• Korean Journal of Clinical Laboratory Science
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• v.38 no.2
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• pp.135-140
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• 2006

Magnetocardiography (MCG) is the measurement and analysis of the magnetic component of the electro-magnetic field of the human heart, usually conducted externally, using extremely sensitive devices such as a Superconducting Quantum Interference Device (SQUID). MCG is a totally noninvasive method, it uses neither radiation nor ultrasonics. The magnetic activity of the heart is registered from outside the thorax. MCG has a very high sensitivity and a high spatial resolution for very a small, local myocardial current. In comparison to the electrical signals measured by an ECG, the magnetic signal does not disturb the boundaries of tissues with different electrical properties. MCG measures the myocardial function rather than describing the morphology. MCG is a relatively new technique that promises good spatial resolution and extremely high temporal resolution, thus complementing other heart activity measurement techniques such as Electrocardiography (ECG). The clinical uses of MCG are in detecting various cardiac disorders including myocardial infarction, ventricular hypertrophy, ventricular conduction defects, Wolff-Parkinson-White (WPW) syndrome, sudden cardiac death and fetal magnetocardiography. Magnetocardiography may be used alone or together with electrcardiography for the measurement of spontaneous or overloaded activity and for research or clinical purposes.

• Journal of Veterinary Clinics
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• v.36 no.4
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• pp.207-211
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• 2019

This study was performed to compare the radiographic and echocardiographic features of cardiovascular changes between small and large dogs with heartworm diseases. Total of 49 dogs from two institutions were included in this study. The dogs were diagnosed with heartworm infestation and underwent thoracic and echocardiography. On thoracic radiographs, vertebral heart scale, reverse D shape, main pulmonary artery dilation, peripheral pulmonary artery dilation, and evidence of right heart failure were evaluated. On echocardiographs, visibility of worms, main pulmonary artery to aortic root (MPA/Ao) ratio, right to left ventricular basal diameter (RVD/LVD) ratio, and pulmonary hypertension were evaluated and analyzed between small and large dogs. The proportion of reverse D shape of the heart and accuracy for right ventricular hypertrophy in small dogs were lower than those of the large dogs. For echocardiographic parameter, the MPA/Ao and RVD/LVD ratio in the small dogs were significantly lower than those of the large dogs. As the results, thoracic radiography have a tendency to underestimate the severity of HWD in small dogs and should be used with echocardiography.

• Journal of Life Science
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• v.17 no.12
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• pp.1717-1722
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• 2007

In the present study, all of the treadmill exercise-trained SHR expressed clear adaptive changes such as reduced resting heart rate and blood pressures, LPOA, homocysteine Therefore, treadmill exercise was sufficient to induce physiological adaptation in the SHR. Endurance training is known to induce physiological cardiac hypertrophy, while hypertension induces patho logical cardiac hypertrophy that increases cardiomyocyte apoptosis. The pathological adaptation to pressure overload has also been associated with a further increase in the expression of several marker genes including cardiomyocyte ET-1 in the SHR, but not in the exercise-trained SHR. Additionally, there is an increase in the endothelial nitricoxide synthases (eNOS) protein expression of soleus, gastrocnemius, and extensor digitorum longus muscle in the exercise-trained SHR but not in the SHR in the present study. Thus, compared to pathological adaptation to pressure overload, physiological adaptation to exercise training is associated with distinct alterations in cardiac and molecular phenotypes. based on these results, exercise training improves hypertension by cardiovascular regulating genes and hemodynamic parameters.

• Clinics in Shoulder and Elbow
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• v.7 no.2
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• pp.98-102
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• 2004

The terrible triad of the shoulder, a combination of anterior shoulder dislocation, massive rotator cuff tear and neurologic injury, is rare. We experienced 4 patients with this condition who were treated with a rotator cuff repair. The mean age was 65 years. Follow-up averaged 27 months. All patients had a history of redislocation after initial traumatic shoulder dislocation and were evaluated with electromyography and magnetic resonance imaging. At the operation, massive rotator cuff tear and hypertrophy of the long head of the biceps were found in all patients. Clinically, 3 patients achieved recovery of their nerve injury by 3 months postoperatively and the final results were fair. In one patient, there was no recovery of deltoid function and this case was rated as a failure. For this injury pattern, the prognosis appears to be dependent on eventual nerve recovery when the rotator cuff has been repaired early.

