• Journal of Chest Surgery
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• v.40 no.5 s.274
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• pp.351-355
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• 2007

Background: Postinfarction ventricular septal rupture is associated with mortality as high as $85\sim90%$, if it is treated medically. This report documents our experience with postinfarction ventricular septal rupture that was treated surgically, Material and Method: We retrospectively reviewed the medical records of 11 patients who were operated on due to postinfarction ventricular septal rupture between August 1996 and August 2006. There were 4 men and 7 women, with a mean age of $70{\pm}11$ years (age range: $50\sim84$ years). The location of the rupture was anterior in 7 cases and posterior in 4 cases. The interval between the onset of acute myocardial infarction and the occurrence of the ventricular septal rupture was $2.0{\pm}1.3$ days (range: $1\sim5$ days). Operation was performed at an average of $2.4{\pm}2.7$ days (range: $0\sim8$ days) after the diagnosis of septal rupture. Preoperative intraaortic balloon pump therapy was performed in 10 patients. Result: The infarct exclusion technique was used in all cases. Coronary artery bypass grafting was done in 8 cases, with the mean number of distal anastomosis being $1.0{\pm}0.8$. There was one operative death. In 2 patients, reoperation was performed due to a residual septal defect. The postoperative morbidities were transient atrial fibrillation (n=7), paroxysmal supraventricular tachycardia (n=1), low cardiac output syndrome (n=3), bleeding reoperation (n=2), delayed sternal closure (n=2), acute renal failure (n=2), pneumonia (n=1), intraaortic balloon pump-related thromboembolism (n=1), and transient delirium (n=2). Nine patients have been followed up for a mean of $38{\pm}40$ months except for one follow-up loss. There have been 3 late deaths. At the latest follow-up, all 6 survivors were in a good functional class. Conclusion: We demonstrated satisfactory operative and midterm results with our strategy of preoperative intraaortic balloon pump therapy, early repair of septal rupture by infarct exclusion and combined coronary revascularization.

• Journal of Chest Surgery
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• v.43 no.5
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• pp.475-481
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• 2010

Background: We evaluated mid-term results of mitral annuloplasty using a flexible band and a completely rigid ring for mitral valve repair in patients with degenerative mitral regurgitation (MR). Material and Method: From January 2004 to September 2008, 71 patients (M:F=36:35, $55{\pm}13$ years) underwent mitral valve repair with mitral annuloplasty for degenerative MR. Ring annuloplasty was done using a Cosgrove-Edwards flexible band (Group I, n=43) or a Carpentier-Edwards classic ring (Group II, n=28). There were no differences in preoperative characteristics of the participants. Average duration of follow-up was 36 months (range: 2~69 mos). Result: There was no in-hospital mortality. Postoperative morbidity, which included atrial fibrillation (n=7) and low cardiac output syndrome (n=5) in groups I and II were similar. There was one late death in group II. The proportion exhibiting freedom from recurrent mitral regurgitation ($\geq$moderate) at 4 years in Groups I and II were, respectively, 94.5 and 91.8%, (p=0.695). Left ventricular ejection fraction decreased in the early postoperative period ($7{\pm}2$ days) and recovered by last follow-up ($25{\pm}16$ mos; p=0.002). The pattern was similar in groups I and II (p=0.905). Re-operation was performed in 3 patients (1 in Group I and 2 in Group II, p=0.316). Four-year event-free survival (free of adverse valve-related events) was 95.2% for Group I and 92.6% for Group II; this difference was not significant, p=0.646). Conclusion: The type of technique used in mitral annuloplasty to repair the mitral valve repair after degenerative MR did not affect mid-term clinical and functional results.

