Location: Home> Login Global Select Abstract Title: Patients with hypoplastic left heart ventricular function deterioration and repeated narrowing of Ann Thorac Surg, 2008 of: Larrazabal LA, Tierney ESS, Brown DW content preview: AbstractBackground: Recurrent coarctation (re- CoA) after stage I palliation in hypoplastic left heart syndrome (HLHS) is deleterious. We studied whether re-CoA had an effect on ventricular systolic function.Methods: Retrospectively reviewed were HLHS patients surviving stage I Norwood palliation (stage I) and cavopulmonary shunt (CPS) between January 2004 and February 2007. Echocardiographic right ventricular fractional area change (RV-FAC) was used to evaluate ventricular systolic function after stage I, before CPS, and before Fontan procedures. Cardiac catheterization and magnetic resonance imaging data before CPS were reviewed to assess re-CoA, using a coarctation index (CI = isthmus diameter / descending aortic diameter). Results: Fifty-one patients were included, and 21 had a CI of less . Please log in to read full text
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Hypoplastic left heart is what causes it?
Hypoplastic left heart is a rare and complex congenital cardiovascular malformations. The genetic disease is related to family history, the complex is between compatriots 0.5% incidence of twins at the same time. This is also a single gene mutation that teratogenic. Pathogenesis is unknown, probably in the fetal ductus arteriosus diameter of the large, large number of blood through the ductus arteriosus is not closed into the descending aorta or the atrial septum and foramen ovale close early, so enter the left heart and aortic arch blood flow reduction the formation of hypoplastic left heart.
What is hypoplastic left heart performance and how to diagnose?
The main pathological features of this disease as follows: atresia or severe aortic stenosis and hypoplastic ascending aorta, about 35 to 80% of cases associated with coarctation of the aorta. mitral valve atresia or hypoplasia. Left Ventricular development. right half of the performance of the right ventricular hypertrophy, atrial and ventricular increased, especially abnormal expansion of pulmonary artery. there thick patent ductus arteriosus, atrial septal defect or patent foramen ovale.
Category: UrbaN and ScHwarzenberg the intrinsic divided into five categories:
︱ Aortic atresia
a. mitral valve hypoplasia or stenosis with
b. with mitral
a. normal aortic mouth
b. associated with aortic valve stenosis
aortic arch hypoplasia
V atresia or aortic arch amputation
Noonan is divided into two categories
Aortic atresia or severe stenosis
Hemodynamics: In hypoplastic left heart, the right atrium and also accept, on the back to the inferior vena cava blood and left atrial septal defect by the inflow of blood. Therefore, systemic and pulmonary venous blood mix in the right atrium from the right ventricle pumps into the lungs after the artery and the left and right pulmonary artery and ductus arteriosus by the thick smooth line into the descending aorta, ascending aorta and retrograde coronary perfusion. Atrial septal defect and patent ductus arteriosus flow is the second punishment children completed hypoplastic left heart and pulmonary circulation during the pre-conditions. Atrial septal defect and the sub-flow and arterial oxygen saturation were associated with atrial septal defect is proportional to the size. After birth, the pulmonary vascular resistance decreased significantly, Pulmonary blood flow, and often accompanied by coarctation of the aorta and patent ductus arteriosus closure, it is systemic vascular resistance is higher. And pulmonary blood flow ratio imbalance, resulting in pulmonary congestion, pulmonary edema and congestive heart failure, and organ hypoperfusion, hypoxemia and acidosis occurs, and ultimately death.
Normal full-term children for children, but there a few hours after birth, progressive cyanosis, shortness of breath or breathing difficulties and heart failure performance. No specific cardiac auscultation noise. Pulmonary valve area 2 tone hyperthyroidism, a single. Thin pulse. Accompanied by acidosis, hypoglycemia, hypoxemia, and shock. If a large atrial septal defect when the sub-flow, cyanosis may be obvious, less hypoxemia. About 90% of the children if prompt diagnosis and treatment is often within 1 month after birth, died.
Hypoplastic left heart check what should be done?
Chest X-ray: Shows the right atrium and right ventricle increased heart shadow spherical, pulmonary congestion, pulmonary edema.
