• Journal of the Korean Society of Radiology
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• v.83 no.1
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• pp.28-41
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• 2022

Acute coronary syndrome involves three types of coronary artery disease associated with sudden rupture of coronary artery plaque, and has a clinical presentation ranging from ST-segment elevation myocardial infarction (STEMI) to non-ST-segment elevation myocardial infarction (NSTEMI) or unstable angina. Cardiac CT can help quantify and characterize atherosclerotic plaques. According to a previous study, low-attenuation plaque, napkin ring sign, positive remodeling, spotty calcification, and increased perivascular fat attenuation are associated with plaque ruptures on cardiac CT. Therefore, coronary artery stenosis, as well as acute coronary artery syndrome, can be diagnosed using cardiac CT.

• Proceedings of the KSMRM Conference
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• 2003.10a
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• pp.45-45
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• 2003

To evaluate remodeling of infarcted myocardium with contrast-enhanced MRI (co-MRI) at true end-diastole (ED) MRI was performed with a Gyroscan Intera (1.5 Tesla, Philips, Netherlands) in 13 patients with acute subendocardial myocardial infarction. The First exam was done 0-15 days (mean 5.2days) after symptom onset and the second exam 28-88days (mean 49 days) after the first exam. Ce-MRI encompassing the entire left ventricle was performed with a multi-shot, turbo-field-echo, breath-hold sequence and a non-selective, inversion prepulse 10 minutes after the intravenous injection of Gd-DTPA at a dose of 0.2 mmol/kg body weight. To allow the long TD, ECG synchronization should use two RR-intervals for one acquisition of a segment of k-space by setting the heart rate to half that of the true heart rate. Trigger delay time (TD) was adjusted to the RR-interval for true end-diastolic imaging. The other typical parameters were TR=5.4ms, TE=1.6ms, voxel size=1.37${\times}$1.37${\times}$10mm, k-space data segmented into 8 segments with 32 lines of segment per two cycles over 16 cardiac circles. The thickness of hyperenhanced myocardium and epicardially nonenhanced myocardium were followed.

• Proceedings of the KSMRM Conference
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• 2003.10a
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• pp.92-92
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• 2003

To evaluate remodeling of infarcted myocardium with contrast-enhanced MRI (co-MRI) at true end-diastole (ED) MRI was performed with a Gyroscan Intera (1.5 Tesla, Philips, Netherlands) in 13 patients with acute subendocardial myocardial infarction. The First exam was done 0-15 days (mean 5.2days) after symptom onset and the second exam 28-88days (mean 49 days) after the first exam. Ce-MRI encompassing the entire left ventricle was peformed with a multi-shot, turbo-field-echo, breath-hold sequence and a non-selective, inversion prepulse 10 minutes after the intravenous injection of Gd-DTPA at a dose of 0.2 mmol/kg body weight. To allow the long TD, ECG synchronization should use two RR-intervals for one acquisition of a segment of k-space by setting the heart rate to half that of the true heart rate. Trigger delay time (TD) was adjusted to the RR-interval for true end-diastolic imaging. The other typical parameters were TR=5.4ms, TE=1.6ms, voxel size=1.37$\times$1.37$\times$10mm, k-space data segmented into 8 segments with 32 lines of segment per two cycles over 16 cardiac cycles. The thickness of hyperenhanced myocardium and epicardially nonenhanced myocardium were followed.

• Journal of the Korean Society of Visualization
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• v.16 no.2
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• pp.31-37
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• 2018

Ischemic mitral regurgitation (IMR) is the primary mitral valve (MV) pathology in the aftermath of myocardial infarction as a consequence of regional left ventricular (LV) remodeling. We investigated the effect of asymmetric papillary muscle (PM) displacement and annular dilation on IMR development. Virtual MV modeling was performed to create a normal human MV. Asymmetric PM displacement, asymmetric annular dilation, and the combination of these two pathologic characteristics were modeled. Dynamic finite element evaluation of MV function was performed across the complete cardiac cycle for the normal and three different IMR MV models. While the normal MV demonstrated complete leaflet coaptation, each pathologic MV model clearly revealed deteriorated leaflet coaptation and abnormal stress distributions. The pathologic MV model having both asymmetric PM displacement and annular dilation showed the worst leaflet malcoaptation. Simulation-based biomechanical evaluation of post-ischemic LV remodeling provides an excellent tool to better understand the pathophysiologic mechanism of IMR development.

