• Journal of Ginseng Research
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• v.47 no.2
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• pp.218-227
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• 2023

Background: Myocardial fibrosis (MF) is an advanced pathological manifestation of many cardiovascular diseases, which can induce heart failure and malignant arrhythmias. However, the current treatment of MF lacks specific drugs. Ginsenoside Re has anti-MF effect in rat, but its mechanism is still not clear. Therefore, we investigated the anti-MF effect of ginsenoside Re by constructing mouse acute myocardial infarction (AMI) model and AngII induced cardiac fibroblasts (CFs) model. Methods: The anti-MF effect of miR-489 was investigated by transfection of miR-489 mimic and inhibitor in CFs. Effect of ginsenoside Re on MF and its related mechanisms were investigated by ultrasonographic, ELISA, histopathologic staining, transwell test, immunofluorescence, Western blot and qPCR in the mouse model of AMI and the AngII-induced CFs model. Results: MiR-489 decreased the expression of α-SMA, collagenI, collagen III and myd88, and inhibited the phosphorylation of NF-κB p65 in normal CFs and CFs treated with AngII. Ginsenoside Re could improve cardiac function, inhibit collagen deposition and CFs migration, promote the transcription of miR-489, and reduce the expression of myd88 and the phosphorylation of NF-κB p65. Conclusion: MiR-489 can effectively inhibit the pathological process of MF, and the mechanism is at least partly related to the regulation of myd88/NF-κB pathway. Ginsenoside Re can ameliorate AMI and AngII induced MF, and the mechanism is at least partially related to the regulation of miR-489/myd88/NF-κB signaling pathway. Therefore, miR-489 may be a potential target of anti-MF and ginsenoside Re may be an effective drug for the treatment of MF.

• Journal of International Academy of Physical Therapy Research
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• v.7 no.1
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• pp.949-955
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• 2016

The purpose of the study was to investigate effects of Low intensity cardiac rehabilitation, using a treadmill, on the myocardial structure. We identified the effects by analyzing changes in the rats' weights and the results of biopsies. Twenty Sprague-Dawley male rats, 50 weeks old, were randomly divided into the exercise group and the control group. myocardial infarction(MI) was induced by ligaturing their left anterior descending artery. After the acute MI induction, two rats of each group began to fall dead, therefore, eight of each group completed at the end of the experiment. We used treadmills for animals for the exercise group. This exercise group performed 30 minutes of exercise five times per week for six weeks, while the control group did not perform any exercise. No statistically significant differences in weight were found in within group comparison and between group comparison. Furthermore, we observed histological changes in the myocardium using Hematoxylin & Eosin and Masson's trichrome staining in both groups. Low-intensity exercise inhibited myocardial fibrosis, may serve as a reference in the cardiopulmonary field, which plays a role in rehabilitating patients with cardiac disorders, including acute MI.

• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.52-52
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• 2003

Junctate is a newly identified integral ER/SR membrane $Ca^{2+}$ binding protein, which is an alternative splicing form of the same gene generating aspartyl $\square$-hydroxylase and junctin. To elucidate the functional role of junctate in heart, transgenic (TG) mice overexpressing mouse cardiac junctate-1 under the control of mouse $\square$$^{~}$ myosin heavy chain promoter were generated. Overexpression of junctate in mouse heart resulted in cardiac hypertrophy, increased fibrosis, bradycardia, arrhythmias and impaired contractility. Overexpression of junctate also led to down-regulation of SERCA2, calsequestrin, calreticulin and RyR, but to up-regulation of NCX and PMCA. The SR $Ca^{2+}$ content decreased and the L-type $Ca^{2+}$ current density and the action potential durations increased in TG cardiomyocytes, which could be the cause for the bradycardia in TG heart. The present work has provided an important example of pathogenesis leading to cardiac hypertrophy and arrhythmia, which was caused by impaired $Ca^{2+}$ handling by overexpression of junctate in heart.n heart.

