• Physical Therapy Rehabilitation Science
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• v.4 no.1
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• pp.17-21
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• 2015

Objective: In this study, we aimed to test the hypothesis that aerobic exercise might exert its cardio-protective effect by preventing oxidative stress and improving cardiac function in rat models with doxorubicin-induced cardiomyopathy. Design: Randomized controlled trial. Methods: We randomly divided experimental rats into four groups: the normal group was used as a non-cardiomyopathy normal control (n=10); the control group included non-aerobic exercise after doxorubicin-induced cardiomyopathy (n=10); the experimental group I included aerobic exercise (3 m/min) after doxorubicin-induced cardiomyopathy (n=10); and experimental group II included aerobic exercise (8 m/min) after doxorubicin-induced cardiomyopathy. Rats in the treadmill training groups underwent treadmill training, which began at 2 weeks after the first intraperitoneal injection. At the end of the exercise period, we determined the heart weight change for each rat. Changes in the levels of oxidative stress enzymes (superoxide dismutase [SOD], thiobarbituric acid-reactive substances [TBARS], and catalase) in the cardiac tissue of rats from all four groups were examined at the end of the experiment. Results: Significant cardiac myocyte injury and increase in myocardial TBARS concomitant with a reduction in myocardial SOD and catalase were observed following cardiomyopathy (p<0.05). Significant cardiac tissue and increase in myocardial TBARS along with reduction in myocardial SOD and catalase were observed following cardiomyopathy (p<0.05). Oxidative parameters were significantly improved in the aerobic exercise groups compared with the control group. Conclusions: These findings indicate that aerobic exercise effectively prevents oxidative stress in rat models with cardiomyopathy.

• Biomolecules & Therapeutics
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• v.27 no.4
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• pp.386-394
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• 2019

Trypanosoma cruzi infection results in debilitating cardiomyopathy, which is a major cause of mortality and morbidity in the endemic regions of Chagas disease (CD). The pathogenesis of Chagasic cardiomyopathy (CCM) has been intensely studied as a chronic inflammatory disease until recent observations reporting the role of cardio-metabolic dysfunctions. In particular, we demonstrated accumulation of lipid droplets and impaired cardiac lipid metabolism in the hearts of cardiomyopathic mice and patients, and their association with impaired mitochondrial functions and endoplasmic reticulum (ER) stress in CD mice. In the present study, we examined whether treating infected mice with an ER stress inhibitor can modify the pathogenesis of cardiomyopathy during chronic stages of infection. T. cruzi infected mice were treated with an ER stress inhibitor 2-Aminopurine (2AP) during the indeterminate stage and evaluated for cardiac pathophysiology during the subsequent chronic stage. Our study demonstrates that inhibition of ER stress improves cardiac pathology caused by T. cruzi infection by reducing ER stress and downstream signaling of phosphorylated eukaryotic initiation factor ($P-elF2{\alpha}$) in the hearts of chronically infected mice. Importantly, cardiac ultrasound imaging showed amelioration of ventricular enlargement, suggesting that inhibition of ER stress may be a valuable strategy to combat the progression of cardiomyopathy in Chagas patients.

• Journal of Chest Surgery
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• v.44 no.4
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• pp.294-297
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• 2011

Stress-induced cardiomyopathy is caused by emotional or physical stressors and mimics acute myocardial infarction, though Stress-induced cardiomyopathy is characterized by reversible left ventricular (LV) apical ballooning in the absence of significant coronary artery disease. We describe a 51-year-old male who underwent left upper lobectomy for non-small cell lung cancer, and during which cardiogenic arrest occurred due to stress-induced cardiomyopathy, successfully managed by intra-aortic balloon pumping and extracorporeal membrane oxygenation.

