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The authors present a review on the frequency and causes of cardiogenic systemic embolism and on the influence of damage of the central nervous system on the heart muscle. 10-20% of ischaemic cerebrovascular attacks are of cardioembolic origin. In patients with chronic atrial fibrillation the risk of a cerebrovascular attack is six times higher than in the corresponding population with a sinus rhythm. Views on the preventive administration of anticoagulants differ so far. In extensive myocardial infarctions of the anterior wall thrombi in the left ventricle are present in 30-40%. Thrombolytic treatment affects their formation; so far it is not clear whether it reduces the risk of embolization. With technical advances in echocardiography, and in particular transoesophageal echocardiography, attention is focused on abnormal findings in patients with cerebrovascular attacks without manifest heart disease. Most frequently in these patients a prolapse of the mitral valve is found, a foramen ovale patents, an aneurysm of the atrial septum, sometimes thrombi in the left auricula atrialis of an otherwise quite normal heart. A rare finding are cardiac tumours, systemic embolism being frequently their first clinical manifestation. An indicator of high risk of thromboembolism is probably a spontaneous echo contrast in the left atrium, detected reliably only from an oesophageal approach. In the second part the authors summarize contemporary knowledge on the effect of damage of the central nervous system on cardiac action. Cerebral injury or haemorrhage accompany kinetic disorders of the left ventricle of varying impact. Myocardial damage is caused by a high catecholamine level and can be prevented by administration of beta blockers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Echocardiographic findings in cerebrovascular accidents]. 175 13

The purpose of this study was to determine the most discriminating clinical and echocardiographic features that are most helpful in correctly identifying Ebstein's anomaly of the tricuspid valve from other causes of tricuspid regurgitation. Ebstein's anomaly is an uncommon malformation of the tricuspid valve with diagnostic echocardiographic features. Other cardiac disorders associated with tricuspid valve regurgitation and predominate right-sided heart chamber enlargement can be misdiagnosed as Ebstein's anomaly. All patients who were referred to our institution between 1982 and 1995 with the diagnosis of Ebstein's anomaly but were found to have other abnormalities of the tricuspid value or right ventricle were identified. Their clinical, echocardiographic, and surgical records were reviewed retrospectively. Twenty-two patients (12 males and 10 females), aged 7 to 68 years (mean 33 years), were referred to our institution with the diagnosis of Ebstein's anomaly but were found to have another abnormality that mimicked clinical and diagnostic features of Ebstein's anomaly. The most common initial symptom was exercise intolerance (13 [59%] patients) followed by atrial arrhythmia (seven [32%] patients). Two patients had cyanosis. Three patients had paroxysmal and six had chronic atrial fibrillation/flutter. Cardiomegaly on chest x-ray film was noted in 18 (82%) patients. Referral diagnosis of Ebstein's anomaly had been made by echocardiography (12 patients), cardiac catheterization (four patients), both techniques (five patients), and echocardiography and magnetic resonance imaging (one patient). All 22 patients had predominate right atrial and right ventricular enlargement, and 18 (82%) of 22 patients also had right ventricular dysfunction. However, Ebstein's anomaly was confidently ruled out with repeat comprehensive echocardiography at our institution by establishing (1) absence of significant apical displacement of the septal tricuspid valve leaflet (> or = 8 mm/m2) and (2) lack of a redundant, elongated, anterior tricuspid valve leaflet in all 22 patients (100%). All had significant tricuspid regurgitation caused by tricuspid valve dysplasia (nine patients), tricuspid valve prolapse (four patients), trauma (four patients), right ventricular dysplasia (three patients), endocarditis (one patient), and annular dilation caused by free pulmonary regurgitation (one patient). In all 15 patients who subsequently underwent surgery (tricuspid valve repair [seven patients] or replacement [eight patients]), the absence of Ebstein's anomaly was confirmed. Echocardiographic absence of the characteristic degree of displacement of the septal leaflet of the tricuspid valve (> or = 8 mm/m2) and the presence of a nonelongated, nonredundant anterior tricuspid valve leaflet consistently excluded the diagnosis of Ebstein's anomaly. Under such circumstances, other anomalies of the tricuspid valve or right ventricle were consistently identified. Recognition of the mimics of Ebstein's anomaly had important surgical implications.
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PMID:Mimics of Ebstein's anomaly. 932 9

A 61-year old man known with chronic atrial fibrillation was referred to our unit via the multidisciplinary team meeting, with severe mitral regurgitation secondary to prolapse of anterior mitral leaflet. In 1968, he had undergone right pneumonectomy due to Scimitar syndrome. Dense adhesions due to previous interventions, such as thoracotomy, make it difficult to insert ports, and this is therefore considered a relative contraindication to port access approach to the mitral valve. The anatomical position of the heart in the mediastinum was completely distorted due to the shift of the mediastinum to the right following previous surgery. Our report illustrates the operative success that can be achieved in such complex situations. Computed tomography scanning and on table transoesophageal and transthoracic echocardiography were the tools used in conjunction to achieve the best possible approach. This case promotes the use of minimal access approach in the experienced hands so that such complex procedures can be carried out without any complication and yield good results.
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PMID:Minimal access mitral valve repair in a patient with a right pneumonectomy for Scimitar syndrome. 2697 55