• Journal of Chest Surgery
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• v.4 no.1
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• pp.43-50
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• 1971

Three patients who sustained penetrating stab wound of the heart have been treated successfully by emergency thoracotomy in the Department of Thoracic Surgery, Chonnam University Hospital. There were two knife and one glass wound. The location of the injury were all on the right ventricle, but in one patient, it was penetrated to ventricular septum. All patients were in shock with a systolic pressure under 60 mmHg when admitted to the emergency room. In one of the three patients, blood pressure was not detectable and subsequently cardiac arrest. Two patients required immediate thoracotomy because of intrathoracic hemorrhage and increased pericardial tamponade and the other one required prompt thoracotomy because of sudden onset of cardiac arrest. There were no death postoperatively. Two patients are living without any complication in 4 years and 4 weeks after operation. One who had penetrating wound to ventricular septum, turned to cardiac decompensation, but he is living now in 4$\frac{1}{2}$ years after operation. Exploratory thoracotomy should be performed immediately in all the patients in whom a penetrating wound of the heart or pericardial tamponade following a penetrating wound of the chest wall is suspected.

• Journal of Chest Surgery
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• v.50 no.5
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• pp.378-381
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• 2017

Patients with an atrial septal defect (ASD) and severe pulmonary arterial hypertension (PAH) are considered ineligible for defect closure surgery because of the risk of right ventricular decompensation and death after the operation. We report the case of a patient with large ASD and severe PAH who was able to undergo defect closure surgery successfully following long-term use of combined oral sildenafil and beraprost.

• Proceedings of the KSME Conference
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• 2002.08a
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• pp.9-10
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• 2002

Human circulatory system between heart and tissue is not directly connected in normal condition but mandatory to go through the capillary system in order to fulfill its physiologic aim to deliver oxygen and nutrients, etc. to the tissue and retrieve used blood together with waste products from the tissue properly. When abnormal connection between arterial and venous system (AV fistula), these two circulatory systems respond differently to the hemodynamic impact of this abnormal connection between high pressure (artery) and low pressure (vein) system. Depending upon the location and/or degree (e.g. size and flow) of fistulous condition, each circulatory system exerts different compensatory hemodynamic response to this newly developed abnormal inter-relationship between two systems in order to minimize its hemodynamic impact to own system of different hemodynamic characteristics. Pump action of the heart can assist the failing arterial system directly to maintain arterial circulation against newly established low peripheral resistance by the AV fistula during the compensation period, while it affects venous system in negative way with increased venous loading. However, the negative impact of increased heart action to the venous system is partly compensated by the lymphatic system which is the third circulatory system to assist venous system independently with different hemodynamics. The lymphatic system with own unique Iymphodynamics based on peristaltic circulation from low resistance to high resistance condition, also increases its circulation to assist the compensation of overloaded venous system. Once these compensation mechanisms should fail to fight to newly established hemodynamic condition due to this abnormal AV connection, each system start to show different physiologic ${\underline{de}compensation}$ including heart and lymphatic system. The vicious cycle of decompensation between arterial and vein, two circulatory system affecting each other by mutually negative way steadily progresses to show series of hemodynamic change throughout entire circulation system altogether including heart. Clinical outcome of AV fistula from the compensated status to decompensated status is closely affected by various biological and mechanical factors to make the hemodynmic status more complicated. Proper understanding of these crucial biomechanical factors iii particular on hemodyanmic point of view is mandatory for the advanced assessment of biomechanical impact of AV fistula, since this new advanced concept of AY fistula based on blomechanical information will be able to improve clinical control of the complicated AV fistula, either congenital or acquired.

• Journal of Chest Surgery
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• v.32 no.1
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• pp.53-57
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• 1999

We describe a case of successful extracorporeal membrane oxygenation(ECMO) in a small infant with cardiopulmonary resuscitation(CPR) failure after an open heart surgery. A 35-day-old male infant weighing 4.4 kg who had congestive heart failure and pulmonary hypertension underwent patch closure of ventricular septal defect without any intraoperative event. Postoperative course was unremarkable in the intensive care uint for about 5 hours before the junctional ectopic tachycardia developed. Sudden cardiac decompensation with bradycardia occurred about 50 minutes after the development of junctional ectopic tachycardia. He was put on ECMO by arterial cannulation at the ascending aorta and by venous cannulation at the right atrial appendage after 4 hours' CPR. The hemodynamics were stable with enough urine output during ECMO. He was weaned from ECMO 38.5 hours after initiation. Delayed sternal closure was attempted. He was extubated on postoperative day 7 and discharged home on postoperative day 21 without any neurologic sequelae.