• Archives of Craniofacial Surgery
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• v.11 no.2
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• pp.120-123
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• 2010

Purpose: Epinephrine itself exhibits some cardiotoxicity. However, it rarely induces cardiomyopathy when used in standard doses during surgery for local hemostasis. This paper reports a rare case of stress-induced cardiomyopathy in a young woman after the local infiltration of epinephrine. Methods: Corrective rhinoplasty was planned in a 20-year-old woman. Lidocaine mixed with epinephrine 1:100,000 was injected around the skin of the nose and nasal septum after inducing anesthesia, which resulted in sinus tachycardia and hypotension. Postoperative ECG showed a T wave inversion in the lead V2 and echocardiography revealed transient hypokinesia in the cardiac apex. Cardiac enzyme was mildly elevated. Results: Symptoms and laboratory findings improved considerably, and the patient was discharged from hospital without complications on the sixth day after surgery. Conclusion: The prognosis of catecholamine-induced cardiomyopathy is generally favorable. However, it is important to be aware of the possible adverse effects of local epinephrine infiltration. This case highlights the need for caution when using epinephrine.

• Archives of Plastic Surgery
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• v.38 no.1
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• pp.85-88
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• 2011

Purpose: Takotsubo cardiomyopathy is a relatively uncommon type of stress-induced cardiomyopathy characterized by transient left ventricular regional wall motion abnormalities. Emotional and physical stresses play a key role in this type of cardiomyopathy in postmenopausal women. The current hypothesis is that the syndrome represents a form of catecholamine surge due to stress or epinephrine-mediated acute myocardial stunning. Methods: A 44-year-old woman had suffered premature ventricular contraction following a cardiogenic shock during a breast augmentation surgery under enflurane anesthesia and tumescent solution infiltration. She was treated with cardiopulmonary resuscitation at a local clinic. Then she was brought to the Emergency Department of the authors' hospital. Results: The woman's echocardiogram showed an ejection fraction of 20~25% with associated basal hyperkinesis and left ventricular apical ballooning. The patient was admitted to the ICU and required inotropic support for two weeks. The patient's condition dramatically improved, and her ejection fraction returned to 70%. Conclusion: It is believed that there were multiple triggering factors of the onset of Takotsubo cardiomyopathy in the woman's social and family history, including infiltration of a large volume of the tumescent solution and VPCs induced by enflurane anesthesia without premedication. The importance of careful history-taking, careful pre-operative consultation on psychological suffering especially for breast surgery, premedication before surgery, patient reassurance, and post-operative psychosocial and emotional assistance was again seen in this case.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.2
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• pp.79-83
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• 2006

We evaluated therapeutic and preventive properties of dehydroepiandrosterone (DHEA), a weak androgenic steroid, against isoproterenol-induced cardiomyopathy. The cardiomyopathy was induced by daily i.p. administration of isoproterenol to rats for five days. One group of rats were given with daily s.c. for 5 days during isoproterenol and the other group with daily s.c. DHEA for total 10 days, including 5 days before and during isoproterenol. The animals were killed after each treatment, and cardiac muscle failure was evaluated using histopathologic examination and biochemical indices. DHEA was found to reduce the damaged area and inhibit the elevation in the serum levels of glutamic oxaloacetic transaminase (SGOT), lactate dehydrogenase (LDH), skeletal muscle creatine kinase (CK) and heart creatine kinase (CK-MB) induced by isoproterenol. We also assayed widely used oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase and glutathion peroxidase (GPx). DHEA decreased the escalated level of TBARS and enhanced the anti oxidant defense reaction with an increase in Mn-SOD and Cu/Zn-SOD. On the other hand, the treatment with DHEA did not affect catalase and GPx activity. The present study indicates that DHEA has a therapeutic and preventive effect against isoproterenol-induced cardiomyopathy and its effects may depend largely on the increase in SOD activity.

• Journal of Yeungnam Medical Science
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• v.33 no.2
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• pp.125-129
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• 2016

Stress induced cardiomyopathy (SC) is characterized by transient left ventricular (LV) dysfunction in the absence of coronary artery disease. We report on a patient with panhypopituitarism who developed SC resulting from withdrawal of hormonal replacement therapy (HRT). A 52-year-old male visited our hospital for progressively worsening dyspnea. The patient had discontinued HRT 7 days ago, which had been administered for 18 months after transsphenoidal adenomectomy for pituitary macroadenoma. Initial electrocardiogram showed marked sinus bradycardia. Transthoracic echocardiography showed apical ballooning with an LV ejection fraction of 25%. No significant obstructive lesions were observed on coronary angiography. With a clinical diagnosis of SC associated with panhypopituitarism, HRT was restarted, including glucocorticoid and thyroxine, along with standard heart failure management. His LV function had normalized at 2-month follow-up. He remains asymptomatic and administration of beta-blocker and angiotensin converting enzyme inhibitor were discontinued He currently only requires HRT.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.6
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• pp.613-619
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• 2016

