From April 1987 to May 1996, 13 infants underwent a Norwood operation for complex congenital heart diseases including hypoplastic left heart syndrome (n : 7), mitral stenosis with small VSD and subaortic stenosis (n : 1), mitral atresia with ventricular septal defect, coarctation of aorta, and subaortic stenosis (n = 1), interrupted aortic arch with ventricular septal defect and subaortic stenosis (n : 1), tricuspid atresia with transposition of the great arteries (n = 1), and complex double-inlet left ventricle (n : 2). All patients without hypoplastic left heart syndrome were associated wit hypoplasia of ascending aorta and arch. Age at operation ranged from 3 days to 8.7 months (mean 60.6 $\pm$ 71.6 days, median 39 days). The operative mortality( < 30 days) was 46% (6 patients). Late mortality was 15% (2 patients). All operative deaths occured during the Erst 24 hours after the operation as a result of cardiopulmonary bypass weaning failure (5 patients) and sudden hemodynamic instability postoperatively (1 patient). Late death was due to aspiration pneumonia in two cases. There are 5 long-term survivals (39%). Three of them have undergone a two-stage repair with a modified Fontan operation in two and total cavopulmonary shunt in one at 12, 17, 4.5 months after Norwood procedure with no mortality. Two patients have entered a three-stage repair strategy by undergoing a bidirectional cavopulmonary shunt at 3 and 5.5 months after initial operation with 1 operative death. The actuarial survival rate for all patients at the first-stage operation, including hospital deaths and ate death was 30.8% at 1 year. In conclusion, the operative mortality of Norwood operation was relatively high compared to other operation for major cardiac anomalies, continuing experience will lead to an improvement in result.
This study was designed 1) to develop a hypertensive animal model in which the blood pressures (BPs) of symmetric regions (right and left upper extremities) are significantly different and 2) to test the effect of BP per se on the contractility and endothelium-dependent relaxation of vascular smooth muscle. Rabbits were anesthetized with sodium pentobarbital and ventilated with room air via animal respirator. The transverse aorta was exposed through the left second intercostal space and the lumen of the aorta was narrowed partially by ligation using 3-0 silk and a probe at a point between the origins of the brachiocephalic trunk and the left subclavian artery. Four to eight weeks postoperatively, BPs were measured in the carotid artery as the high BP area (proximal to coactation site) and in the femoral artery as the low BP area (distal to coarctation site). In the animal model, pressure-overload hypertension was developed and the BP of the right subclavian artery was higher than that of the left subclavian artery. The concentrations of circulating epinephrine, norepinephrine, angiotensin I, and angiotensin II were measured. The right and left subclavian arteries and their branches were used for isometric tension recording in organ baths and their responsiveness to phenylephrine, serotonin, acetylcholine, and sodium nitroprusside were examined. The BPs of carotid and femoral artery in control animals were $116{\pm} 12/75{\pm}9\;mmHg (mean ${\pm}SEM$) and $130{\pm}16/68{\pm}9\;mmHg$ respectively, while those of carotid and femoral artery in the hypetensive animals were $172{\pm}6/111{\pm}10\;mmHg$ and 136{\pm} 4/100 {\pm}9\;mmHg$ respectively. There were no significant differences in the concentrations of circulating epinephrine, norepinephrine, angiotensin I, and angiotensin II between controls and the animal models. No significant differences were found in the vascular sensitivities to phenylephrine and serotonin between the high pressure-exposed vessels and the low pressure-exposed vessels. However, the endothelium-dependent relaxation to acetylcholine and nitroprusside-induced relaxation showed significant differences between the high pressure-exposed and the low pressure-exposed subclavian arteries. From the above results, we suggest that the contractility of vascular smooth muscle is unchanged by the elevated pressure per se. However, the endothelium-dependent relaxation to acetylcholine and the nitroprusside-induced relaxation are attenuated by pressure.