• Korean Journal of Radiology
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• v.25 no.6
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• pp.540-549
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• 2024

Objective: This study investigated the feasibility and prognostic relevance of threshold-based quantification of myocardial delayed enhancement (MDE) on CT in patients with nonischemic dilated cardiomyopathy (NIDCM). Materials and Methods: Forty-three patients with NIDCM (59.3 ± 17.1 years; 21 male) were included in the study and underwent cardiac CT and MRI. MDE was quantified manually and with a threshold-based quantification method using cutoffs of 2, 3, and 4 standard deviations (SDs) on three sets of CT images (100 kVp, 120 kVp, and 70 keV). Interobserver agreement in MDE quantification was assessed using the intraclass correlation coefficient (ICC). Agreement between CT and MRI was evaluated using the Bland-Altman method and the concordance correlation coefficient (CCC). Patients were followed up for the subsequent occurrence of the primary composite outcome, including cardiac death, heart transplantation, heart failure hospitalization, or appropriate use of an implantable cardioverter-defibrillator. The Kaplan-Meier method was used to estimate event-free survival according to MDE levels. Results: Late gadolinium enhancement (LGE) was observed in 29 patients (67%, 29/43), and the mean LGE found with the 5-SD threshold was 4.1% ± 3.6%. The 4-SD threshold on 70-keV CT showed excellent interobserver agreement (ICC = 0.810) and the highest concordance with MRI (CCC = 0.803). This method also yielded the smallest bias with the narrowest range of 95% limits of agreement compared to MRI (bias, -0.119%; 95% limits of agreement, -4.216% to 3.978%). During a median follow-up of 1625 days (interquartile range, 712-1430 days), 10 patients (23%, 10/43) experienced the primary composite outcome. Event-free survival significantly differed between risk subgroups divided by the optimal MDE cutoff of 4.3% (log-rank P = 0.005). Conclusion: The 4-SD threshold on 70-keV monochromatic CT yielded results comparable to those of MRI for quantifying MDE as a marker of myocardial fibrosis, which showed prognostic value in patients with NIDCM.

• Journal of the Korean Society of Radiology
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• v.81 no.2
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• pp.302-309
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• 2020

Fabry disease is a rare X-linked metabolic disorder that is characterized by the accumulation of glycosphingolipids in various organs, resulting from the deficiency of alpha-galactosidase A. Cardiac involvement is relatively common; myocardial inflammation, left ventricular hypertrophy, and myocardial fibrosis secondary to abnormal lipid deposition in myocytes are often observed. Hence, the diagnosis of cardiac involvement is crucial for evaluating patient prognosis. Cardiac MRI is the standard technique for measuring the function, volume, and mass of the ventricles. It is also useful for myocardial tissue characterizations. The evaluation of native myocardial T1 values can facilitate early diagnosis of cardiac involvement, while measurements of left ventricular myocardial mass can be used to monitor treatment outcomes, in patients with Fabry disease. Consequently, cardiac MRI can provide useful information for diagnosing, monitoring, and treating patients with Fabry disease.

• Journal of Chest Surgery
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• v.51 no.2
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• pp.149-152
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• 2018

A 76-day-old infant weighing 3.4 kg was referred for surgical intervention for severe mitral valve stenoinsufficiency caused by leaflet fibrosis and calcification. He had ex perienced a cerebral infarction in the left middle cerebral artery territory, which was deemed attributable to an embolism of a calcified particle from the dysmorphic mitral valve. Because mitral valve replacement using a prosthetic valve was not feasible in this small baby, mitral valve replacement with a pulmonary autograft was performed. After a brief period of extracorporeal membrane oxygenation (ECMO) support, he was weaned from ECMO and was discharged home without further cardiovascular complications.

• Korean Journal of Radiology
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• v.23 no.6
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• pp.581-597
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• 2022

Left ventricular (LV) wall thickening, or LV hypertrophy (LVH), is common and occurs in diverse conditions including hypertrophic cardiomyopathy (HCM), hypertensive heart disease, aortic valve stenosis, lysosomal storage disorders, cardiac amyloidosis, mitochondrial cardiomyopathy, sarcoidosis and athlete's heart. Cardiac magnetic resonance (CMR) imaging provides various tissue contrasts and characteristics that reflect histological changes in the myocardium, such as cellular hypertrophy, cardiomyocyte disarray, interstitial fibrosis, extracellular accumulation of insoluble proteins, intracellular accumulation of fat, and intracellular vacuolar changes. Therefore, CMR imaging may be beneficial in establishing a differential diagnosis of LVH. Although various diseases share LV wall thickening as a common feature, the histologic changes that underscore each disease are distinct. This review focuses on CMR multiparametric myocardial analysis, which may provide clues for the differentiation of thickened myocardium based on the histologic features of HCM and its phenocopies.