ECG: p wave height sharp, right axis deviation and right ventricular hypertrophy.
Echocardiography: Two-dimensional imaging shows a huge right atrium and right ventricle, and left ventricular cavity is small wall thickness, mitral valve dysplasia, small ascending aorta and arch.
Right heart catheterization: the level of atrial shunt can be displayed and confirmed the presence of patent ductus arteriosus, but the pressure of circulation and oxygen saturation close to the pulmonary circulation, then the atrial shunt can not be measured.
Cardiovascular Imaging; pulmonary artery catheter angiography can be found into the aortic coarctation of the aorta can be displayed. Retrograde aortic angiography showed the ascending aorta and aortic arch hypoplasia or coarctation of the aorta with or amputation. Left atrial angiography can understand the developmental status of mitral valve.
Hypoplastic left heart disease easily confused with what?
The disease to be with aortic, mitral phase identification.
Artery valve insufficiency in patients with left ventricular diastolic blood while receiving an additional left atrium to accept the blood from the aortic regurgitation, leading to left ventricular diastolic volume increases, left ventricular myofibrils section as compensatory mechanisms, a centrifugal left ventricular hypertrophy, left ventricular compliance increased to gradually adapt to chronic left ventricular volume overload, guarantee - left ventricular end-diastolic volume and left ventricular end-diastolic pressure increased in the normal range, this compensatory mechanism to maintain myocardial for a long time, resulting in asymptomatic patients. But with the progression of ventricular hypertrophy caused by the aggravation of left ventricular endocardium under the major regions, with left ventricular systolic and diastolic dysfunction, symptoms, and soon left ventricular dysfunction is irreversible; Therefore, such compensatory mechanism for cardiac patients are often in a very long period of time without any symptoms due to failure to timely treatment. Once symptoms appear, and soon lead to irreversible changes in left ventricular function, even if the surgery, the prognosis is relatively poor.
Coronary Heart Disease Transcatheter check about 3% of mitral regurgitation. Mitral regurgitation caused by coronary heart disease may be acute or chronic ischemia caused by papillary muscle. Myocardial infarction, papillary muscle may be due to acute ischemic necrosis in a few hours completely broken. Although the valve leaflets and chordae no abnormal lesions, but the corresponding loss of parts of the mitral valve leaflets open and close function, in the event of early stage after infarction showed severe mitral regurgitation. In cases of acute myocardial infarction due to papillary muscle rupture and died suddenly of severe mitral regurgitation account for about 0.4 to 5%. Although some patients caused by myocardial infarction papillary muscle necrosis, but not immediately and completely broken, or due to chronic ischemia, necrosis of cardiac tissue is gradually replaced by fibrous tissue, papillary muscle thinning, elongation, reduction or loss of systolic function, in cardiac embolism more than 2 months after mitral regurgitation was present. Early symptoms can be intermittent disease occurs, then the degree of mitral regurgitation gradually increased. Ventricle and left atrium was enlarged and showed heart failure cardiac dysfunction.
Hypoplastic left heart how to prevent it?
The disease is congenital cardiovascular malformations, no effective preventive measures. Early detection, early diagnosis and early treatment are the only measures to treat the disease.
Hypoplastic left heart can be complicated by the diseases?
The disease is often accompanied by acidosis, hypoglycemia, hypoxemia, and shock. If a large atrial septal defect when the sub-flow, cyanosis may be obvious, less hypoxemia. About 90% of the children if prompt diagnosis and treatment is often within 1 month after birth, died.
Hypoplastic left heart should be treated?
Preoperative treatment: a clear diagnosis of the prostaglandin E10.01 g / (kg min) continuous intravenous infusion, control about 21% oxygen concentration, the purpose is to promote arterial catheter remain open, to avoid over-ventilation using a ventilator to maintain arterial partial pressure of carbon dioxide in the 4.0 ~ 5.33kPa (30 ~ 40mmHg) than to promote pulmonary vasoconstriction, increased resistance, decreased pulmonary blood flow, thereby increasing the arterial catheter into the descending aorta blood flow. Maintaining water, electrolyte and blood pH and other normal indicators, requiring oxygen saturation of 80 to 85%.