Background: The purpose of this study was to evaluate and analyze the surgical techniques and postoperative complications in patients undergoing operations for descending thoracic aortic aneurysms. Material and Method: The data of 22 major operations between March 1987 and August 1997 were retrospectively reviewed. Result: There were 18 men and 4 women with a mean age of 49 years (range 33 years to 82 years). The cause of the aneurysm was aortic dissection in 13 patients, atherosclerosis in 3, mycotic in 3, trauma in 2 and uncertain in 1. The operative techniques were resection and graft replacement in 16, axillofemoral bypass graft in 2, femorofemoral bypass graft in 2, exclusion, aneurysmorrhaphy in 1 and transfemoral stent insertion in 1. During the operation, 16 cases were performed under total aortic clamp. Among the 16 patients, femorofemoral bypass was used in 14 cases and previously made shunt in 2 cases. The mean total aortic clamp time was 91 minutes and the mean extracorporeal circulation time was 116 minutes. One death occurred in an excluded patient on the 52 postoperative day due to a rupture of the aneurysm. Postoperative complications were paraplegia in 1 case, acute renal failure in 1 case and acute respiratory failure in 1 case. Conclusion: Although surgical treatment of the descending thoracic aneurysm has many postoperative complications, good surgical results can be achieved with a proper patient selection and fine surgical techniques.
Background: Thoracic aortomyoplasty is one of the surgical treatment for heart failure and has advantages over artificial heart or intraaortic balloon pumps. It uses autogenous skeletal muscles and solves problems such as energy source. However its use in clinical settings has been limited. This preliminary study was designed to develop surgical technique and to determine the effect of acute descending thoracic aortomyoplsty. Material and Method: Thirteen adult Mongrel dogs were used. The left latissimus dorsi muscle was wrapped around the descending aorta under general anesthesis. Swan-Ganz and microtipped Millar catheter were used for the hemodynamics and endocaridial viability ratio. Data were collected with myostimulator on and off in normal hearts and the ischemic hearts. Result: In normal hearts, the mean aortic diastolic pressure increased from 72$\pm$15mmHg at baseline to 78$\pm$13mmHg with stimulator on. Coronary perfusion pressure increased from 61$\pm$11mmHg to 65$\pm$9mmHg. Diastolic time increased from 0.288$\pm$0.003 msec to 0.290$\pm$0.003msec. Systolic time decreased from 0.164$\pm$0.002msec to 0.160$\pm$0.002 msec. Endocardial viability ratio increased from 1.21$\pm$0.22 to 1.40$\pm$0.18. In ischemic hearts, mean aortic diastolic pressure incrased from 56$\pm$21mmHg at baseline to 61$\pm$15mmHg with stimulator on. Coronary perfusion pressure increased from 48$\pm$17mmHg to 52$\pm$15mmHg. Diastolic time increased from 0.290$\pm$0.003 msec to 0.313$\pm$0.004msec. Systolic time decreased from 0.180$\pm$0.002 msec to 0.177$\pm$0.003 msec. Endovascular viability ratio increased from 0.9$\pm$0.31 to 1.1$\pm$0.31. The limited number of cases ruled out the statistic significance. Conclusion: Descending thoracic aortomyoplasty is a simple operation designed to use patient's own skeletal muscles. It trends to increase diastolic augmentation and coronary perfusion pressure. Modification of surgical technique and stimulator protocol would maximize the effect to assist the heart.
It has not been clear whether L-arginine plays solely a role contributing to vascular nitric oxide (NO) synthesis. To investigate the mechanisms by which L-arginine induces vasorelaxation, effects of L-arginine on the isometric tension, and tissue NOx and cyclic guanosine monophosphate(cGMP) contents were examined in the isolated rat thoracic aorta. L-Arginine induced a dose-dependent relaxation of aortic rings only with intact endothelium only. The vasorelaxation response to low concentrations of L-arginine was abolished by the pretreatment with NG-nitro-L-arginine methyl ester(L-NAME, 10-4 mol/L), whereas the relaxation caused by higher concentrations L-arginine(10-5-10-3 mol/L) was maintained and even more pronounced in the presence of L-NAME. L-Arginine did not affect the vascular tension precontracted with KCl. The vascular tissue contents of NOx/cGMP were not significantly affected by L-arginine, while they were decreased by L-NAME. L-Arginine could not completely recover the NOx/cGMP decreased by L-NAME. Methylene blue only partially antagonized the relaxation response to L-arginine. Indomethacin did not affect the L-arginine-induced vasorelaxation, whereas ouabain markedly attenuated the relaxation. It is suggested that L-arginine induces vasorelaxation not only through its contribution to NO synthesis, but also through enhancing another endothelium-dependent mechanism which is NO/cGMP-independent and cyclooxygenase- independent.
