• Korean Journal of Clinical Laboratory Science
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• v.44 no.3
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• pp.136-141
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• 2012

The hearts of highly trained athletes show morphologic and electrocardiographic (ECG) changes that suggest the presence of cardiovascular disease, including sinus bradycardia, a striking increase in precordial R-wave or S-wave voltages, ST segment depression, and T-wave inversions. Despite a number of previous observational surveys, the determinants of abnormal ECG patterns in trained athletes remain largely unresolved. In this study, we compared the electrocardiographic characteristics of athletes to determine any sensitive indicators. Comparison between ECG patterns and cardiac physiology was performed in 21 junior athletes and 25 untrained subjects with no signs of cardiac disease. Sinus bradycardia was detected in a subset of athletes but not statistically significant between the athletes ($69.9{\pm}11.1bpm$) and the control ($72.7{\pm}9.9bpm$) group. The mean values of the PR and QTc intervals in the athletes' group were $149.2{\pm}15.4ms$ and $402.3{\pm}28.8ms$, respectively. Also, there were no significantly differences between control group and the athletes' group. In addition, the athletes demonstrated a spectrum of alterations in the 12-lead ECG pattern, including marked increase in precordial R-wave or S-wave voltages ($$SV_1+RV_5{\geq_-}35mm$$, 23.8%), QRS duration ($${\geq_-}90ms$$, 90.5%), suggestive of left ventricular hypertrophy. However, left axis deviation, ST segment depression, and T-wave changes in V5, V6 were not observed in either the athletes or control group. Our findings suggest that sinus bradycardia, precordial R-wave or S-wave voltages, and QRS duration seem to be more sensitively detected in athletes than in control group. Further researches on the electrocardiographic patterns of athletes should be carried out to improve the sensitivity and specificity of diagnostic criteria.

• Clinical and Experimental Pediatrics
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• v.60 no.11
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• pp.365-372
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• 2017

Purpose: The mechanism for the pathogenesis of adriamycin (ADR)-induced cardiomyopathy is not yet known. Different hypotheses include the production of free radicals, an interaction between ADR and nuclear components, and a disruption in cardiac-specific gene expression. Apoptosis has also been proposed as being involved in cardiac dysfunction. The purpose of this study was to determine if apoptosis might play a role in ADR-induced cardiomyopathy. Methods: Male Sprague-Dawley rats were separated into 2 groups: the control group (C group) and the experimental group (ADR 5 mg/wk for 3 weeks through intraperitoneal injections; A group). Echocardiographic images were obtained at week 3. Changes in caspase-3, B-cell leukemia/lymphoma (Bcl)-2, Bcl-2-associated X (Bax), interleukin (IL)-6, tumor necrosis $factor-{\alpha}$, brain natriuretic peptide (BNP), troponin I, collagen 1, and collagen 3 protein expression from the left ventricle tissues of C and A group rats were determined by Western blot. Results: Ascites and heart failure as well as left ventricular hypertrophy were noted in the A group. Ejection fraction and shortening fraction were significantly lower in the A group by echocardiography. The expression of caspase-3, Bax, IL-6, BNP, collagen 1, and collagen 3 were significantly higher in the A group as compared with the C group. Protein expression of Bcl-2 decreased significantly in the A group compared with the C group. Conclusion: ADR induced an upregulation of caspase-3, Bax, IL-6, and collagen, as well as a depression in Bcl-2. Thus, apoptosis and fibrosis may play an important role in ADR-induced cardiomyopathy.

• Journal of Chest Surgery
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• v.2 no.2
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• pp.155-166
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• 1969

Heterotopic abdominal homograft of canine heart was carried out in 20 pairs of dogs. Of these 12 cases were subjected as a control and 8 were subjected to immunosuppressive group. The dosage of immunosuppressive agent was 5mg/kg/day of Imuran [Azathioprine] for 3 days preoperatively, 10mg/kg on operative day and 5mg/kg/day postoperatively. For reducing the metabolic demand, the donor heart was preserved in 4degree heparinized saline solution for approximately I4 minutes. In the most of the cases, transplantation was performed with the technique of end-to-side aorto-aortic anastomosis and end-to-side pulmonary artery-inferior vena cava anastomosis at the infrarenal portion. Five out of 20 grafted dogs were survived more than one day. The longest survived 18 days in the control group and survive more than 60 days in the treated group. The survival cases were 3 out of 8[37. 5%] in the group of dogs treated with lmuran and 2`out of 12 [16.6%] in the group of non-treated. A prominent gross findings of the grafted heart was a minimal to moderate degree of dilatation of the heart with or without thrombosis in the cardiac chambers and/or anastomotic site. The case number 10, 15, and 19 showed moderate hypertrophy in grossly. The microscopic findings were as follows; 1. There were early hypersensitive histologic reactions such as interstitial edema, cellular infiltrations and early degenerative changes in the myocardium in the cases of 3 hour survival. 2. In the cases of more than 6 hours survival, organizing thrombosis of myocardial vessels, vasculitis,myocardial necrosis and lymphocyte, plasma cell, round cell infiltrations were noted. In the cases of more than 12 hours survival, the degree of these histologic changes especially in the non-treated group were more intensified than in the treated. 3. In the cases which survived more than one day, so called homograft specific histologic changes were milder in the immunosuppressive group compared with the control. 4. All the host hearts showed no evidence of pathologic findings histologically. Among the homologous canine cardiac transplantation tissue reaction, was milder and suvival time longer in the group treated with immunosuppressive drug.

