Síndrome de Eisenmenger em um gato / Eisenmenger syndrome in cat

A 6-month-old female, 1.0kg, uncastrated female Persian cat was brought to the Veterinary Hospital at State University of Ceara, with a history of dyspnea, prostration, hyporexia and progressive weight loss for a month. On physical examination, systolic cardiac murmur, cyanosis and dyspnea were detected. Unfortunately, the cat died during oxygen therapy. Necropsy examination revealed an increase in cardiac silhouette and ventricular septal defect of 2cm in diameter. Macroscopically the lungs were collapsed, with absent and diffusely reddish blackish crepitus, and the liver with blackish red coalescent multifocal areas, interspersed with lighter areas and lobular pattern with irregular brownish multifocal areas intercepted by brownish areas. Thus, the necropsy results together with the history and physical examination of the animal confirmed the diagnosis of Eisenmenger Syndrome, becoming the report of the first case, in a cat, in Brazil.(AU)

Eisenmenger syndrome in pregnancy

Abstract Eisenmenger syndrome is very rare in pregnant women. Debates remain concerning the management of Eisenmenger syndrome in this patient population and the prognosis is unclear in terms of maternal and fetoneonatal outcomes. Epidural analgesia is preferred for Cesarean section as it alleviates perioperative pain and reduces the pulmonary and systemic vascular resistances. Maternal mortality in the presence of Eisenmenger syndrome is reported as 30-50% and even up to 65% in those with Cesarean section. The major causes of death could be hypovolemia, thromboembolism and preeclampsia. Pregnancy should ideally be avoided in a woman with Eisenmenger syndrome concerning the high maternal mortality rate and probable poor prognosis of the baby. A short labour and an atraumatic delivery under epidural block are preferred in the women with a strong desire of pregnancy. The purpose of this article is to discuss the debates of Eisenmenger syndrome in pregnancy and the possible resolutions.

Eisenmenger syndrome: a silent killer in adults born with heart septal defect: experience from cardiac centre at Faisalabad

Eisenmenger syndrome is a term used to any large shunt between systemic and pulmonary circulation which results in high pulmonary arterial pressure and irreversible changes in pulmonary vascular bed with bidirectional shunt with physical limitation and shortness of breath. Eisenmenger syndrome particularly creates problems to fetus and mother in pregnancy and there is a particularly risk during aneasthesia while performing general surgery. We collected all consecutive patients above age 12 with atrial septal defect [ASD], ventricular septal defect [VSD] and patent ductus arteriosus [PDA] who attended echocardiography department between June 2008 to October 2010. We also analysed all pregnant females with Eisenmenger complex during this period. Out of 309 patients diagnosis of one of three shunts was confirmed either by transthorasic echocardiography with intravenous saline infusion or transesophageal echocardiography Eisenmenger syndrome was diagnosed in 39 patients [19 patients with ASD, 11 patients with VSD and 09 patients with PDA]. All 39 patients were followed till October 2010 and were alive. Among 03 pregnant females, 02 completed pregnancy without any hazard to child and mother. However tubal ligation was opted at time of delivery. One lady opted abortion and ligation to prevent further pregnancy. 05 patients underwent non cardiac surgery under general anesthesia without any complication. Eisenmenger syndrome a silent killer in a congenital treatable disease which is being neglected and diagnosis is being delayed. It seems Eisenmenger syndrome is on rise in Pakistan. We need to establish adult congenital heart disease department in each cardiac centre where trained persons should be appointed who had experience of congenital heart disease. Screening clinics need to be established at school and community level to diagnose this silent killer at a stage when pulmonary artery pressure is still reversible

Undiagnosed sinus venosus atrial septal defect giving rise to eisenmenger syndrome: a case report

Atrial septal defects are communications of variable size that occur in the heart and allow interatrial shunting. We report a 49-year-old lady with sinus venosus type ASD, diagnosed by trans-esophageal echocardiography

Hipertensão arterial pulmonar associada a cardiopatias congênitas / Pulmonary hypertension in congenital heart disease

A hipertensão arterial pulmonar é frequentemente encontrada nas cardiopatias congênitas associadas a hiperfluxo pulmonar secundário a grandes shunts da esquerda para a direita. A hipertensão pulmonar é um fator complicador importante no tratamento desses pacientes, podendo impedir a correção cirúrgica da cardiopatia naqueles com doença vascular pulmonar já estabelecida. O diagnóstico precoce e o conhecimento da história natural do defeito cardíaco usualmente levam à prevenção da doença vascular pulmonar, por permitir seu fechamento em tempo adequado. Nos pacientes com doença vascular pulmonar irreversível, o tratamento clínico convencional continua indicado, embora novos medicamentos demonstrem seus efeitos potenciais sobre variáveis hemodinâmicas e sobrevida. Após a falência ao tratamento clínico otimizado, existe a opção de transplante pulmonar.

Total Occlusion of Left Main Coronary Artery by Dilated Main Pulmonary Artery in a Patient with Severe Pulmonary Hypertension

A 34-year-old woman was admitted to the hospital because of recently aggravated right heart failure without angina for 5 months. When she was 25 years old, patch repair with Polytetrafluoroethylene (PTFE) was performed for the secondum type of atrial septal defect (ASD) with moderate pulmonary hypertension. The chest PA, echocardiography and cardiac catheterization at current admission revealed Eisenmenger syndrome without intracardiac shunt. Chest CT scan with contrast revealed markedly dilated pulmonary trunk, both pulmonary arteries and concave disfigurement of the left side of the ascending aorta suggesting extrinsic compression, as well as total occlusion of the ostium of the left main coronary artery that was retrogradly filled with collateral circulation from the right coronary artery. The coronary angiography showed normal right coronary artery and the collaterals that come out from the conus branch to the mid-left anterior descending artery (LAD) and that from distal right coronary artery to the left circumflex artery (LCX) and to the distal LAD, respectively. On aortography, the left main coronary artery was not visualized with no stump, suggestive of total occlusion of the ostium of the left main coronary artery. From our experience, it is possible to say that the occlusion of the ostium of the left main coronary can be induced by the dilated pulmonary artery trunk due to ASD with pulmonary hypertension and that, if the ASD closure was too late, the narrowing or obstruction of the left coronary artery could not be resolved even after operation owing to irreversible pulmonary hypertension.

Clinical course of isolated ventricular septal defect: an Indian experience.

To define the clinical course of ventricular septal defect, 410 consecutive patients with isolated ventricular septal defect were evaluated over a period of 13 years. Their age ranged from 12 days to 24 years at the time of first visit to the hospital. Patients with less than 2 years follow-up period were excluded. One hundred and fifty seven patients were one year of age or less. The left to right shunt size remained the same in 52.4% of cases. In 34.4% the shunt size decreased, with complete closure of ventricular septal defect in 8.8%. Closure of ventricular septal defect was observed even in patients who had initially presented with large left to right flow, and congestive heart failure in infancy. Right ventricular outflow tract obstruction developed in 8.5% of patients usually between 2 and 10 years of age. Murmur of aortic regurgitation appeared in 8.9% on follow-up. Infective endocarditis developed in 6 cases. The unfortunate complication of Eisemenger's complex was seen in 3 patients; they had not returned for follow up for a long period of time. Hence, our data show that the left to right shunt across the ventricular septal defect decreases in about one-third of patients. However, a regular follow up is essential to prevent development of Eisenmenger's complex and for early detection of other complications like aortic regurgitation and right ventricular outflow tract obstruction.