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Ebstein's anomaly is a congenital heart defect in which the septal and posterior leaflets of the tricuspid valve are displaced downwards towards the apex of the right ventricle of the heart. [1] EA has great anatomical heterogeneity that generates a wide spectrum of clinical features at presentation and is complicated by the fact that the ...
EBV+ LG usually (~90% of cases) presents as a lung disorder with coughing, hemoptysis, shortness of breath, and chest X-rays showing multiple nodular lesions at the base of both lungs. It may also evidence signs and symptoms caused by nodular or infiltrative lesions in the skin, central nervous system, [36] kidney, liver, [1] and/or peripheral ...
English: 12-lead ECG of a woman with Ebstein's anomaly (a congenital heart defect in which the opening of the tricuspid valve is displaced towards the apex of the right ventricle of the heart, resulting in a large right atrium). The ECG shows signs of right atrial enlargement, best seen in V1.
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Ebstein's anomaly [31] – about 50% of individuals with Ebstein anomaly have an associated shunt between the right and left atria, either an atrial septal defect or a patent foramen ovale. [32] Fetal alcohol syndrome – about one in four patients with fetal alcohol syndrome has either an ASD or a ventricular septal defect. [33]
Signs and symptoms depend on the specific type of defect. [3] Symptoms can vary from none to life-threatening. [7] When present, symptoms are variable and may include rapid breathing, bluish skin , poor weight gain, and feeling tired. [2] CHD does not cause chest pain. [2] Most congenital heart defects are not associated with other diseases. [3]
The symptoms and the severity of these symptoms vary between patients where most patients experience nephritis in childhood and then progress to kidney failure in adolescence. [5] In macrothrombocytopenia platelet sizes can reach to approximately 6.6 um compared to a normal platelet size of 2.5 um where 30% platelets can reach the size of an ...
The condition is named after Wilhelm Ebstein and P. K. Pel who both published papers in 1887 noting the phenomenon. [5] [6] [7] Both doctors published in the same journal, though Pel published first by several months. A long-term dispute persisted between Pel and Ebstein on the etiology of the condition. [citation needed]