• Journal of Ginseng Research
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• v.45 no.6
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• pp.683-694
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• 2021

Background: Ginsenoside Rg1 (Rg1) has been well documented to be effective against various cardiovascular disease. The aim of this study is to evaluate the effect of Rg1 on mechanical stress-induced cardiac injury and its possible mechanism with a focus on the calcium sensing receptor (CaSR) signaling pathway. Methods: Mechanical stress was implemented on rats through abdominal aortic constriction (AAC) procedure and on cardiomyocytes and cardiac fibroblasts by mechanical stretching with Bioflex Collagen I plates. The effects of Rg1 on cell hypertrophy, fibrosis, cardiac function, [Ca²⁺]_i, and the expression of CaSR and calcineurin (CaN) were assayed both on rat and cellular level. Results: Rg1 alleviated cardiac hypertrophy and fibrosis, and improved cardiac decompensation induced by AAC in rat myocardial tissue and cultured cardiomyocytes and cardiac fibroblasts. Importantly, Rg1 treatment inhibited CaSR expression and increase of [Ca²⁺]_i, which similar to the CaSR inhibitor NPS2143. In addition, Rg1 treatment inhibited CaN and TGF-b1 pathways activation. Mechanistic analysis showed that the CaSR agonist GdCl₃ could not further increase the [Ca²⁺]_i and CaN pathway related protein expression induced by mechanical stretching in cultured cardiomyocytes. CsA, an inhibitor of CaN, inhibited cardiac hypertrophy, cardiac fibrosis, [Ca²⁺]_i and CaN signaling but had no effect on CaSR expression. Conclusion: The activation of CaN pathway and the increase of [Ca²⁺]_i mediated by CaSR are involved in cardiac hypertrophy and fibrosis, that may be the target of cardioprotection of Rg1 against myocardial injury.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.1
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• pp.63-70
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• 2019

We aimed to propose a novel computational approach to predict the electromechanical performance of pre- and post-mitral valve cerclage annuloplasty (MVCA). Furthermore, we tested a virtual estimation method to optimize the left ventricular basement tightening scheme using a pre-MVCA computer model. The present model combines the three-dimensional (3D) electromechanics of the ventricles with the vascular hemodynamics implemented in a lumped parameter model. 3D models of pre- and post-MVCA were reconstructed from the computed tomography (CT) images of two patients and simulated by solving the electromechanical-governing equations with the finite element method. Computed results indicate that reduction of the dilated heart chambers volume (reverse remodeling) appears to be dependent on ventricular stress distribution. Reduced ventricular stresses in the basement after MVCA treatment were observed in the patients who showed reverse remodeling of heart during follow up over 6 months. In the case who failed to show reverse remodeling after MVCA, more virtual tightening of the ventricular basement diameter than the actual model can induce stress unloading, aiding in heart recovery. The simulation result that virtual tightening of the ventricular basement resulted in a marked increase of myocardial stress unloading provides in silico evidence for a functional impact of MVCA treatment on cardiac mechanics and post-operative heart recovery. This technique contributes to establishing a pre-operative virtual rehearsal procedure before MVCA treatment by using patient-specific cardiac electromechanical modeling of pre-MVCA.

• Journal of Chest Surgery
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• v.38 no.5 s.250
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• pp.323-334
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• 2005

