Transesophageal echocardiography in patients with recent stroke and normal carotid arteries

Abstract

E of cardiac origin are the second most frequent cause of stroke. Transesophageal echocardiography (TEE) has been increasingly used to diagnose intracardiac thrombus as well as a number of other cardiac abnormalities. Evaluation of a suspected cardiac source of embolism is currently the most common indication for TEE in many centers because of transesophageal echocardiographic superiority over transthoracic echocardiography. The aim of the present prospective study was to evaluate the clinical significance of transesophageal echocardiographic findings in patients with normal carotid arteries who had suffered cerebral ischemia. • • • The study group consisted of 245 of the 458 patients referred to 3 institutions. Patients ranged in age from 36 to 86 years (mean 65.7 21); 77 were women and 168 were men (Table 1). All patients were selected on the basis of a recent unexplained cerebral ischemia and were included in the study if they had normal carotid arteries (group A). These patients were compared with 245 ageand sex-matched patients (mean age 64.7 23 years, range 29 to 86) who underwent transesophageal echocardiographic examination during the same period for indication other than cerebral ischemia (group B). Exclusion criteria were chronic atrial fibrillation, mitral prosthesis, and mitral stenosis. In group A, we excluded patients with evidence of a mass or hemorrhage on a computer tomographic head scan. In the study population (group A), a trained neurologist established a clinical diagnosis of transient ischemic attack or stroke. A computed tomographic scan (CT) was performed in all patients, and magnetic resonance imaging in 100 of the 245 patients. Cerebral ischemia was defined as: (1) stroke, sudden development of a permanent focal neurologic deficit after which a brain CT scan establishes a cerebrovascular accident as the cause; (2) reversible ischemic attack with complete or almost complete recovery without the need for therapeutic rehabilitation; (3) transient ischemic attack, which is completely resolved within 24 hours; and (4) reversible ischemic neurologic deficit in which there is full clinical recovery within 7 days. A cardioembolic source was suspected on clinical findings, brain imaging, and on normal duplex carotid ultrasound examination. All patients underwent complete transthoracic and transesophageal echocardiographic studies. In group A patients, the examinations were performed 1 to 7 days after the cerebral ischemic event. A Commercial Hewlett-Packard system (Andover, Massachusetts) with 2.5and 3.5-MHz probes and a 5-MHz biplane or multiplane frequency probe with color Doppler and spectral pulsed Doppler was used. Standard views from the gastric and lower esophageal windows were obtained from every patient. All patients who underwent TEE were given diazepam and pharyngeal xilocaine. Each study was assessed for the presence or absence of the following: left atrial enlargment, mass, thrombus, spontaneous echo-contrast, atrial septal defect, atrial septal aneurysm, patent foramen ovale (PFO), mitral annular calcium, mitral valve prolapse, vegetation or strands, left ventricular dilatation and dysfunction, and ascending aortic arch and descending aortic atherosclerotic plaque. Left atrial enlargment was diagnosed if the left atrial cavity was found to be 40 mm. Thrombus in the left atrium or appendage was defined as the presence of a clearly defined intracavitary mass acoustically distinct from underlying endocardium and not caused by the pectinate ridges of the left atrial appendage. Spontaneous echo contrast was defined as dynamic, smoke-like echoes with a characteristic swirling motion, distinct from the echoes caused by excessive gain. Gain controls had been adjusted optimally to minimize artifact by the physician performing the echo examination. Atrial septal aneurysm was defined as a bulge of 15 mm beyond the plane of the atrial septum as measured by TEE. Atrial septal aneurysm was classified according to Hanley’s diagnostic criteria, and modified by PearFrom the Department of Cardiology, Pierantoni Hospital, Forli; Department of Cardiology, University of Modena, Modena; and School of Medicine, University of Ferrara, Ferrara, Italy. Dr. Mattioli’s address is: Department of Cardiology, University of Modena, Via del pozzo 71, 41100 Modena, Italy. E-mail: mattioli.annavittoria@ unimo.it. Manuscript received February 19, 2001; revised manuscript received and accepted May 17, 2001.