Background: Pulmonary endarterectomy is widely accepted as a treatment for chronic thromboembolic pulmonary hypertension. Based on our experiences, we sought to find ways to reduce perioperative complications and to improve surgical outcomes in patients undergoing pulmonary endarterectomy. Material and Method: This study was designed as a retrospective analysis of 20 patients with pulmonary hypertension who underwent pulmonary endarterectomy between January 1998 and March 2008. All patients presented with chronic dyspnea. Deep vein thrombosis (DVT) was the major cause of chronic pulmonary thromboembolism (55%). Seventeen patients (85%) underwent inferior vena cava (IVC) filter placement. Thirteen patients underwent surgery under total circulatory arrest, while the others underwent surgery while on low flow cardiopulmonary bypass. Concomitant tricuspid annuloplasty was done in 6 patients (66%) whose tricuspid regurgitation was as severe as grade IV/IV. The mean follow-up duration was $45{\pm}32$ months. Result: Using of University of California, San Diego (UCSD), thromboembolism classification, 4 patients (20%) were type 1, 8 patients (40%) were type II, and 8 patients (40%) were type III. Right ventricular systolic pressure was reduced significantly from $77{\pm}29$ mmHg to $37{\pm}19$ mmHg after pulmonary endarterectomy (p<0.001). The degree of tricuspid regurgitation and the NYHA functional class were all improved postoperatively. Reperfusion edema occurred in 7 cases (35%). The incidence of reperfusion edema was higher in the UCSD type III group than in the other group (25% vs 50%, p=0.25) and the length of postoperative intensive care unit stay was longer in type III group ($5{\pm}2$ days vs $9{\pm}7$ days, p=0.07). The early mortality rate was 10%, and the late mortality rate was 15% (n=3); one death was due to progression of underlying non-Hodgkin's lymphoma, and the other deaths were related to recurrent thromboembolism and persistent pulmonary hypertension, respectively. Conclusion: Pulmonary endarterectomy, as a curative surgical method for treating chronic thromboernbolic pulmonary hypertension, should be performed aggressively in patients diagnosed with chronic thromboembolic pulmonary hypertension, and an effort should be made to reduce the frequency of perioperative complications and to improve surgical outcomes.
Jang Won-Chae;Jeong In-Suk;Cho Kyu-Sung;Oh Bong-Suk
Journal of Chest Surgery
/
v.39
no.9
s.266
/
pp.659-667
/
2006
Background: Experimental studies of vascular remodeling in the pulmonary arteries have been performed actively. These models required a persistent vascular insult for intimal injury induced by chronic hypoxia, monocrotaline intoxication or chronic air embolism and characterized medial hypertrophy and neointimal formation by active synthesis of the extracellular matrix protein. The purpose of this study was to determine the pattern of pulmonary vascular remodeling after obstruction of the pulmonary vein. Material and Method: Obstruction of the right pulmonary vein with a metal clip was performed in Sprague-Dawley rats $(352{\pm}18g,\;n=10)$ to cause pulmonary vascular disease. Fifteen days later, experimental studies were done and finally the both lungs and hearts were extirpated for experimental measurement. Pulmonary arterial pressure, weight ratio of right ventricle (RV) to left ventricle (LV) and ventricular septum (S) (RV/LV +S weight ratio), and pulmonary artery morphology (percent wall thickness, %WT) were evaluated and compared with normal control groups. Result: Pulmonary hypertension $(38{\pm}12mmHg\;vs\;13{\pm}4mmHg;\;p<0.05)$ and right ventricular hypertrophy (right ventricular/left ventricular and septal weight ratio, $0.52{\pm}0.07\;vs\;0.35{\pm}0.04;\;p<0.05$) with hypertrophy of the muscular layer of the pulmonary arterial wall (percent wall thickness, $22.4{\pm}6.7%\;vs\;6.7{\pm}3.4%;\;p<0.05$) were developed by 15 days after obstruction of the pulmonary vein. Conclusion: Obstruction of the pulmonary vein developed elevation of pulmonary blood pressure and medial hypertrophy of the pulmonary artery. These results are a part of the characteristic vascular remodeling. Theses results demonstrate that obstruction of the pulmonary vein can develope not only high pulmoanry blood flow of contralateral lung but also intima injury inducing vascular remodeling.