The studies on cryopreserved arterial allograft have been focused on cooling methods, pre-treatment, cryoprotectant agents, and preservation temperature. But recently, several studies have reported that thawing methods also play an important role in the occurrence of macroscopic and microscopic cracks. This study was designed to investigate the cell injury after thawing, using a rabbit model to clarify the effect of thawing methods on cryopreserved arteries. Material and Method: Segments of the rabbit aorta were obtained and divided into 3 groups (n=60) according to whether the specimens were fresh (control, n=20), cryopreserved and rapidly thawed (RT) at 37$^{\circ}C$ (n=20), or cryopreserved and subjected to controlled, automated slow thawing (ST)(n=20). Cell damage was established using the TUNEL method and the morphological changes were also evaluated. Result: In the group that was rapidly thawed, the expression of TUNEL (+) cells increased significantly more than in the slowly thawed group. In addition, the endothelial denudation, microvesicles and edema were significant in the rapidly thawed group compared with those changes in the slowly thawed group. Conclusion: Our study suggests that the rapid thawing method may be one of the major causes of cellular damage and delayed rupture in cryopresewed arterial allografts. The expression of TUNEL (+) cells and structural changes were significantly low in the slowly thawed group, which might have contributed to the improvement of graft failure after transplantation.
For years, physicians and anatomists have been interested in the heart that has one functioning ventricle. Various terms have been suggested for this entity including single ventricle, common ventricle, double-inlet left ventricle, cor biatriatum triloculare, and primitive ventricle. In this report, the term "single ventricle" is utilized as suggested by Van Praagh, and is defined as that congenital cardiac anomaly in which a common or separate atrioventricular valves open into a ventricular chamber from which both great arterial trunks emerge. An outlet chamber, or infundibulum, may or may not be present and give rise to the origin of either of the great arteries. This definition excludes the entity of mitral and tricuspid atresia. An 11 year old cyanotic boy was admitted chief complaints of exertional dyspnea and frequent upper respiratory infection since 2 weeks after birth. He was diagnosed as inoperable cyanotic congenital heart disease, and remained without any corrective treatment up to his age of 11 year when he suffered from aggravation of symptoms and signs of congestive heart failure for 2 months before this admission. On 22nd of May 1979, he was admitted for total corrective operation under the impression of tricuspid atresia suggested by a pediatrician. Physical check revealed deep cyanosis with finger and toe clubbing, and grade V systolic ejection murmur with single second heart sound was audible at the left 3rd intercostal space. Development was moderate in height [135 cm] and weight[28Kg]. Routine lab findings were normal except increased hemoglobin [21.1gm%], hematocrit [64 %], and left axis deviation with left ventricular hypertrophy on EKG. Cardiac catheterization and angiography revealed 1-transposition of aorta, pulmonic valvular stenosis, double inlet of a single ventricle with d-loop, and normal atriovisceral relationship [Type III C solitus according to the classification of Van Praagh]. At operation, longitudinal incision at the outflow tract of right ventricle in between the right coronary artery and its branch [LAD from RCA] revealed high far anterior aortic valve which had fibrous continuity with mitral annulus, and pulmonic valve was stenotic up to 4 mm in diameter positioned posterolaterally to the aorta. Ventricular septum was totally defective, and one markedly hypertrophied moderator band originated from crista supraventricularis was connected down to the imaginary septum of the ventricular cavity as a pseudoseptum of the ventricle. Size of the defect was 3X3 cm2 in total. Patch closure of the defect with a Teflon felt of 3.5 x 4 cm2 was done with interrupted multiple sutures after cut off of the moderator band, which was resutured to the artificial septum after reconstruction of the ventricular septum. Pulmonic valvotomy was done from 4 mm to 11 mm in diameter thru another pulmonary arteriotomy incision, and right ventriculotomy wound was closed reconstructing the right ventricular outflow tract with pericardial autograft of 3 x 4 cm2. Atrial septal defect of 2 cm in diameter was closed with 3-0 Erdeck suture, and atrial wall was sutured also when rectal temperature reached from 24`C to 35.5`C. Complete A-V block was managed with temporary external pacemaker with a pacing rate of 110/min. thru myocardial wire, and arterial blood pressure of 80/50 mmHg was maintained with Isuprel or Dopamine dripping under the CVP of 25-cm saline. Consciousness was recovered one hour after the operation when his blood pressure reached 100 /70 mmHg, but vital signs were not stable, and bleeding from the pericardial drainage and complete anuria were persisted until his heart could not capture the pacemaker impulse, and patient died of low output syndrome 320 min after the operation.