• Journal of Chest Surgery
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• v.21 no.4
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• pp.672-680
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• 1988

Munro is generally considered the first person to have demonstrated, in 1888, in an infant cadaver, the feasibility of dissection and ligation of a persistently patent ductus arteriosus. In august, 1938, Robert Gross reported first successful division and suture of the patent ductus of 7 year old girl. Interruption of a ductus is one of the most satisfactory and curative operations in the field of surgery for congenital heart disease. Seventy-eight consecutive cases of closure of patent ductus arteriosus were operated from June 1980 to June 1988 in the department of thoracic and cardiovascular surgery in Maryknoll Hospital. Retrospective clinical analysis of the patients were 1. There were 24 males, 54 females. 2. The age range of the patients were from 7 months to 32 years with the mean age 9.8 years. 3. Chief complaints of the patients were frequent URI[70.5%], dyspnea on exertion[36.9%], palpitation[10.3%], but 15 patients[19.2%] had no subjective symptoms. 4. Continuous machinery murmur could be heard at the 2nd or 3rd intercostal space on the left sternal border in 66 patients[84.6%]. The other 12 patients made systolic murmur. 5. Radiographic findings of the Chest P-A were cardiac enlargement in 55 patients[70%], enlargement of pulmonary conus and/or increasing density of pulmonary vascularity in 68 patients[87%]. 6. Electrocardiographic findings of the patients were within normal limit in 23 patients[36%], LVH in 38 patients[48.7%], RVH in 7 patients[9%], biventricular hypertrophy in 5 patients[6%]. 7. Cardiac catheterization performed in 62 patients. Mean Qp/Qs=2.5, mean pulmonary arterial pressure=45 mmHg. 8. 73 patients were operated through left posterolateral thoracotomy: Closure of the ductus by ligation in 64 cases, division with suture in 6 cases, and division with aortopatch in 3 cases. Ligation through median sternotomy under cardiopulmonary bypass were 5 cases. 9. There was no death associated with operation, but one case was experienced with intraoperative tearing of ductus resulting in massive bleeding. The other complications were transient hoarseness in 2 patients, chylothorax in 2 patients.

• 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.

• Biomolecules & Therapeutics
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• v.25 no.5
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• pp.471-481
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• 2017

The canonical transient receptor potential channels (TRPCs) constitute a series of nonselective cation channels with variable degrees of $Ca^{2+}$ selectivity. TRPCs consist of seven mammalian members, TRPC1, TRPC2, TRPC3, TRPC4, TRPC5, TRPC6, and TRPC7, which are further divided into four subtypes, TRPC1, TRPC2, TRPC4/5, and TRPC3/6/7. These channels take charge of various essential cell functions such as contraction, relaxation, proliferation, and dysfunction. This review, organized into seven main sections, will provide an overview of current knowledge about the underlying pathogenesis of TRPCs in cardio/cerebro-vascular diseases, including hypertension, pulmonary arterial hypertension, cardiac hypertrophy, atherosclerosis, arrhythmia, and cerebrovascular ischemia reperfusion injury. Collectively, TRPCs could become a group of drug targets with important physiological functions for the therapy of human cardio/cerebro-vascular diseases.

• Journal of Chest Surgery
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• v.20 no.2
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• pp.404-410
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• 1987

An 18-day-old male neonate with hypoplastic left heart syndrome underwent surgical intervention by modification of the Norwood procedure on September 23, 1986. Hypoplastic left heart syndrome is a serious congenital cardiac anomaly that has a fatal outlook if left untreated. Included in this anomaly are [1] aortic valve atresia, and hypoplasia of the ascending aorta and aortic arch, [1] mitral valve atresia or hypoplasia, and [3] diminutive or absent left ventricle. Patent ductus arteriosus is essential for any survival, and there is usually a patent foramen ovale. Coarctation of the aorta is frequently associated with the lesion.z With a limited period of cardiopulmonary bypass, deep hypothermia, and circulatory arrest, the ductus arteriosus was excised. The main pulmonary artery was divided immediately below its branches, and the distal stump of the divided pulmonary artery was closed with a pericardial patch. The aortic arch was incised, and a 1 5mm tubular Dacron prosthesis was inserted between the main pulmonary artery and the aortic arch. A 4mm shunt of polytetrafluoroethylene graft was established between the new ascending aorta and the right pulmonary artery to provide controlled pulmonary blood flow. Following rewarming, the heart started to beat regularly, but the patient could not be weaned from cardiopulmonary bypass. At autopsy, the patient was found to have hypoplasia of the aortic tract complex with mitral atresia and aortic atresia. A secundum atrial septal defect was noted. Right atrial and ventricular hypertrophy was present, and the left ventricle was entirely absent. Although unsuccessful in this case report, continuing experience with hypoplastic left heart syndrome will lead to an improvement in result.

