This 3-year-old girl was observed frequent exertional dyspnea and cyanosis at crying since birth. She was not premature baby and delivered at full term normally. On physical examination, she was underdeveloped-body weight 13.5 kg, height 99 cm.- and cyanotic. There was severe clubbing on fingers. There was grade II/VI ejection systolic murmur on left lateral border of the sternum. The preoperative examinations [EKG, echocardiogram, cardiac catheterization and biventriculogram] showed that complicated T.G.A. combined vena cava[S.D.D.]. Preoperatively, we decided the corrective surgery of Rastelli operation using a. pulmonary valved conduit. The operation was performed under total circulatory arrest using deep profound hypothermia combining with extracorporeal circulation. On operation, the anatomy of the heart showed that, 1. The subaortic conus was seen and subaortic muscles were hypertrophied. 2. The VSD[type II], behind the subaortic conus-about 1 cm. in diameter, was visible only through LV cavity and, 3. The pulmonary valve ring was hypoplastic and pulmonary valvular stenosis was seen also. The subpulmonic area [LV outflow tract] was obstructed with hypertrophied muscle and mitral valve. 4. Left superior vena cava was drained to RA via coronary sinus. 5. LAD coronary artery was originated from right coronary artery and ran anterior to the pulmonary artery. According to above anatomy, we performed the VSD closure with Teflon patch, and Mustard operation combined with LV-to-pulmonary artery bypass graft using the valve contained [Hancock 16 mm] conduit. Postoperatively, adequate blood pressure could be maintained under the state of using inotropic agent [epinephrine]. On the second postoperative day, the patient died of cardiac arrest due to low cardiac output syndrome, acute renal failure and pulmonary edema.
Park, Chan-Soh;Chin, Hyun-Jung;Kim, Seok-Min;Son, Chang-Woo;Yu, Sung-Ken;Chung, Jin-Hong;Lee, Kwan-Ho
Journal of Yeungnam Medical Science
/
v.25
no.1
/
pp.50-57
/
2008
Pulmonary hypertension is an increase in blood pressure in the pulmonary artery, pulmonary vein or pulmonary capillaries. Depending on the cause, pulmonary hypertension can be a severe disease with markedly decreased exercise tolerance and right-sided heart failure. Pulmonary hypertension can present as one of five different types: arterial, venous, hypoxic, thromboembolic, or miscellaneous. Chronic obstructive pulmonary disease with severe pulmonary hypertension is a rare disease. A 52-year-old man presented with a complaint of aggravating dyspnea. The mean pulmonary arterial pressure was 61.5 mmHg by Doppler echocardiogram. The patient was prescribed diuretics, digoxin, bronchodilator, sildenafil, bosentan and an oxygen supply. However, he ultimately died of cor pulmonale. Thus, diagnosis and early combination therapy are important.
Certain oriental medication have been shown to be effective in decreasing pulmonary vascular resistance and increasing cardiac output in primary pulmonary artery pressure secondary to pulmonary edema. So oleic acid was administered in 14 dogs in order to induce acute lung injury. And we studied the hemodynamics and blood gas changes of Pyengpaetang(50mg, 100mg) with continuous postive pressure was ventilation in pulmonary edema. The pulmonary edema group, arterial oxygenation was improved after 5 and $10cmH_2O$ PEEP(positive end expiratory pressure), but cardiovascular system was depressed. Blood pressure and cardiac output were decreased, and CVP, MP AP, PCWP were increased. In Pyengpaetang(50mg) group, mean aortic pressure was decreased and PCWP(pulmonary capillary wedge pressure) was decreased remarkably, while there was a significant increase in cardiac output. And there was improvement in $PaO_2$ and $PaCO_2$ without hemodynamic changes after applying 5cm $H_2O$ PEEP, but arterial blood gases$(PaO_2,\;PaCO_2)$ were improved, while cardiovascular effects were depressed after cm $H_2O$ PEEP. In Pyengpaetang(100mg) treated group, there was no significant hemodynamic change. But mean pulmonary arterial pressure was significantly increased, and cardiac output was decreased significantly after applying the more degree of PEEP. And blood gases were not changed significantly after applying the more degree of PEEP. The above results suggest that the effects of Pyengpaetang(50mg) group is superior to those of Pyengpaetang(100mg) group on the effects of hemodynamics and gas exchanges in acute lung injury in dogs. So we can conclude that lower degree PEEP 5cm $H_2O$ is more beneficial in Pyengpaetang(50mg) treated group.