• Reproductive and Developmental Biology
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• v.34 no.2
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• pp.81-88
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• 2010

Our objective of current study was to investigate the development of bone and heart in association with diabetes mellitus (DM). DM was induced by administering an intraperitoneal injection of streptozotocin (STZ; 60 mg/kg) to 4-week-old Sprague-Dawley rats. Body weight and blood glucose were monitored, and rats were sacrificed after 2 or 5 weeks. The left ventricle (LV), including the interventricular septum, was weighed, and body weight and tibial bone length were assessed. Young diabetic rats showed reduced growth in terms of tibial length and body weight compared to controls. Moreover, diabetic males showed more significant growth suppression and reduced LV size than diabetic females. Morphometric analysis of tibiae from diabetic rats revealed suppressed bone growth at 2 and 5 weeks, with no difference between genders. STZ-induced diabetes decreased bone growth and retarded pre-pubertal heart development. As a result, diabetes may increase cardiovascular risk factors and lead to eventual heart failure. Therefore, new therapeutic approaches are required for diabetic children exhibiting growth retardation. Heart growth factor, exercise, and cardiopulmonary physical therapy may be required to promote heart development and physiological function.

• Integrative Medicine Research
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• v.3 no.4
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• pp.204-210
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• 2014

The aim of this review was to understand the effects of ${\beta}$-adrenergic stimulation on oxidative stress, structural remodeling, and functional alterations in the heart and cerebral artery. Diverse stimuli activate the sympathetic nervous system, leading to increased levels of catecholamines. Long-term overstimulation of the ${\beta}$-adrenergic receptor (${\beta}AR$) in response to catecholamines causes cardiovascular diseases, including cardiac hypertrophy, stroke, coronary artery disease, and heartfailure. Although catecholamines have identical sites of action in the heart and cerebral artery, the structural and functional modifications differentially activate intracellular signaling cascades. ${\beta}AR$-stimulation can increase oxidative stress in the heart and cerebral artery, but has also been shown to induce different cytoskeletal and functional modifications by modulating various components of the ${\beta}AR$ signal transduction pathways. Stimulation of ${\beta}AR$ leads to cardiac dysfunction due to an overload of intracellular $Ca^{2+}$ in cardiomyocytes. However, this stimulation induces vascular dysfunction through disruption of actin cytoskeleton in vascular smooth muscle cells. Many studies have shown that excessive concentrations of catecholamines during stressful conditions can produce coronary spasms or arrhythmias by inducing $Ca^{2+}$-handling abnormalities and impairing energy production in mitochondria, In this article, we highlight the different fates caused by excessive oxidative stress and disruptions in the cytoskeletal proteome network in the heart and the cerebral artery in responsed to prolonged ${\beta}AR$-stimulation.

• Journal of Chest Surgery
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• v.40 no.8
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• pp.552-557
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• 2007

Background: B-type natriuretic peptide (BNP) is a cardiac hormone that is primarily synthesized by the ventricular cardiac myocytes. Increased plasma BNP levels have been observed in patients suffering with congestive heart failure, ventricular hypertrophy and myocaridits and also during heart transplantation rejection. We investigated the serum BNP level as a predictive marker for rejection after heart transplantation. Material and Method: To test the usefulness of measuring the BNP level in cardiac transplant patients, consecutive blood samplings for BNP, right ventricular endomyocardial biopsies, hemodynamic measurements and transthoracic echocardiogram were all done in 10 such patients between January 2004 and August 2005 at the Department of Thoracic and Cardiovascular Surgery in Asan Medical Center. Two groups were identified with using the median value: the low BNP group (n=28, BNP: ${\le}290$ pg/mL) and the high BNP group (n=29, BNP: >290 pg/mL). We retrospectively analyzed rejection, the ejection fraction, tricuspid regurgitation, left ventricular hypertrophy, the pulmonary capillary wedge pressure and the right atrial pressure between the 2 groups. Result: There were no differences in age, gender, rejection, the ejection fraction, tricuspid regurgitation, left ventricular hypertrophy and the right atrial pressure between the 2 groups (p>0.05). However, a higher pulmonary capillary wedge pressure and a higher mean pulmonary atrial pressure were observed in the high BNP group (p<0.05). Further, BNP has linear correlation with the pulmonary capillary wedge pressure (r=0.590, p<0.001). Using the cut-off value of 620 pg/mL, the BNP predicted a high PCWP (>12 mmHg) with a sensitivity of 83.3% and a specificity of 91.1% (AUC: $0.900{\pm}0.045$, p<0.001). Conclusion: The BNP level after heart transplantation does not show any significant correlation with rejection, yet it might be a predictive marker of ventricular diastolic dysfunction.

