ABSTRACT
Introduction: One in six ischemic strokes is caused bycardiogenic embolism. The current knowledge regardingthe natural history, diagnosis, prevention, and treatment ofcardioembolic stroke is reviewed in this study. Nonrheumaticatrial fibrillation is the most frequent substrate for brainembolism and patients with this dysrhythmia have a fivefoldincrease in the risk of stroke. Study aimed to evaluate theclinical assessment of the patients with ischemic stroke lessthan 45 years of age.Material and Methods: 50 patients who were admitted inthe medical and neurology wards of Govt. Stanley medicalcollege, Chennai during the study period from December 2003to May 2004 for ischaemic stroke were clinically examined.The inclusion and exclusion criteria were satisfied, resultswere clinically and statistically assessed and the relevance oftransthoracic echocardiography was studied in them.Results: Cardiogenic embolism mostly affects the malepopulation more frequently and the most commonly affectedage group is 30-45 years. The clinically identifiable cardiaclesion was present in 77% of the cases. The most commondisease is rheumatic valvular disease as seen in about 5 casesfollowed by ischemic heart disease which was found in about3 cases. Abnormal ECG findings were observed in 12% ofcases in the form of atrial fibrillation. Left atrial enlargement,old infarct changes, conduction abnormality and recurrentstroke(12%) were the other findings. In these, 66% (4 cases)were due to the cardioembolic origin. The echocardiographicstudy increases the sensitivity of detecting cardiac lesion by22%.Conclusion: Cardiac lesion accounts for 36% of brainembolism. Hemiparesis is the most common presentation(88% of cases) followed by Hemiplegia. The middle cerebralartery is most commonly affected by embolism. Rheumaticheart disease (39%) and Ischemic heart disease are theimportant causes of brain embolism in this study.
ABSTRACT
A 69-year-old woman had syncope and aphasia. Magnetic resonance imaging showed multiple cerebral infarctions in both hemispheres. Cardiogenic embolisms were suspected, but no arrhythmic causes were shown. Transesophageal echocardiography revealed a highly calcified mitral annulus (MAC) with a rough intraluminal surface and mild mitral regurgitation, but no thrombus or tumor in the left heart system. However, recurrent multiple cerebral embolisms occurred in spite of strict anticoagulation therapy. We speculated that spontaneous rupture of the MAC was the cause of the scattered cerebral embolisms, and we therefore planned to remove the MAC as safely as possible and to endothelialize the deficit of MAC with autologous pericardium. Operative findings revealed that the MAC in P2-P3 had ruptured longitudinally and the ostium of the left atrium was connected to the ostium of the left ventricle as an inter-atrioventricular tunnel beneath the posterior mitral annulus with a fragile calcified wall. The finding suggested that calcified particles that had peeled away from the MAC by normal heart beating resulted in the cerebral infarctions. Therefore, she underwent resection of the MAC and mitral valve replacement with reinforcement of the decalcified posterior mitral annulus between the posterior left ventricular wall and the left atrial wall using autologous pericardium, which enabled both appropriate insertion of a mechanical prosthetic valve and endothelial continuity covering the surface of the residual MAC. No systemic embolism has occurred for two and a half years after surgery. This is the first case report of cerebral embolism caused by a spontaneously ruptured MAC.