Background: Retrograde cerebral perfusion(RCP) is one of the methods used for brain protection during aortic arch surgery. The author previously published the data, however, for the safety of it, there still remains many controversies. The author performed RCP and checked various parameters to clarify the possibility of early detection of cerebral injury. Material and Method: The author used pigs(Landrace species) weighing 25 to 30kg and performed RCP for 120 minutes. After weaning of cardiopulmonary bypass, we observed pigs for another 120 minutes. Rectal temperature, jugular venous oxygen saturation, central venous pressure were continuously monitored, and the hemodynamic values, histological changes, and serum levels of neuron-specific enolose(NSE) and S100$\beta$ protein were checked. Central venous pressure during RCP was maintained in the range of 20 to 25 mmHg. Result: Flow rates(ml/min) during RCP were 224.3$\pm$87.5(20min), 227.1$\pm$111.0(40min), 221.4$\pm$119.5(60min), 230.0$\pm$136.5(80min), 234.3$\pm$146.1(100min), and 184.3$\pm$50.5(120min). Serum levels of NSE did not increase after retrograde cerebral perfusion. Serum levels of S100$\beta$ protein(ng/ml) were 0.12$\pm$0.07(induction of anesthesia), 0.12$\pm$0.07(soon after CPB), 0.19$\pm$0.12(20min after CPB), 0.25$\pm$0.06(RCP 20min), 0.29$\pm$0.08(RCP 40min), 0.41$\pm$0.05(60min), 0.49$\pm$0.03(RCP 80min), 0.51$\pm$0.10(RCP 100min), 0.46$\pm$0.11(RCP 120min), 0.52$\pm$0.15(CPBoff 60min), 0.62$\pm$0.15(60min after rewarming), 0.76$\pm$0.17(CPBoff 30min), 0.81$\pm$0.20(CPBoff 60min), 0.84$\pm$0.23(CPBoff 90min) and 0.94$\pm$0.33(CPBoff 120min). The levels of S100$\beta$ after RCP were significantly higher than thosebefore RCP(p<0.05). The author could observe the mitochondrial swellings using transmission electron microscopy in neocortex, basal ganglia and hippocampus(CA1 region). Conclusion: The author observed the increase of serum S100$\beta$ after 120 minutes of RCP. The correlation between its level and brain injury is still unclear. The results should be reevaluated with longterm survival model also considering the confounding factors like cardiopulmonary bypass.
Jang Woo-Sung;Lim Cheong;Lim Hong-Kook;Min Sun-Kyung;Kwak Jae-Kun;Chung Eui-Seuk;Kim Dong-Jin;Kim Woong-Han
Journal of Chest Surgery
/
v.39
no.6
s.263
/
pp.434-439
/
2006
Background: Deep hypothermic circulatory arrest during repair of aortic arch anomalies may induce neurological complications or myocardial injury. So we surveyed if the regional cerebral and myocardial perfusion might eliminate those potential side effects. Material and Method: From March 2000 to December 2004, 62 neonates or infants with aortic arch anomaly underwent one stage biventricular repair using the regional perfusion technique by single surgeon. Preoperative diagnosis of the arch anomaly consisted of coarctation (n=46), interruption of the aorta (n=12), hypoplastic left heart syndrome (n=2) and truncus areteriosus (n=2). Combined anomalies were ventricular septal defect (n=51), TAPVR (n=1), PAPVR (n=1) and atrioventricular septal defect (n=2). Arterial cannula was inserted at the innominate artery. Result: The mean regional perfusion time of brain was $28{\pm}10min$. Operative mortality rates was 0 (0/62). Late death was 1 (1/62) during $11{\pm}7$ months of follow-up. Neurologic complications consisted of transient chorea in 1 case. There was no reoperation associated with arch anolamy. Pulmonary complication associated with arch repair occurred in f case which was managed by aortopexy. Conclusion: One-tage rch repair using the regional profusion is safe and effective in minimizing the neurologic and myocardial complications.
background: In an attempt to investigate the role of oxidants in the activation of phospholipase $A_2$(PLA$_2$) and endogenous oxidative stress in the lung. acute inflammatory lung injury was induced by the instillation of hydrogen peroxide into the trachea of Sprague-Dawley rats. Material and Method: To prove the hypothesis thats released oxidants from neutrophils activate the PLA$_2$ retrogradely, activities of PLA$_2$ and lysoplatelet activating factor acetyltransferase(lysoPAF AT) were assayed i hours after instillation of hydrogen peroxide. In addition, to confirm the impairing effects of the activation of PLA$_2$ associated with endogenous oxidative stress, lung weight/body weight ratio(L$\times$10$^{-3}$ B), protein contents(mg/two lungs) in bronchoalveolar lavage(BAL) were measured. As neutrophilic respiratory burst has been known to play a pivotal role in the genesis of endogenous oxidative stress associated with acute inflammatory lung injury, BAL neutrophils counts and level of lung myelperoxidase(MPO) were measured after hydorgen peroxide insult. Morphological and histochemical studies were also performed to identify the effect of the endogenous oxidative stress. Result: Five hours after hydrogen peroxide instillation, lungs showed marked infiltration of neutrophils and increased weight. Protein contents in BAL increased significantly compared to those of normal rats. PLA$_2$ activity was enhanced in the hydrogen peroxide instilled group. Interestingly, the accelerated production of platelet activating factor(PAF) was confirmed by the increased activity of lysoPAF AT in the $H_2O$$_2$ employed lung. Morphologically, light microscopic findings of lungs after instillation of hydrogen peroxide showed atelectasis and infiltration of inflammatory cells, which was thought to be caused by lipid mediators produced by PLA$_2$ activation. In cerium chloride cytochemical electron microscopy, dense deposits of cerrous perhydroxide were identified. In contrast, no deposit of cerrous perhydroxide was found in the normal lung.