• Journal of Chest Surgery
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• v.31 no.6
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• pp.586-590
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• 1998

Background: The regression of the left ventricular hypertrophy after prosthetic valve replacement in patients with aortic valvular stenosis is an important factor to determine the appropriateness of the replaced prosthetic valvular size. Methods: To assess the regression of myocardial hypertrophy, a retrospective analysis of Doppler echocardiographic and electrocardiographic data was undertaken before, soon after(7.5$\pm$2.1 day), and late after(10.7$\pm$1.8 months) surgery in 36 patients(22 males, 14 female, mean age 54$\pm$12.1 years, mean BSA 1.61$\pm$0.15m2) with predominant aortic valvular stenosis. The patients underwent St. Jude Medical aortic valve replacement. By the size of the valves used, the patients were divided into three groups(19, 21 and 23+). Results: The mean body surface area(1.48$\pm$0.13) in the patients with the 19 mm valve was smaller than that in the other groups(1.63$\pm$0.12)(p<0.05). No significant changes of ejection fraction were detected in all groups over time. Left ventricular muscle mass index(gm/m2) was reduced significantly in the 21 and 23+ groups over time(p<0.05), but there were no significant changes in the 19 mm valve group. The electric voltage height on EKG at the period of late after surgery was reduced significantly in all groups(p<0.05). Conclusion: Despite clinical improvement, the LVH was not reduced significantly in 19 mm valve group. Thus we suggest that more attention and additional procedures such as annular enlargement should be taken in patients who will undergo the replacement of 19 mm prosthetic valve.

• BMB Reports
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• v.52 no.10
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• pp.595-600
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• 2019

Cardiac fibrosis is a common feature in chronic hypertension patients with advanced heart failure, and endothelial-to-mesenchymal transition (EndMT) is known to promote Angiotensin II (Ang II)-mediated cardiac fibrosis. Previous studies have suggested a potential role for the transcription factor, ETS-1, in Ang II-mediated cardiac remodeling, however the mechanism are not well defined. In this study, we found that mice with endothelial Ets-1 deletion showed reduced cardiac fibrosis and hypertrophy following Ang II infusion. The reduced cardiac fibrosis was accompanied by decreased expression of fibrotic matrix genes, reduced EndMT with decreased Snail, Slug, Twist, and ZEB1 expression, as well as reduced cardiac hypertrophy and expression of hypertrophy-associated genes was observed. In vitro studies using cultured H5V cells further confirmed that ETS-1 knockdown inhibited $TGF-{\beta}1$-induced EndMT. This study revealed that deletion of endothelial Ets-1 attenuated Ang II-induced cardiac fibrosis via inhibition of EndMT, indicating an important ETS-1 function in mediating EndMT. Inhibition of ETS-1 could be a potential therapeutic strategy for treatment of heart failure secondary to chronic hypertension.

• Journal of Oriental Neuropsychiatry
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• v.18 no.3
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• pp.309-319
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• 2007

Chest pain is classified into two major categories of cardiac chest pain and non-cardiac chest pain. Cardiac chest pain is caused by cardiovascular disease, for example, myocardial infarction, angina pectoris, valvular heart disease, cardiac enlargement or hypertrophy, dissecting aortic aneurysm, pericarditis, myocarditis, etc. When the chest pain is not attributed to heart disease, it is termed non-cardiac chest pain. Non-cardiac chest pain is caused by pulmonary, gastrointestinal, musculoskeletal disease, psychiatric factor, etc. In tills case, we treated a 54-year old female patient who was diagnosed with dilated cardiomyopathy and suspicious sick sinus syndrome. She complained of chest pain, exertional dyspnea, dizziness and headache. For treatment, we made use of Yugultangami(六鬱湯加味) and Daejobwan(大造丸). Before and after treatment, we measured Heart rate variability(HRV). In result, the clinical symptoms were improved and there was a significant increase in assessmeut by Heart rate variability(HRV). Tills result suggests that Yugultaugami aud Daejowhan have a good effect on cardiac chest pain.