For years, physicians and anatomists have been interested in the heart that has one functioning ventricle. Various terms have been suggested for this entity including single ventricle, common ventricle, double-inlet left ventricle, cor biatriatum triloculare, and primitive ventricle. In this report, the term "single ventricle" is utilized as suggested by Van Praagh, and is defined as that congenital cardiac anomaly in which a common or separate atrioventricular valves open into a ventricular chamber from which both great arterial trunks emerge. An outlet chamber, or infundibulum, may or may not be present and give rise to the origin of either of the great arteries. This definition excludes the entity of mitral and tricuspid atresia. An 11 year old cyanotic boy was admitted chief complaints of exertional dyspnea and frequent upper respiratory infection since 2 weeks after birth. He was diagnosed as inoperable cyanotic congenital heart disease, and remained without any corrective treatment up to his age of 11 year when he suffered from aggravation of symptoms and signs of congestive heart failure for 2 months before this admission. On 22nd of May 1979, he was admitted for total corrective operation under the impression of tricuspid atresia suggested by a pediatrician. Physical check revealed deep cyanosis with finger and toe clubbing, and grade V systolic ejection murmur with single second heart sound was audible at the left 3rd intercostal space. Development was moderate in height [135 cm] and weight[28Kg]. Routine lab findings were normal except increased hemoglobin [21.1gm%], hematocrit [64 %], and left axis deviation with left ventricular hypertrophy on EKG. Cardiac catheterization and angiography revealed 1-transposition of aorta, pulmonic valvular stenosis, double inlet of a single ventricle with d-loop, and normal atriovisceral relationship [Type III C solitus according to the classification of Van Praagh]. At operation, longitudinal incision at the outflow tract of right ventricle in between the right coronary artery and its branch [LAD from RCA] revealed high far anterior aortic valve which had fibrous continuity with mitral annulus, and pulmonic valve was stenotic up to 4 mm in diameter positioned posterolaterally to the aorta. Ventricular septum was totally defective, and one markedly hypertrophied moderator band originated from crista supraventricularis was connected down to the imaginary septum of the ventricular cavity as a pseudoseptum of the ventricle. Size of the defect was 3X3 cm2 in total. Patch closure of the defect with a Teflon felt of 3.5 x 4 cm2 was done with interrupted multiple sutures after cut off of the moderator band, which was resutured to the artificial septum after reconstruction of the ventricular septum. Pulmonic valvotomy was done from 4 mm to 11 mm in diameter thru another pulmonary arteriotomy incision, and right ventriculotomy wound was closed reconstructing the right ventricular outflow tract with pericardial autograft of 3 x 4 cm2. Atrial septal defect of 2 cm in diameter was closed with 3-0 Erdeck suture, and atrial wall was sutured also when rectal temperature reached from 24`C to 35.5`C. Complete A-V block was managed with temporary external pacemaker with a pacing rate of 110/min. thru myocardial wire, and arterial blood pressure of 80/50 mmHg was maintained with Isuprel or Dopamine dripping under the CVP of 25-cm saline. Consciousness was recovered one hour after the operation when his blood pressure reached 100 /70 mmHg, but vital signs were not stable, and bleeding from the pericardial drainage and complete anuria were persisted until his heart could not capture the pacemaker impulse, and patient died of low output syndrome 320 min after the operation.
