LVEF) and left ventricular end-diastolic/end-systolic volumes (LVEDV/LVESV) were measured by echocardiography, myocardial SPECT, and cardiac catheterization and angiography performed at the sequence of preoperative, early postoperative, and one year postoperative stage. Result: Cardiopulmonary bypass and aortic clamp times were mean 141$\pm$64, 69$\pm$24 minutes, respectively. Intraaortic balloon pump (IABP) therapy was required in 19 patients (42%; 7 preoperatively, 9 intraoperatively, 3 postoperatively). Operative mortality rate was 2.2% (1/45). Postoperative morbidities were low cardiac output syndrome (12), atrial fibrillation (5), acute renal failure (4), and postoperative bleeding (4). Functional class (NYHA) was improved from classes 2.8 to 1.1 (p < 0,01). When we compared between the preoperative and early postoperative values, LVEF was improved from 32$\pm$9% to 52$\pm$11% (p<0.01). The asynergy portion decreased from 57$\pm$12% to 22$\pm$9%, and LVEDV/LVESV indexes improved from 125$\pm$39 mL/$m^2$, 85$\pm$30 mL/$m^2$ to 66$\pm$23 mL/$m^2$, 32$\pm$16 mL/$m^2$ (p<0.01). Although these changes in volumes were relatively preserved at postoperative one year, the left ventricular volumes showed a tendency to increase. Conclusion: After the Dor procedure for ischemic left ventricular dysfunction, LVEF improvement and left ventricular volume reduction were maintained till postoperative one year. The tendency for left ventricular volume to increase at postoperative one year suggested the requirement of strict medical management.