During the Off-Pump Coronary Arterial Bypass surgery (OPCAB), the manipulation of the heart can depress cardiac contractility and cause hemodynamic instability. In this study, hemodynamic parameters were measured during operation and the laboratory and clinical data were investigated to evaluate their effects on postoperative outcome. Material and Method: From March 2001 to August 2002, 50 consecutive patients who underwent OPCAB were included in this study. During the same period, total number of CABG was 71 The blood pressure, pulmonary artery pressure, mixed venous oxygen saturation, and cardiac index were measured before manipulation, after application of stabilizer, and at the end of anastomosis. Postoperatively, we measured the cardiac enzymes such as CK-MB, troponin 1 and checked the amount of inotropes required, chest tube drainage, the amount of transfusion, duration of ventilator support, and duration of ICU stay. Result: The number of mean distal anastomoses was 2.8$\pm$0.9 per patient. On elevation and stabilization of the heart, systolic blood pressure was depressed and pulmonary artery pressure was elevated significantly, but during each anastomosis no significant changes were detected. The peak level of cardiac markers was 29.2$\pm$46.7 for CK-MB, 0.69$\pm$0.86 for troponin 1 on postoperative day f. Among the intraoperative hemodynamic parameters, the ischemic change of EKG and bolus injection of inotropes significantly affected the posteroperative cardiac enzymes. But, no difference other than the level of cardiac enzymes between the two groups with or without the ischemic change of EKG and bolus injection of inotropes was noticed. Conclusion: The significant hemodynamic changes occurred when the heart was elevated and stabilized, however during anastomoses there were no significant changes. Serum cardiac enzymes rose significantly in the group that showed the ischemic charge of EKG or needed the bolus injection of inotropes for maintaining hemodynamic stability intraoperatively, but it did not affect the postoperative outcome. In conclusion, the ischemic change of EKG and the need for bolus injection of intropes during operation may be very indicative for probable ischemia.
Background: The femoral artery is the most common site of canuulation for cardiopulmonary bypass in surgery for type A aortic dissection. Recently, many surgeons prefer the axillary artery to the femoral artery as the arterial cannulation site for several benefits. We evaluated the safety and usefulness of axillary artery cannulation in surgery for acute type A aortic dissection. Material and Method: Between Oct. 1995 and Sep. 2001, 71 patients underwent operations for acute type A aortic dissection. The arterial cannula was inserted into the axillary artery in 31 patients (AXILLARY group, mean age=56), and into the femoral artery in 40 patients (FEMORAL group, mean age=57). We retrospectively compared the incidence of mortality, morbidities, and hospital course. Result: The mean duration of cardiopulmonary bypass and circulatory arrest were significantly shorier in the AXILLARY group (207 min and 39min, respectively) than in the FEMORAL group (263min and 49 min, respectively; P<0.05). Postoperative hospital stay was significantly shorter in the AXILLARY group than in the FEMORAL group (mean 15 days vs. 35 days, p<0.05). Although there was no difference in the incidence of new-onset permanent neurological dysfunction (3.2%, in the AXILLARY group, 2.5% in the FEMORAL group), the incidence of transient neurological dysfunction was significantly lower in the AXILLARY group (12.9% vs. 25%, p<0.05). In the FEMORAL group, two patients needed urgent conversion to cannulation site due to arch vessel malperfusion. In the AXILLARY group, there was only one patient who had a complication related to the cannulation, i.e., median nerve injury. Conclusion: Axillary artery cannulation was safe and helpful in decreasing the cerebral ischemic time and incidence of transient neuroligcal dysfunction in surgery for acute type A aortic dissection, It enabled us to approach the patients with aortic arch pathology more aggressively.