• Journal of Chest Surgery
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• v.37 no.1
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• pp.27-34
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• 2004

Background: Infective endocarditis shows higher operative morbidity and mortality rates than other cardiac diseases. The vast majority of studies on infective endocarditis have been made on aortic endocarditis, with little attention having been paid to infective endocarditis on the mitral valve. This study attempts to investigate the clinical aspects and operative results of infective endocarditis on the mitral valve. Meterial and Method: The subjects of this study consist of 23 patients who underwent operations for infective endocariditis on the mitral valve from June 1995 to May 2003. Among them, 2 patients suffered from prosthetic valvular endocarditis and the other 21 from native valvular endocarditis. The subjects were evenly distributed age-wise with an average age of 44.8$\pm$15.7 (11∼66) years. Emergency operations were performed on seventeen patients (73.9%) due to large vegetation or instable hemodynamic status. In preoperative examinations, twelve patients exhibited congestive heart failure, four patients renal failure, two patients spleen and renal infarction, and two patients temporary neurological defects, while one patient had a brain abscess. Based on the NYHA functional classification, seven patients were determined to be at Grade II, 9 patients at Grade III, and 6 patients at Grade IV. Vegetations were detected in 20 patients while mitral regurgitation was dominant in 19 patients with 4 patients showing up as mitral stenosis dominant on the preoperative echocardiogram. Blood cultures for causative organisms were performed on all patients, and positive results were obtained from ten patients, with five cases of Streptococcus viridance, two cases of methicillin-sensitive Staphylococcus aureus, and one case each of Corynebacteriurn, Haemophillis, and Gernella. Operations were decided according to the AA/AHA guidelines (1988). The mean follow-up period was 27.6 $\pm$23.3 (1 ∼ 97) months. Result: Mitral valve replacements were performed on 43 patients, with mechanical valves being used on 9 patients and tissue valves on the other 4. Several kinds of mitral valve repair or mitral valvuloplasty were carried out on the remaining 10 patients. Associated procedures included six aortic valve replacements, two tricuspid annuloplasty, one modified Maze operation, and one direct closure of a ventricular septal defect. Postoperative complications included two cases of bleeding and one case each of mediastinitis, low cardiac output syndrome, and pneumonia. There were no cases of early deaths, or death within 30 days following the operation. No patient died in the hospital or experienced valve related complications. One patient, however, underwent mitral valvuloplasty 3 months after the operation. Another patient died from intra-cranial hemorrhage in the 31st month after the operation. Therefore, the valve-related death rate was 4.3%, and the valve-related complication rate 8.6% on mid-term follow-up. 1, 3-, and 5-year valve- related event free rates were 90.8%, 79.5%, and 79.5%, respectively, while 1, follow-up. 1, 3-, and 5-year valve- related event free rates were 90.8%, 79.5%, and 79.5%, respectively, while 1, 3-, and 5-year survival rates were 100%, 88.8%, and 88.8%, respectively. Conclusion: The findings suggest that a complete removal of infected tissues is essential in the operative treatment of infectious endocarditis of the mitral valve. It is also suggested that when infected tissues are completely removed, neither type of material nor method of operation has a significant effect on the operation result. The postoperative results also suggest the need for a close follow-up observation of the patients suspected of having brain damage, which is caused by preoperative blood contamination or emboli from vegetation, for a possible cerebral vascular injury such as mycotic aneurysm.

• Journal of Chest Surgery
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• v.37 no.1
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• pp.19-26
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• 2004