• Experimental and Molecular Medicine
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• v.50 no.11
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• pp.1.1-1.10
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• 2018

Bone marrow-derived mesenchymal stem cells (BMMSCs) are used extensively for cardiac repair and interact with immune cells in the damaged heart. Macrophages are known to be modulated by stem cells, and we hypothesized that priming macrophages with BMMSCs would enhance their therapeutic efficacy. Rat bone marrow-derived macrophages (BMDMs) were stimulated by lipopolysaccharide (LPS) with or without coculture with rat BMCs. In the LPS-stimulated BMDMs, induction of the inflammatory marker iNOS was attenuated, and the anti-inflammatory marker Arg1 was markedly upregulated by coculture with BMMSCs. Myocardial infarction (MI) was induced in rats. One group was injected with BMMSCs, and a second group was injected with MIX (a mixture of BMMSCs and BMDMs after coculture). The reduction in cardiac fibrosis was greater in the MIX group than in the BMC group. Cardiac function was improved in the BMMSC group and was substantially improved in the MIX group. Angiogenesis was better in the MIX group, and anti-inflammatory macrophages were more abundant in the MIX group than in the BMMSC group. In the BMMSCs, interferon regulatory factor 5 (IRF5) was exclusively induced by coculture with macrophages. IRF5 knockdown in BMMSCs failed to suppress inflammatory marker induction in the macrophages. In this study, we demonstrated the successful application of BMDMs primed with BMMSCs as an adjuvant to cell therapy for cardiac repair.

• Korean Journal of Radiology
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• v.22 no.10
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• pp.1619-1627
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• 2021

Objective: This study used cardiac magnetic resonance imaging (MRI) to compare the characteristics of left ventricular remodeling in patients with primary aldosteronism (PA) with those of patients with essential hypertension (EH) and healthy controls (HCs). Materials and Methods: This prospective study enrolled 35 patients with PA, in addition to 35 age- and sex-matched patients with EH, and 35 age- and sex-matched HCs, all of whom underwent comprehensive clinical and cardiac MRI examinations. The analysis of variance was used to detect the differences in the characteristics of left ventricular remodeling among the three groups. Univariable and multivariable linear regression analyses were used to determine the relationships between left ventricular remodeling and the physiological variables. Results: The left ventricular end-diastolic volume index (EDVi) (mean ± standard deviation [SD]: 85.1 ± 13.0 mL/m² for PA, 75.9 ± 14.3 mL/m² for EH, and 77.3 ± 12.8 mL/m² for HC; p = 0.010), left ventricular end-systolic volume index (ESVi) (mean ± SD: 35.2 ± 9.8 mL/m² for PA, 30.7 ± 8.1 mL/m² for EH, and 29.5 ± 7.0 mL/m² for HC; p = 0.013), left ventricular mass index (mean ± SD: 65.8 ± 16.5 g/m² for PA, 56.9 ± 12.1 g/m² for EH, and 44.1 ± 8.9 g/m² for HC; p < 0.001), and native T1 (mean ± SD: 1224 ± 39 ms for PA, 1201 ± 47 ms for EH, and 1200 ± 44 ms for HC; p = 0.041) values were higher in the PA group compared to the EH and HC groups. Multivariable linear regression demonstrated that log (plasma aldosterone-to-renin ratio) was independently correlated with EDVi and ESVi. Plasma aldosterone was independently correlated with native T1. Conclusion: Patients with PA showed a greater degree of ventricular hypertrophy and enlargement, as well as myocardial fibrosis, compared to those with EH. Cardiac MRI T1 mapping can detect left ventricular myocardial fibrosis in patients with PA.

• Korean Journal of Veterinary Research
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• v.44 no.1
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• pp.125-129
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• 2004

A 2-year-old, female, American cocker spaniel dog presented for a 1-year history of severe ascites, exercise intolerance, tachypnea. At that time, she was in an emergency state. First, the dog was stabilized with oxygen therapy. A diagnosis of cardiac problem was made from history, auscultation, radiograph, ECG, and echocardiography. Jugular pulsation was palpated and a harsh, systolic murmur of tricuspid regurgitation was prominent at the right cardiac apex. Tricuspid valve dysplasia (TVD) was confirmed with echocardiography, accompanying enormous myocardial hypertrophy. The clinical signs had been improved for 8 months with careful therapy and periodic abdominocentesis, and ascites was well controlled. The situation, however, became worse quickly in a week because the client did not follow our management schedule. Finally, she died due to dyspnea and shock. After the spontaneous death, necropsy and histopathological examination were performed and when we opened the thorax, a significantly large heart was observed. On histopathological findings, grossly myocardium appeared pale initially, then progressed to yellow and white. Microscopically, there was an extensive hemorrhage along with loss of myocardial striations. Interstitial fibrosis and various degenerative alterations in myocytes were also present.