Background: Despite the relatively high mortality rates in the chronic heart failure model induced by coronary artery ligation are relatively high, this model has been a subject of continuos research because of its clinical correlation. Chronic heart failure model of large-sized animals is very useful to analyse mechanical or biological effects on circulatory system which is difficult in small-sized animals. The purpose of this study is to establish the heart failure model by coronary artery ligation in sheep. Material and Method: Among 9 Corridale sheep, the homonymous artery and the diagonal branch were ligated simultaneously in 2 sheep and remaining 7 sheep were assigned to successive ligation of both arteries at an interval of 1 hour. Both coronary arteries were ligated from the point 40% proximal to the apex of the heart. Hemodynamic and echocardiographic parameters were analyzed before the ligation of the coronary artery, after the ligation of the homonymous artery, and after additional ligation of the diagonal branch. The experimental animals were sacrificed after 2 or 3 months of growth and histopathologic studies were performed Result: Immediate postoperative death occurred in the 2 sheep that had received simultaneous ligation of the homonymous artery and diagonal branch. On the other hand, all the 7 sheep that were lifated in succession were survived up to 3 months. Arterial pressure was sifnificantly decreased immediately after ligation of the homonymous artery(p<0.05), and the cardiac output was decreased and pulmonary capillary wedge pressure was increased after further ligation of the diagonal branch(p<0.05). Central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, left ventricular end-diastolic dimension and end-systolic dimension were markedly increased 3 months after ligation of coronary arteries. Anteroseptal akinesia or dyskinesia was developed after the ligation of coronary arteries. Histopathologic study revealed we]1-demarcated ischemic area of fibrosis. Conclusion: Using methods of successive ligation of the homonymous artery and diagonal branch, chronic heart failure model could be reliably established in sheep.
BACKGROUND: Right ventricular (RV) dysfunction is a significant risk of major adverse cardiac events in patients with acute heart failure (AHF). In this study, we evaluated RV-pulmonary artery (PA) coupling, assessed by tricuspid annular plane systolic excursion (TAPSE)/pulmonary artery systolic pressure (PASP) and assessed its prognostic significance, in AHF patients. METHODS: We measured the TAPSE/PASP ratio and analyzed its correlations with other echocardiographic parameters. Additionally, we assessed its prognostic role in AHF patients. RESULTS: A total of 1147 patients were included in the analysis (575 men, aged 70.81 ± 13.56 years). TAPSE/PASP ratio exhibited significant correlations with left ventricular (LV) ejection fraction(r = 0.243, p < 0.001), left atrial (LA) diameter(r = -0.320, p < 0.001), left atrial global longitudinal strain (LAGLS, r = 0.496, p < 0.001), mitral E/E' ratio(r = -0.337, p < 0.001), and right ventricular fractional area change (RVFAC, r = 0.496, p < 0.001). During the median follow-up duration of 29.0 months, a total of 387 patients (33.7%) died. In the univariate analysis, PASP, TAPSE, and TAPSE/PASP ratio were significant predictors of mortality. After the multivariate analysis, TAPSE/PASP ratio remained a statistically significant parameter for all-cause mortality (hazard ratio [HR], 0.453; p = 0.037) after adjusting for other parameters. In the receiver operating curve analysis, the optimal cut-off level of TAPSE/PASP ratio for predicting mortality was 0.33 (area under the curve = 0.576, p < 0.001), with a sensitivity of 65% and a specificity of 47%. TAPSE/PASP ratio < 0.33 was associated with an increased risk of mortality after adjusting for other variables (HR, 1.306; p = 0.025). CONCLUSIONS: In AHF patients, TAPSE/PASP ratio demonstrated significant associations with RVFAC, LA diameter and LAGLS. Moreover, a decreased TAPSE/PASP ratio < 0.33 was identified as a poor prognostic factor for mortality.
This is one case report of the extremely rare congenital cardiac malformation, Double-outlet of left ventricle in corrected transposition of great arteries. 11-year-old boy complained acrocyanosis and exertional dyspnea, the parents noticed cyanosis since birth. Physical examination revealed acrocyanosis, clubbed fingers and toes, G-III pansystolic murmur on 2nd and 3rd ICS, LSB. Right heart catheterization revealed significant $O_2$ jump in ventricular level. Right and left ventriculography showed the both catheters arriving in the same ventricle i.e. anterior chamber, morphological left ventricle was in right and anterior position, simultaneous visualization of aorta and pulmonary artery and aorta locating anterior and right side of pulmonary artery. Echo cardiogram surely disclosed interventricular septum. Conclusively it was clarified that the patient has Double-outlet of left ventricle and corrected transposition of great arteries [S.L.D.]. Operation was performed to correct the anomalies under extracorporeal circulation with intermittent moderate hypothermia. Right-sided ventriculotomy disclosed the following findings. 1. Right-sided ventricle was morphological left ventricle. 2. Left-sided ventricle was morphological right ventricle. 3. Right side atrioventricular valve was bicuspid. 4. Left side atrioventricular valve was tricuspid. 5. Aortic valve was superior, anterior and right side of pulmonary valve. 6. Subpulmonary membranous stenosis. 7. Non-committed ventricular septal defect. We made a tunnel between VSD and aorta with Teflon patch so that arterial blood comes through VSD and the tunnel into aorta. After correction the patient needed assisted circulation for 135 min. to have adequate blood pressure. Postoperatively by any means, adequate blood pressure could not be maintained and expired in the evening of operation day.