Background: The aims of this study are to verify the result of the surgical treatment of ALCAPA and to identify the postoperative changes of left ventricular dimensions and mitral regurgitation (MR), Material and Method: Fifteen patients operated on since 1985 were included in the study. The patients operated on before 1998 (n=9) showed heterogeneous properties with various surgical strategies and cardiopulmonary bypass techniques. However, six patients were operated on with the established surgical strategy since 1998; 1) Dual perfusion and dual cardioplegic solution delivery through ascending aorta and main pulmonary artery, 2) Coronary transfer by rolled-conduit made of pulmonary artery wall flap, and 3) Additional mitral valvular procedure was not peformed. Result: Median age of the study group was 6 months (1 month to 34 years). The operative methods were left subclavian artery to left coronary artery anastomosis in 1, simple ligation in 2, Takeuchi operation in 2, and coronary reimplantation in 10 patients. The mean follow up period was 5.5<5.8 years (2 months 14 years), There were one early death (6.7%) and one late death. Overall 5-year survival rate was 85.6$\pm$9.6%. The Z-value of left ventricular end-diastolic and end-systolic dimensions were 6.4$\pm$3.0 and 5.1 $\pm$3.6 preoperatively, and decreased to 1.7$\pm$ 1.9 and 0.8$\pm$ 1.6 in 3 months (p<0.05). Significant preoperative MR was identified in 6 patients (40%) and all the patients showed immediate improvement of MR within f month postoperatively. There were 3 cases of reoperation due to coronary anastomosis site stenosis and recurrence of MR. However, there was no mortality nor late reoperation in the patients operated on after 1998. Conclusion: The surgical treatment of ALCAPA showed favorable survival and early recovery of ventricular dimensions and mitral valvular function. Although long-term reintervention was required in some cases of earlier period, all the cases after 1998 showed excellent surgical outcome without long-term problem.

• Journal of Chest Surgery
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• v.36 no.8
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• pp.545-558
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• 2003

Adult respiratory distress syndrome (ARDS) is of particular interest because of its severity of the associated lung injury and its high mortality. However, the pathophysiologies of ARDS in infant and childhood groups are still not well clarified inspite of many previous investigations. To investigate the time course of pathophysiology of ARDS in infant and childhood groups, this study was designed with experimental endotoxin-induced ARDS model using young rabbits (8 week-old). Material and Method: Rabbits were divided into the control group (n=8) and the endotoxin-treated group (n=32). The endotoxin group was subdivided into 4 groups by the sampling times as 3, 6, 12 and 24 hr-groups (G- $E_{3,6,12,24,}$ each n=8). The experimental ARDS was made by a bolus injection of endotoxin (Escherichia coli serotype 055 : B5, 0.50 mg/kg) via rabbit ear vein. For evaluation of the hematologic and inflammatory markers, and superoxide dismutase (SOD) concentrations, the blood samples were taken from the heart. The bronchoalveolar lavage fluid (BALF) were obtained for analysis of the leukocytes and protein concentration. With biopsy of the lung, histopathologic changes of the lung were also evaluated. Result: In the endotoxin groups, significant leukopenia (owing to pancytopenia) occurred in 3 and 6-hr groups, which was followed by significant leukocytosis (owing to neutrophilia) in the 12 and 24-hr groups (p<0.05). Serum levels of tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and interleukin-1 $\beta$ (IL-1 $\beta$) in the endotoxin groups were higher than those of control group (p<0.05). Serum levels of superoxide dismutase (SOD) of G- $E_{3}$ and G- $E_{6}$ were higher than those of control group, whereas those of G- $E_{12}$ were lower than those of control groups (p<0.05). Total leukocyte counts and protein con-centrations in BALF were significantly elevated in the endotoxin groups compared to the control group (p < 0.05). The hemorrhagic pattern of BALF showed occurred in the endotoxin groups. The endotoxin groups (in G- $E_{6}$) had severe infiltration of inflammatory cells (lymphocyte and monocyte) in the pulmonary interstitium and parenchyma, migrations of neutrophil and eosinophil into alveolar spaces and interstitial widening, which are the evidences of acute lung injury. In the endotoxin groups, there were significant positive correlations between the BALF findings and the immunologic markers (TNF-$\alpha$, IL-1$\beta$, SOD) (p<0.05). Conclusion: Severe acute lung injury occurred in all the endotoxin-treated rabbits. The pathophysiologic findings were so progressive until 6-hr by time dependant pattern, and then recovered slowly, Variable hematologic, immuno-logic, and pathologic factors were well correlated in the development and progression of endoxin-induced lung injury. The pathophysiologic responses were sensitive and rapid in young rabbit Young rabbit seemed to be a useful experimental animal model for infant and childhood groups.roups.

