==== Front Ann Saudi MedAnn Saudi MedAnnals of Saudi Medicine0256-49470975-4466King Faisal Specialist Hospital and Research Centre 1652187410.5144/0256-4947.2006.43asm-1-43Brief ReportCardiac sources of embolic cerebral infarction in transesophageal echocardiography Zibaeenezhad Mohammad Javad *Mowla Ashkan *Salahi R. *Nikseresht Ali Reza †Shariat Hamid †Ashjaezadeh Nahid †Banani Seyyed Javad * * Cardiovascular Research Centre, Shiraz, Iran † Department of Neurology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, IranCorrespondence: Mohammad Javad Zibaeenezhad, MD, AFACA, P.O. Box 71935-1161, Cardiovascular Research Center, Nemazi Hospital, Shiraz, Iran, Fax: +98-711-230-7594, zibaeem2@sums.ac.irJan-Feb 2006 26 1 43 45 01 8 2005 Copyright © 2006, Annals of Saudi Medicine2006This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. ==== Body Previous reports have suggested that 6% to 39% of ischemic strokes are caused by cardiogenic emboli.1 Thrombus formation associated with atrial fibrillation has been reported as one of the most important cardiac sources of embolism.2 Using transesophageal echocardiography (TEE), other possible sources of embolism, including atrial septal aneurysm,3 patent foramen ovale (PFO),4 aortic atherosclerotic plaque,5 annular calcification of the mitral valve,6 mitral valve prolapse (MVP),7 prosthetic cardiac valves and endocarditis,8 mural thrombi,9 cardiac tumors,10 and cardiac transplants11 have been reported as risk factors for ischemic stroke. TEE is considered more sensitive than transthoracic echocardiography (TTE) in detecting cardiac abnormalities in patients with stroke and transient ischemic attacks.12 As there is no data available in Iran regarding TEE findings after embolic cerebrovascular accident (CVA), this study was undertaken to assess the prevalence of cardiac abnormalities by the TEE technique in patients with stroke. Patients and Methods Between September 2001 and July 2002, 98 consecutive patients, including 54 males and 44 females (mean age, 50.82 ± 18.1, years; range, 16–81 years) admitted to the neurology ward of Nemazi Hospital of Shiraz University of Medical Sciences, Shiraz, Iran were prospectively enrolled in this study. The inclusion criteria were: 1) completed embolic CVA confirmed by two expert neurologists considering neurological deficits, age of the patient, the form of the lesion in a computed tomography (CT) scan 12 hours after the beginning signs and symptoms of CVA, the existence of risk factors for defining embolic CVA from other types of CVA, the ability of patients to cooperate, and the patient’s consent to undergo a detailed etiological investigation. Patients with hemorrhagic stroke proven by MRI or brain CT scanning, were excluded from the study. All patients underwent a general medical examination, electrocardiogram, general blood chemistries and complete blood count, and TEE using a standard protocol. Established risk factors for stroke such as hypertension, diabetes, a history of myocardial infarction, hypercholesterolemia, alcoholism, obesity and smoking habits were assessed. TEE was performed with a 5.0 MHz biplane probe using air contrast, introduced after topical oropharyngeal anesthesia. Cardiac pathologies were evaluated and the echocardiographic images were recorded for later analysis. No complications occurred during TEE. Statistical analyses were performed using SPSS version 8.01-J (SPSS, Chicago, IL). Results Five patients (5.1%) had no significant pathology by TEE. The most prevalent congenital abnormality was PFO (Table 1) and the least frequent was ventricular septal defect (VSD). Valvular findings included mitral regurgitation and mitral valve vegetation associated with a prosthetic valve (Table 2). Among the other cardiac pathologies, the most prevalent abnormality was decreased left ventricular systolic function and the least was pericardial effusion (Table 3). More thrombi were observed in the left ventricle (6 patients) than the left atrium (2 patients), and the presence of any masses was more common in the left atrium and ventricle (2 patients for each) than the right atrium (1 patient). Discussion This study confirmed earlier observations that patients with a clinical diagnosis of embolic stroke have a high prevalence of certain specific cardiac abnormalities found by TEE. Left atrial and ventricular thrombi, atrial septal aneurysm, atrial septal defect, PFO and MVP have all been reported as possible sources of cerebral embolism.13 Barkin et al demonstrated that the frequency of cerebral infarction was 28% in patients with atrial septal aneurysm.14 In the present study, atrial septal aneurysm was detected in 3% of patients, which can be expected based on previous studies that include a wide age range of patients.15–18 PFO is present in 3.2% to 22% (average 12%) of normal subjects by TEE.19 Left atrial pressure may remain higher than the right atrial pressure after the Valsalva maneuver in some PFO cases. In this study, we found that the overall prevalence of PFO was similar to that previously reported in all age groups. Several investigators have reported