Surgery as the only effective method. As early neonatal pulmonary vascular resistance higher operative mortality of radical correction of the high purposes of staging surgery Guchang.
Combination of the first phase of cardiopulmonary bypass surgery in low temperature or under deep hypothermic circulatory arrest may be through pulmonary artery or arterial catheter and right atrial cannulation to establish cardiopulmonary bypass. The basic principles of operation are as follows: removed most of the atrial septum, the shape of a large atrial septal defect or a similar single atrium, eliminating the left and right atrial pressure, left atrial blood flow to the right to enter the mixing room to improve the oxygen saturation degrees. aortic arch coarctation of the aorta and the lifting of forming lesions: right innominate artery to the descending aorta starting at the aortic arch, along the lower edge of the upper longitudinal incision, and the level of the flat transverse sinus lack of pulmonary artery, distal pulmonary artery sutured incision proximal artificial fabrics (Gortex or PTFE) patch and the aortic arch incision, the lower edge of the match, the right ventricle can flow smoothly into the aorta and coronary arteries. However, consistent and easy bleeding or artificial fabric folding of blood flow. Therefore, the pulmonary artery incision JoNas under such move on the level of pulmonary valve and pulmonary artery bifurcation in the cross-sectional, will be cut after the replacement of pulmonary artery wall of artificial fabrics, to expand the reconstruction of the aortic arch and connected with the right ventricular outflow tract. Lau reported in pulmonary artery posterior wall of the longitudinal incision, re-4mm of the pulmonary artery and pulmonary artery for anastomosis with the aortic arch. ligation of patent ductus arteriosus, re-fit body - pulmonary shunt pathway, early implementation of more pulmonary artery and right subclavian artery anastomosis (Blalock-Taussimg surgery), in recent years, respected central shunt, that is, between the aorta and pulmonary artery for 3 ~ 4mm in shunt.
Postoperative treatment: Early If there is excessive pulmonary blood, pulmonary vascular resistance by increasing the pressure and to reduce pulmonary blood flow. 21% of inhaled oxygen given to maintain partial pressure of carbon dioxide higher than the 4.0 ~ 5.33kPa (30 ~ 40mmHg). Treatment of metabolic acidosis, increased assisted ventilation when PEEP. If it is found for the reconstruction of the pulmonary artery diameter caused by excessive pulmonary blood too, may be a pulmonary artery cerclage. If there is too little pulmonary blood, were treated with pure oxygen hyperventilation to reduce carbon dioxide partial pressure required to 4.0kPa (30mmHg) below, to promote pulmonary vasodilation, resistance decreased adrenergic drugs can increase vascular resistance, thereby increasing the pulmonary shunt ratio, increase of pulmonary blood. However, if systemic vascular resistance less than 8.67kPa (65mmHg), and carbon dioxide partial pressure of less than 2.67 ~ 3.33kPa (20 ~ 25mmHg), compared with stoma is too small, conservative treatment with poor prognosis.
Half a year after routine cardiac catheterization were reviewed and, if found too small atrial septal defect or aortic stenosis, may further the purposes of balloon catheter dilation.
Physiological correction of technique: the first takes 12 to 18 months after surgery may be a rational correction of Shi Xingsheng surgery. Surgical methods: septal resection, line patch to the left atrium through the tricuspid valve port into the blood room right ventricle, atrial septal defect repair. suture ligation or the main pulmonary artery shunt site, keep right ventricular outflow tract or proximal pulmonary artery and aortic arch anastomosis, the right ventricle to the blood supply to the systemic circulation. Ministry of right atrial appendage and right pulmonary artery anastomosis, anterior pericardium patch can be used to expand or valved external conduit connecting the modified Fontan operation. Determine the level of pulmonary artery pressure key to the success of surgery.
The physiological correction of about 1 / 5 cases, receive a more satisfactory outcome, but the long-term right ventricular pressure to withstand the systemic circulation, and its long-term effects have yet to be followed up.
Heart transplantation is an effective radical surgery.