• Tuberculosis and Respiratory Diseases
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• v.44 no.2
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• pp.360-378
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• 1997

Background : Severe acute lung injury(ALI), also known as the adult respiratory distress syndrome(ARDS), is a heterogenous nature of dynamic and explosive clinical synrome that exacts a mortality of approximately 50%. Endotoxin(ETX) is an abundant component of the outer membrane of gram-negative bacteria capable of inducing severe lung injury in gram-negative sepsis and gram-negative bacterial pneumonia, which are among the most common predisposing causes of ARDS. The influx of PMNs into airway tissue is a pathological hallmark of LPS-induced lung injury. And there is a substantial evidence suggesting that cytokines are important mediators of lung injury in gram-negative sepsis. However, the kinetics of phagocytes and cytokines by an exact time sequence and their respective pathogenic importance remain to be elucidated. This study was performed to investigate the role of phagocytes and proinflammatory cytokines in ETX-induced ALI through a time course of changes in the concentration of protein, $TNF{\alpha}$ and IL-6, and counts of total and its differential cells in BALF. The consecutive histologic findings were also evaluated. Method : The experimental animals, healthy male Sprague-Dawley, weighted $200{\pm}50g$, were divided into control- and ALI- group. ALI was induced by an intravenous administration of ETX, 5mg/kg. Above mentioned all parameters were examined at 0(control), 3, 6, 24, 72 h after administration of ETX. $TNF{\alpha}$ and IL-6 cone. in BALF were measured by a bioassay. Results : The protein concentration and total leukocyte count(TC) in BALF was significantly increased at 3h compared to controls(p < 0.05). The protein conc. was significantly elavated during observation period, but TC was significantly decreased at 72h(p < 0.05 vs. 24h). There was a close relationship between TC and protein cone. in BALF(r = 0.65, p < 0.001). The PMN and monocyte count was well correlated with TC in BALF, and the correlation of PMN(r = 0.97, p < 0.001) appeared to be more meaningful than that of monocyte(r = 0.61, p < 0.001). There was also a significant correlation between protein cone. and PMN or monocyte count in BALF(PMN vs. monocyte : r = 0.55, p < 0.005 vs. r = 0.64, p < 0.001). The count of monocyte was significantly elavated during observation period though a meaningful reduction of PMN count in BALF at 72h, this observation suggested that monocyte may, at least, partipate in the process of lung injury steadly. In this study, there was no relationship between IL-6 and $TNF{\alpha}$ cone., and $TNF{\alpha}$ but not IL-6 was correlated with TC(r = 0.61, p < 0.05) and monocyte(r = 0.67, p < 0.05) in BALF only at 3, 6h after ETX introduced. In particular, the IL-6 cone. increased earlier and rapidly peaked than $TNF{\alpha}$ cone. in BALF. In histologic findings, the cell counts of lung slices were increased from 3 to 72h(p < 0.001 vs. NC). Alveolar wall-thickness was increased from 6 to 24h(p < 0.001 vs. NC). There was a significant correlation between the cell counts of lung slices and alveolar wall-thickness(r= 0.61, p < 0.001). This result suggested that the cellular infiltrations might be followed by the alterations of interstitium, and the edematous change of alveolar wall might be most rapidly recovered to its normal condition in the process of repair. Conclusion : We concluded that although the role of PMN is partly certain in ETX-induced ALI, it is somewhat inadequate to its known major impact on ALL Alveolar macrophage and/or non-immune cells such as pulmonary endothelial or epithelial cells, may be more importantly contributed to the initiation and perpetual progression of ETX-induced ALI. The IL-6 in ETX-induced ALI was independent to $TNF{\alpha}$, measured by a bioassay in BALF. The early rise in IL-6 in BALF implies multiple origins of the IL-6.