Background: The washing of packed red blood cells could remove pro-inflammatory mediators, cell debris, and micro-particles contained in packed red blood cells, and the preci-rculation-ultrafiltration (recirculation and ultrafiltration of circuit itself before cardiopulmonary bypass) could attenuate the initial inflammatory reaction and remove the initial proinflam-matory mediators. This study was performed to evaluate whether the washing of packed red blood cells and precirculation-ultrafiltration can reduce the production of cytokines that have an important role in myocardial reperfusion injury. This study investigated the effects of washing the packed red blood cells and precirculation-ultrafiltration on the production of cytokines during and after cardiopulmonary bypass and open heart surgery. Material and Method: Forty eight infants with VSD undergoing open heart surgery under cardiopulmonary bypass were randomized into control group (group C, n=12), washing group (group W, n= 12), precirculation-ultrafiltration group (group F, n: 12), and combined group(washing and precirculation-ultrafiltration, group WF, n=12). Blood samples were obtained before, during, and after the bypass to assess plasma level of tumor necrosis factor-$\alpha$(TNF-$\alpha$), interleukin-6(IL-6), and interleukin-8 (IL-8). Results: Expressions of TNF-$\alpha$ were significantly reduced in combined group (group WF) compared with group C, group W, and group F (p<0.05). Expression of IL-6 were significantly reduced in group W, group F, and group WF compared with group C (p<0.05), but similar among group W, group F, and group WF (p=0.053). Expression of IL-8 were reduced in group W and group WF compared with group C (p<0.05), but similar among group W, group F, and group WF (p=0.067). Conclusion: In conclusion, the washing of packed red blood cells and precirculation-ultrafiltration blunted the increase of TNF-$\alpha$ , IL-6, and IL-8 during and after open heart surgery with cardiopulmonary bypass. However, the clinical benefits of these treatments remains unproven.
Kim, Kwan-Chang;Lee, Cheul;Choi, Chang-Hue;Lee, Chang-Ha;Oh, Sam-Sae;Park, Seong-Sik;Kim, Kyung-Hwan;Kim, Woong-Han;Kim, Yong-Jin
Journal of Chest Surgery
/
v.41
no.2
/
pp.170-176
/
2008
Background: Bioprosthetic devices for treating cardiovascular diseases and defects may provide alternatives to autologous and homograft tissue. We evaluated the mechanical and physical conditions of a porcine pericardial bioprosthesis treated with Glutaraldehyde (GA), Ethanol, or Sodium dodecylsulfate (SDS) before implantation. Material and Method: 1) Thirty square-shaped pieces of porcine pericardium were fixed in 0.625%, 1.5% or 3% GA solution. 2) The tensile strength and thickness of these and other bioprosthesis, including fresh porcine pericardium, fresh human pericardium, and commercially produced heterografts, were measured. 3) The tensile strength and thickness of the six treated groups (GA-Ethanol, Ethanol-GA, SDS only, SDS-GA, Ethanol-SDS-GA and SDS-Ethanol-GA) were measured. Result: 1) Porcine pericardium fixed in 0.625% GA the thinnest and had the lowest tensile strength, with thickness and tensile strength increasing with the concentration of GA solution. The relationship between tensile strength and thickness of porcine pericardium increased at thicknesses greater than 0.1mm (correlation-coefficient 0.514, 0<0.001). 2) There were no differences in tensile strength or thickness between commercially-produced heterografts. 3) Treatment of GA, ethanol, or SDS minimally influenced thickness and tensile strength of porcine pericardium, except for SDS alone. Conclusion: Porcine pericardial bioprosthesis greater than 0.1 mm thick provide better handling and advantageous tensile strength. GA fixation did not cause physical or mechanical damage during anticalcification or decellularization treatment, but combining SDS-ethanol pre-treatment and GA fixation provided the best tensile strength and thickness.
The Aspergillus species produces metabolic products that play a significant role in the destructive processes in the lung. We experienced a case of chronic necrotizing pulmonary aspergillosis caused by an Aspergillus niger infection, which contained numerous calcium oxalate crystals in the necrotic lung tissue. A 46-year-old man, who had a history of pulmonary tuberculosis, presented with high fever, intermittent hemoptysis and pulmonary infiltrations with a cavity indicated by the chest radiograph. Despite being treated with several antibiotics and anti-tuberculosis regimens, the high fever continued. The sputum cultures yielded A. niger repeatedly, and intravenous amphotericin B was then introduced. The pathological specimen obtained by a transbronchial lung biopsy revealed numerous calcium oxalate crystals in a background of acute inflammatory exudates with no identification of the organism. Intravenous amphotericin B was continued at a total dose of 1600 mg, and at that time he was afebrile, although the intermittent hemoptysis continued. On the $63^{rd}$ hospital day, a massive hemoptysis (about 800 mL) developed, which could not be controlled despite embolizing the left bronchial artery. He died of respiratory failure the next day. It is believed that the oxalic acid produced by A. niger was the main cause of the patient's pulmonary injury and the ensuing massive hemoptysis.
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