Background: The optimal therapeutic strategies for patients with coarctation of the aorta(CoA) and ventricular septal defect(VSD) remain controversial. This study was undertaken to determine the outcome and the need for reintervention following single-stage repair of coarctation with VSD in infants younger than 6 months. Material and Method: Thirty three consecutive patients who underwent single-stage repair of CoA with VSD, from January 1995 to December 2000, at Sejong General Hospital were reviewed retrospectively. Mean age and body weight at repair were 54$\pm$37 days(12 days-171 days) and 3.9$\pm$1.1 kg(1.5~6 kg), respectively. The surgical repair of CoA was performed under deep hypothermic circulatory arrest(CA) in the early period of the study and under regional cerebral perfusion through a direct innominate arterial cannulation without CA in the later period. The technique used in the repair of the CoA was resection and extended end-to-end anastomosis(EEEA; n=16) and extended side-to-side anastomosis(ESSA; n=2) in the early period, and resection and extended end-to-side anastomosis(EESA; n= 15) in the later period. The simultaneous closure of VSD was done with a Dacron patch(n= 16) and autologous pericardium(n=17). Aortic arch hypoplasia was present in 29 patients(88%) and its types were distal(n=18), complete(n=5), and complex(n=6)
Park, Kwang-Joo;Kim, Eun-Sook;Kim, Hyung-Jung;Chang, Joon;Ahn, Chul-Min;Kim, Sung-Kyu;Lee, Won-Young;Kim, Sang-Jin;Lee, Doo-Yun
Tuberculosis and Respiratory Diseases
/
v.44
no.2
/
pp.401-408
/
1997
Background : Pulmonary sequestration is a rare congenital malformation, which is manifested by formation of nonfunctioning lung tissue lacking normal communication with the tracheobronchial tree. The preoperative diagnostic rate has been relatively low, and without consideration of pulmonary sequestration, unexpected bleeding from aberrant vessels may be a serious problem during the operation. The purpose of our study is to describe the clinical features of pulmonary sequestration based on a review of 15 cases treated by operation. Method : Fifteen patients with pulmonary sequestration who had undergone surgical treatment from 1991 through May 1996 at Yongdong Severance Hospital and Severance Hospital were reviewed retrospectively. Results : The mean age of the patients was 22.5 years (range 5~57), and male to female ratio was 9 : 6. Clinical presentations varied from recurrent respiratory infections such as fever, cough, and sputum or chest pain to no symptom. The chest simple X-rays showed multicystic shadow(10/15) and solid mass-like shadow(5/15). The chest CT scans, done in twelve cases, showed multicystic lesion with or without lung infiltration(8/12), solid mass-like lesion(4/12), The chest MRIs, done in three cases, revealed the aberrant arteries originating from descending aorta(2/3). Aortograms, done in four cases, showed the aberrant arteries originating from descending thoracic aorta(2/4), abdominal aorta(I/4), and intercostal artery(1/4). and the venous returns were via the pulmonary veins. Pulmonary sequestration was considered preoperatively in six patients of fifteen. Other preliminary diagnosis were lung tumor(3/15), lung abscess(21/15), bronchiectasis(2/15), and mediastinal tumor(2/15). In the operative findings, twelve cases were of intralobar type and three cases of extralobar type. The left lower lobe was most often affected(9/15) and one extralobar sequestration was in the pericardium. The aberrant arteries originated from descending thoracic aorta(6/15), abdominal aorta(1/15), internal thoracic arteries (2/15), intercostal artery(1/15), pericardiophrenic artery(1/15), but in four cases, the origins could not be defined. There was no mortality or complication postoperatively. Conclusion : In our study, preoperative diagnostic rate was relatively low, and clinical features were similar to previous reports. Preoperative vigorous diagnostic approach including aortography is strongly advocated not only for its diagnostic value, but also for accurate localization of the aberrant vessels, which is major concern to surgical procedure.
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