• Journal of Chest Surgery
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• v.23 no.5
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• pp.871-880
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• 1990

We clinically evaluated 182 cases of the ventricular septal defect that we experienced at the Department of Thoracic and Cardiovascular Surgery, Maryknoll Hospital from March 1986 through June 1990. Of the 182 cases, 95 patients were male and 87 patients were female. Their age distribution ranged from 8 month to 37 years and their mean age was 8.1 years. The most common chief complaint was frequent upper respiratory infection. Among them, 46 patients had associated cardiac anomalies, which were subdivided as follow; 9 cases of patent foramen ovale, 8 cases of infundibular stenosis, 6 cases of pulmonary valvular stenosis, 4 cases of left superior vena cava, and etc. The most common preoperative abnormal EKG finding was left ventricular hypertrophy in 22 cases. Ninety-three patients[51.1%] underwent simple closure of the VSD and the rest[48.0%] underwent patch closure. In anatomical classification by Kirklin type I constituted 24.2%; type II, 74.8%, type III, 0.7%, and the mixed type of type I and II, 0.5%, The important postoperative EKG changes were noted in 38 cases[20.9%], 18 cases of which were incomplete right bundle branch block. Thirty-three patients[18.1%] developed minor and major complications, and five patients died, overall operative mortality being 2.7%.

• Journal of Chest Surgery
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• v.28 no.6
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• pp.601-605
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• 1995

Clinical evaluations were performed on 54 cases of the traumatic sternal fracture, those were admitted and treated at the department of Thoracic and Cardiovascular Surgery in Chosun University Hospital during the past 5 years period from January 1990 to December 1994. The frequency was about 7.8% of the nonpenetrating chest trauma. The ratio of male to female was 2 : 1 in male predominance. Average age was 45.7 years old and age distribution was from 18 to 80 years old. The most common cause in the sternal fracture were high decelerating injury[ 38 cases . The most common fracture site was sternal body. Associated intrathoracic organ injuries were cardiac contusion[11cases , hemopneumothorax and pulmonary contusion. Added, thoracic cage and extrathoracic organ injuries were rib fracture, head injuries, thoracic spinal fracture and long bone fracture. Abnormal ECG findings were sinus bradycardia[4 cases , sinus tachycardia[3 cases , bundle branch block, atrial fibrillaton, left ventricular hypertrophy and myocardial ischemia. The average days of admission was 19.1 days. All patients were treated with conservative treatment. The complications after treatment were atelectasis[2 cases ,empyema[1 cases , ARDS[1 cases .

• Clinical and Experimental Pediatrics
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• v.57 no.1
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• pp.19-25
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• 2014

Recently, surgical outcomes of repair of tetralogy of Fallot (TOF) have improved. For patients with TOF older than 3 months, primary repair has been advocated regardless of symptoms. However, a surgical approach to symptomatic TOF in neonates or very young infants remains elusive. Traditionally, there have been two surgical options for these patients: primary repair versus an initial aortopulmonary shunt followed by repair. Early primary repair provides several advantages, including avoidance of shunt-related complications, early relief of hypoxia, promotion of normal lung development, avoidance of ventricular hypertrophy and fibrosis, and psychological comfort to the family. Because of advances in cardiopulmonary bypass techniques and accumulated experience in neonatal cardiac surgery, primary repair in neonates with TOF has been performed with excellent early outcomes (early mortality<5%), which may be superior to the outcomes of aortopulmonary shunting. A remaining question regarding surgical options is whether shunts can preserve the pulmonary valve annulus for TOF neonates with pulmonary stenosis. Symptomatic neonates and older infants have different anatomies of right ventricular outflow tract (RVOT) obstructions, which in neonates are nearly always caused by a hypoplastic pulmonary valve annulus instead of infundibular obstruction. Therefore, a shunt is less likely to preserve the pulmonary valve annulus than is primary repair. Primary repair of TOF can be performed safely in most symptomatic neonates. Patients who have had primary repair should be closely followed up to evaluate the RVOT pathology and right ventricular function.