• Journal of Chest Surgery
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• v.46 no.4
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• pp.285-288
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• 2013

Prosthetic valves are being widely used in the treatment of heart valve disease. Prosthetic valve endocarditis (PVE) is one of the most catastrophic complications seen in these patients. In particular, prosthetic valve dehiscence can lead to acute decompensation, pulmonary edema, and cardiogenic shock. Here, we discuss the medical management of late PVE in a patient with a prior history of late and redo early PVE and recurrent dehiscence. According to the present case, we can summarize the learning points as follows. A prior history of infective endocarditis increases the risk of relapse or recurrence, and these patients should be evaluated very cautiously to prevent late complications. Adequate debridement of infected material is of paramount importance to prevent relapse. A history of dehiscence is associated with increased risk of relapse and recurrent dehiscence.

• Clinical and Experimental Pediatrics
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• v.50 no.3
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• pp.268-271
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• 2007

Purpose : Premature narrowing of the foramen ovale is rare but serious clinical entity. Prenatal narrowing or obstruction of the foramen ovale shows symptoms such as right heart failure, fetal hydrops, triscupid regurgitation, left heart obstructive disease, and supraventricular tachycardia. This study aimed to assess the prenatal diagnosis and postnatal clinical course of restrictive foramen ovale in utero in otherwise normal heart. Methods : The subjects were five patients diagnosed with restrictive foramen ovale in utero from January 2001 to June 2005 at Chungnam National University Hospital. The diagnostic criteria was defined when the maximum diameter in a 4-chamber view is less than 2.5 mm and there is a continuous doppler velocity at the foramen ovale of more than 0.6m/s. Results : At the time of diagnosis of restrictive foramen ovale, gestation age was 34~37 wks, and chief complaints were fetal arrhythmia(2 cases), pericardial effusion, Ebstein anomaly and subaortic stenosis. Two cases which were diagnosed fetal hydrops and supraventricular tachycardia delivered by emergent cesarian section. Five cases were found to have right heart dilatation on echocardiogram after birth, but right heart dilatation became normalized at day 7 after birth and the clinical courses were not eventful. Conclusion : Identifying an obstructed foramen ovale in the fetus warrants the further search for additional cardiac and extracardiac anomalies, which may alter the prognosis. Delivery should be induced if possible in cases of foramen ovale obstruction with signs of cardiac decompensation.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.21 no.1
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• pp.22-27
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• 2021

Propionic acidemia (PA) is an inherited autosomal recessive disorder, due to the deficiency of propionyl-CoA carboxylase (PCC). PCC is the enzyme which catalyzes the conversion of propionyl-CoA to D-methylmalonyl-CoA, and it is critical for the metabolism of amino acids, odd-chain fatty acids, and side chains of cholesterol. The clinical manifestations present mostly at the neonatal period with life-threatening metabolic acidosis and hyperammonemia. Here, we described a case of a 16-year-old Korean boy with late-onset PA who presented with embolic cerebral infarction due to dilated cardiomyopathy (DCMP) with left ventricular noncompaction. And he has family history of sudden cardiac death, so we performed metabolic screening and genetic tests. Elevated levels of 3-hydroxypropionic acid, methylcitric acid and propionylglycerine were detected in urine. Plasma acylcarnitine profile showed elevated propionylcarnitine (C3). Diagnosis of PA was confirmed by genetic analysis, which revealed compound heterozygous mutations, c.[1151T>G] (p.[Phe384Cys]) and c.[1228C>T] (p.[Arg410Trp]) in PCCB gene. His heart function is in improving state and the results of biochemical analysis are stable with heart failure medication and metabolic managements. We present a case of patient without episodes of metabolic decompensation who manifests DCMP as the first symptom of PA.