a strong association between atherosclerotic plaque of the aorta and ischemic stroke.16 Large and complex atheromas are reported to be risk factors for aorta-arterial embolization.21 We found aortic atheromas in 4% of our patients, supporting other reports.21 TEE is obviously useful for assessing the hemodynamic consequences of the lesions and can detect giant ball thrombi associated with mitral stenosis. Mitral stenosis leads to disturbed flow, which can be detected with TEE. TEE is useful for difficult cases, such as those with rheumatic involvement of the valves but is limited in stenosis, or in those with only mild or moderate mitral regurgitation, especially in patients who have other apparent risk factors for the event. In some echogenic patients with mitral stenosis or a mitral valve prosthesis, these echoes appear to overflow into the left ventricle,22 and they can also be detected in the body of dyskinetic ventricles. In some circumstances platelet aggregation may contribute toward this phenomena. These echoes can coexist with intracardiac thrombus and be associated with an increased risk of systemic embolism.23 Annular calcification of the mitral valve is also believed by some to be associated with embolic events. This abnormality is relatively common, especially in elderly women and is associated with enlargement of the left atrium and atrial fibrillation leading to left atrial thrombus formation. It is also associated with aortic stenosis, mitral regurgitation and thromboembolism.6 Embolic stroke in young patients with mitral prolapse is reported to be associated with atrial septal defect, PFO and atrial septal aneurysm, which are all alternative sources for a presumed embolic event.24 Table 1 TEE congenital abnormalities in patients with embolic cerebrovascular accident. TEE findings Number Percent (%) Patent foramen ovale 9 9.1 Bicuspid aortic valve 6 6.1 Atrial septal defect 3 3 Ventricular septal defect 2 2 Aneurismal interatrial septum 2 2 Table 2 TEE valvular abnormalities in patients with embolic cerebrovascular accident. TEE findings Number Percent (%) Mitral regurgitation 51 52 Mitral valve prolapse 31 31.6 Mitral stenosis 8 8.1 Thick aortic valve 6 6.1 Aortic stenosis 5 5.1 Mass on aortic valve 7 7.1 Prolapse of aortic valve 2 2 Mitral valve vegetation (prosthetic valve) 1 1 Table 3 Other TEE findings in patients with embolic cerebrovascular accident. TEE findings Number Percent (%) Decreased left ventricular systolic function 12 12.2 Clot 8 8.1 Mass in LV* or LA** 5 5.1 Aorta atherosclerosis 4 4 Left ventricular hypertrophy 3 3 Pericardial effusion 1 1 * Left ventricle ** Left atrium ==== Refs References 1 Hart RG Cardiogenic embolism to the brain Lancet 1992 339 589 594 1347101 2 Fatkin D Kelly RP Feneley MP Relation between left atrial appendage blood flow velocity, spontaneous schocardiographic contrast and thromboembolic risk in vivo J Am Coll Cardiol 1994 23 961 969 8106703 3 Mugge A Daniel WG Atrial septal aneurysm in adult patients: a milticenter study using transthoracic and TEE Circulation 1995 91 2785 2792 7758185 4 Hanna JP Sun JP Patent foramen ovale and brain infarction: echocardiographic predictors, recurrence and prevention Stroke 1994 25 782 786 8160221 5 The French study of aortic plaque in stroke group Atherosclerotic disease of the aortic arch as a risk factor for recurrent ischemic stroke N Eng J Med 1996 334 1216 1221 6 Aronow WS Mitral annular calcification: significant and worth acting upon Geriat 1991 46 73 86 7 Rahko PS Xu QB Increased prevalence of atrial septal aneurysm in mitral valve prolapse Am J Cardiol 1990 66 235 237 2091625 8 Keyser DL Biller J Neurologic complications of late prosthetic valve endocarditis Stroke 1990 21 472 475 2309273 9 Vechio C Chiarella F Left ventricular thrombus in anterior acute MI after thrombolysis Circulation 1991 84 512 519 1860196 10 Verkkala K Primary cardiac tumors: operative treatment of 20 patients Cardiovasc Surg 1989 37 361 364 11 Counihan PJ Yelland A Infective endocarditis in a heart transplant recipient J Heart Lung Transplant 1991 10 275 279 2031925 12 Streifler JY Katz M Cardiogenic cerebral embolic: diagnosis and treatment Curr Opin Neurol 1995 8 45 54 7749516 13 Mendel T Pasierski T Transesophageal echocardiographic findings in patients with anterior and posterior circulation infarcts Acta Neurol Scand 1998 97 63 97 9482680 14 Belkin RN Hurwitz BJ Atrial septal aneurysm: association with cerebrovascular and peripheral embolic events Stroke 1987 18 856 862 3629643 15 Mugge A Daniel WG Cardiogenic embolism Williams and Wilkins Co Baltimore 1996 159 168 16 Okura H Iroue H Transesophageal echocardiographic detection of cardiac sources of embolism in elderly patients with ischemic stroke Intern Med 1999 38 766 772 10526938 17 Among Y Khandeheria BK Frequency of atrial septal aneurysm in patients with cerebral ischemic events Circulation 1999 99 1942 1944 10208995 18 Meissner I Whisnant JP Prevalence of potential risk factors for stroke assessed by transesophageal echocardiography and carotid ultrasonography. 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