Diabetic cardiomyopathy (DCM), a serious complication of diabetes mellitus, is associated with changes in myocardial structure and function. This study sought to explore the ability of insulin-like growth factor-1 (IGF-1) to modulate DCM and its related mechanisms. Twenty-four male Wistar rats were injected with streptozotocin (STZ, 60 mg/kg) to mimic diabetes mellitus. Myocardial fibrosis and apoptosis were evaluated by histopathologic analyses, and relevant proteins were analyzed by Western blotting. Inflammatory factors were assessed by ELISA. Markers of oxidative stress were tested by colorimetric analysis. Rats with DCM displayed decreased body weight, metabolic abnormalities, elevated apoptosis (as assessed by the bcl-2/bax ratio and TUNEL assays), increased fibrosis, increased markers of oxidative stress (MDA and SOD) and inflammatory factors (TNF-${\alpha}$ and IL-$1{\beta}$), and decreased phosphorylation of Akt and glycogen synthase kinase (GSK-$3{\beta}$). IGF-1 treatment, however, attenuated the metabolic abnormalities and myocardial apoptosis, interstitial fibrosis, oxidative stress and inflammation seen in diabetic rats, while also increasing the phosphorylation levels of Akt and GSK-$3{\beta}$. These findings suggest that IGF-1 ameliorates the pathophysiological progress of DCM along with an activation of the Akt/GSK-$3{\beta}$ signaling pathway. Our findings suggest that IGF-1 could be a potential therapeutic choice for controlling DCM.

• Biomolecules & Therapeutics
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• v.21 no.5
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• pp.371-380
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• 2013

Doxorubicin is still main drug in chemotherapy with limitation of use due to adverse drug reaction. Increased oxidative stress and alteration of nitric oxide control have been involved in cardiotoxicity of doxorubicin (DOX). A Disintegrin And Metalloproteinase (ADAMs) are transmembrane ectoproteases to regulate cell-cell and cell-matrix interactions, but role in cardiac disease is unclear. The aim of this study was to determine whether DOX activates peroxynitrite and ADAM 10 and thus ADAM and matrix metalloproteinase (MMP) induce cardiac remodeling in DOX-induced cardiomyopathy. Adult male Sprague-Dawley rats were subjected to cardiomyopathy by DOX (6 times of 2.5 mg/kg DOX over 2-weeks), and were randomized as four groups. Then followed by 3, 5, 7, and 14 days after cessation of DOX injection. DOX-injected animals significantly decreased left ventricular fractional shortening compared with control by M-mode echocardiography. The expressions of cardiac nitrotyrosine by immunohistochemistry were significant increased, and persisted for 2 weeks following the last injection. The expression of eNOS was increased by 1.9 times (p<0.05), and iNOS was marked increased in DOX-heart compared with control (p<0.001). Compared to control rats, cardiac ADAM10- and MMP 9- protein expressions increased by 20 times, and active/total MMP 9 proteolytic activity showed increase tendency at day 14 after cessation of DOX injection (n=10, each group). DOX-treated $H_9C_2$ cell showed increased ADAM10 protein expression with dose-dependency (p<0.01) and morphometric changes showed the increase of ventricular interstitial, nonvascular collagen deposition. These data suggest that activation of cardiac peroxynitrite with increased iNOS expression and ADAM 10-dependent MMP 9 expression may be a molecular mechanism that contributes to left ventricular remodeling in DOXinduced cardiomyopathy.

• Tuberculosis and Respiratory Diseases
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• v.77 no.1
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• pp.24-27
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• 2014

Takotsubo cardiomyopathy (TTC) is defined as a reversible, acute ventricular dysfunction without any evidence of coronary artery obstruction. There have been reports of TTC caused by emotional or physical stress, drug use, hormone imbalance, or medical conditions such as pulmonary disease, sepsis, and trauma, but a relationship between TTC and pulmonary tuberculosis has not previously been reported. From our knowledge, this is the first report of TTC caused by pulmonary tuberculosis.