Background: Gene therapy is a new and promising option for the treatment of severe myocardial ischemia by therapeutic angiogenesis. The goal of this study was to elucidate the efficacy of therapeutic angiogenesis by using VEGF165 in large animals. Material and Method: Twenty-one pigs that underwent ligation of the distal left anterior descending coronary artery were randomly allocated to one of two treatments: intramyocardial injection of pCK-VEGF (VEGF) or intramyocardial injection of pCK-Null (Control). Injections were administered 30 days after ligation. Seven pigs died during the trial, but eight pigs from VEGF and six from Control survived. Echo-cardiography was performed on day 0 (preoperative) and on days 30 and 60 following coronary ligation. Gated myocardial single photon emission computed tomography imaging (SPECT) with $^{99m}Tc-labeled$ sestamibi was performed on days 30 and 60. Myocardial perfusion was assessed from the uptake of $^{99m}Tc-labeled$ sestamibi at rest. Global and regional myocardial function as well as post-infarction left ventricular remodeling were assessed from segmental wall thickening; left ventricular ejection fraction (EF); end systolic volume (ESV); and end diastolic volume (EDV) using gated SPECT and echocardiography. Myocardium of the ischemic border zone into which pCK plasmid vector had been injected was also sampled to assess micro-capillary density. Result: Micro-capillary density was significantly higher in the VEGF than in Control ($386\pm110/mm^{2}\;vs.\;291\pm127/mm^{2};\;p<0.001$). Segmental perfusion increased significantly from day 30 to day 60 after intramyocardial injection of plasmid vector in VEGF ($48.4\pm15.2\%\;vs.\;53.8\pm19.6\%;\;p<0.001$), while no significant change was observed in the Control ($45.1\pm17.0\%\;vs.\;43.4\pm17.7\%;\;p=0.186$). This resulted in a significant difference in the percentage changes between the two groups ($11.4\pm27.0\%\;increase\;vs.\;2.7\pm19.0\%\;decrease;\;p=0.003$). Segmental wall thickening increased significantly from day 30 to day 60 in both groups; the increments did not differ between groups. ESV measured using echocardiography increased significantly from day 0 to day 30 in VEGF ($22.9\pm9.9\;mL\;vs.\;32.3\pm9.1\;mL;\; p=0.006$) and in Control ($26.3\pm12.0\;mL\;vs.\;36.8\pm9.7\;mL;\;p=0.046$). EF decreased significantly in VEGF ($52.0\pm7.7\%\;vs.\;46.5\pm7.4\%;\;p=0.004$) and in Control ($48.2\pm9.2\%\;vs.\;41.6\pm10.0\%;\;p=0.028$). There was no significant change in EDV. The interval changes (days $30\~60$) of EF, ESV, and EDV did not differ significantly between groups both by gated SPECT and by echocardiography. Conclusion: Intramyocardial injection of pCK-VEGF165 induced therapeutic angiogenesis and improved myocardial perfusion. However, post-infarction remodeling and global myocardial function were not improved.

• 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.

• Molecules and Cells
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• v.40 no.1
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• pp.66-72
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• 2017

Pathological hypertrophy of the heart is closely associated with endoplasmic reticulum stress (ERS), leading to maladaptations such as myocardial fibrosis, induction of apoptosis, and cardiac dysfunctions. Salubrinal is a known selective inhibitor of protein phosphatase 1 (PP1) complex involving dephosphorylation of phospho-eukaryotic translation initiation factor 2 subunit $(p-eIF2)-{\alpha}$, the key signaling process in the ERS pathway. In this study, the effects of salubrinal were examined on cardiac hypertrophy using the mouse model of transverse aortic constriction (TAC) and cell model of neonatal rat ventricular myocytes (NRVMs). Treatment of TAC-induced mice with salubrinal ($0.5mg{\cdot}kg^{-1}{\cdot}day^{-1}$) alleviated cardiac hypertrophy and tissue fibrosis. Salubrinal also alleviated hypertrophic growth in endothelin 1 (ET1)-treated NRVMs. Therefore, the present results suggest that salubrinal may be a potentially efficacious drug for treating pathological cardiac remodeling.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.6
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• pp.607-616
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• 2018

The effect of melatonin on juveniles with cardio fibrosis is poorly understood. We investigated whether HDACs participate in the anti-fibrotic processes regulated by melatonin during hypertrophic remodeling. Abdominal aortic constriction (AAC) was employed in juvenile rats resulting in pressure overload-induced ventricular hypertrophy and melatonin was subsequently decreased via continuous light exposure for 5 weeks after surgery. AAC rats displayed an increased cross-sectional area of myocardial fibers and significantly elevated collagen deposition compared to sham-operated rats, as measured by HE and Masson Trichrome staining. Continuous light exposure following surgery exacerbated the increase in the cross-sectional area of myocardial fibers. The expression of HDAC1, HDAC2, HDAC3, HDAC4 and HDAC6 genes were all significantly enhanced in AAC rats with light exposure relative to the other rats. Moreover, the protein level of $TNF-{\alpha}$ was also upregulated in the AAC light exposure groups when compared with the sham. However, Smad4 protein expression was unchanged in the juveniles' hearts. In contrast, beginning 5 weeks after the operation, the AAC rats were treated with melatonin (10 mg/kg, intraperitoneal injection every evening) or vehicle 4 weeks, and sham rats were given vehicle. The changes in the histological measures of cardio fibrosis and the gene expressions of HDAC1, HDAC2, HDAC3, HDAC4 and HDAC6 were attenuated by melatonin administration. The results reveal that melatonin plays a role in the development of cardio fibrosis and the expression of HDAC1, HDAC2, HDAC3, HDAC4 and HDAC6 in cardiomyocytes.