From January 1989 to December 1993, cardiac catheterization and open heart surgery for ventricular septal defect closure were performed in 115 pediatric patients who were selected as meeting the criteria for elective closure of restrictive ventricular septal defect. These criteria included age greater than 1 year and less than 15 years, no evidence of congestive heart failure, Qp/Qs 2.0, pulmonary artery systolic pressure 35mmHg, and no associated cardiac anomalies. Mean age of patients was 5.25$\pm$ 3.53, and 72 patients were male, 43 patients were female[male:female=1.9:1 . Mean systolic pulmonary artery pressure was 19.66$\pm$4.79mmHg, and mean pulmonary to systemic flow ratio was 1.27$\pm$ 0.28. Aortic cusp prolapse was present in 30 patients [26% , aortic insufficiency was present in 1 paient, and 1 patient had prior bacterial endocarditis. There were no instances of complete atrioventricular dissociation, reoperations for bleeding, or reoperations for recurrent ventricular septal defect, but wound infection was present in 1 patient, and there were 7 patients who had the hemodynamically insignificant remnant shunt. There were no early or late deaths or major morbidity.
Between September 1986, and August 1989, eight infants underwent operation for repair of coarctation of the aorta in the first year of life. The patients included 7 males and 1 female ranging in age 19 days and 9 months. Weights ranged from 3.5 Kg to 7 Kg [mean 5 Kg]. All patients had preductal coarctation of the aorta. Each infant had associated cardiac anomalies, including ventricular septal defect [7 infants] and patent ductus arteriosus [5 infants]. All had intractable congestive heart failure, despite aggressive medical therapy. Pressure gradient across the coarctation ranged from 10 mmHg to 60 mmHg. Operative techniques were subclavian flap aortoplasty in five cases, Gore-Tex patch aortoplasty in three cases. In addition to coarctation repair, six infants had concomitant banding of the pulmonary artery. Four infants required ventilator support for several days. There was no operative death. Complications developed in two. One infant had tracheal stenosis after a tracheostomy. Another infant had restenosis of the aorta revealed by cardiac catheterization 30 months after surgery. The pressure gradient was 30 mmHg, necessitating balloon dilatation aortoplasty. Results were satisfactory. During follow up, we performed total correction procedures [patch closure of the ventricular septal defect, infundibulectomy, pulmonary valvotomy and pulmonary artery angioplasty] in one case. Continuing follow-up finds all patients in good condition.
The effect of captopril on the lung angiotensin converting enzyme (ACE) was investigated after 3 weeks oral administration (120~160 mg/kg/day) through drinking water in SpragueDawley rats. On the $^{125}$I-351A, an ACE inhibitor, binding assay in the isolated perpused lungs, the number of ACE molecules at the intrapulmonary endothelial cell surface was significantly decreased (p<0.001), and recovered to the normal level 7 days after discontinuation of captopril treatment. Intrapulmonary conversion ratio of Al to All was also significantly decreased (p<0.05) in the isolated perpused lungs. Bolus intravenous injection of angiotensin I did not showed pressor response in the both of systemic and pulmonary blood pressure of the anesthetized rats. ACE activity of the lung homogenates was also significantly reduced. These data consistently indicate the decrease of functionally active ACE molecule at the pulmonary artery after chronic captopril treatment. However, serum ACE activity was increased three fold in captopril treated rats compared to the normal rats. So, these results suggest that the functionally active ACE molecule at the pulmonary artery was still inhibited, which is directly associated with the antihypertensive effects, even if the total angiotensn converting enzyme induction was resulted after chronic captopril treatment.
The Fontan procedure was physiological correction which was initially applied to tricuspid atresia. We had used the modified Fontan operation in 8 cases at National Medical Center, Seoul, from Aug. 1984 to Oct. 1986. Age range was 20 months to 15 years [mean: 9 years] and male: female ratio was 5:3. 5 patients had tricuspid atresia [lb: 2 cases, Ic: 1 case, lib: 1 case, & llc: 1 case], 2 Patients had univentricular heart of left ventricular type, and one patient had transposition of great arteries with complete endocardial cushion defect. The operative principle was direct anastomosis between right atrium and pulmonary artery, whether main pulmonary artery or right pulmonary artery without any conduits. Postoperatively all patients needed high central venous pressure for adequate hemodynamic status in both survival [20-24 CmH2O] and mortality groups [20-24 CmH2O]. The fatal complications were as follows: empyema with bronchopleural fistula [1 case], bleeding tendency & brain damage [1 case], low cardiac output syndrome & acute renal failure [2 cases], and right to left shunt of unknown origin [1 case]. There were 5 hospital deaths; 3 of 5 tricuspid atresia patients, 1 of 2 univentricular heart patients, and 1 of 1 transposition of great arteries with complete endocar4ial cushion defect patient. The overall mortality was 62.5%. 3 survivors were nearly compatible with Choussat & Fontan criteria. Thus appropriate patient selection and experienced surgical technique were required for good results.
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