Cardiological diagnosis in arterial embolism]

Potential cardiac sources of arterial embolism are in particular thrombi within the left atrium or ventricle, or attached to a prosthetic valve, intracardiac tumors, and vegetations due to endocarditis. Patent foramen ovale and atrial septal defect may lead to paradoxical embolism, and spontaneous echo contrast within the heart has to be considered as a parameter of increased thromboembolic risk. In rare cases, atrial septal aneurysm, mitral valve prolapse or annulus calcification and calcified aortic stenosis has to be taken into consideration. Current method of choice for diagnosis of these abnormalities is echocardiography. When the transthoracic approach fails, transesophageal echocardiography (TEE) leads to a definite diagnosis in most cases. Precordial echocardiography allows the detection of left ventricular thrombi with a sensitivity ranging between 72 and 95%, and monoplane TEE does usually not increase these numbers. In contrast, thrombi within the left atrium and particularly in the left atrial appendage can be detected with a significantly higher detection rate when TEE is used. The same is true for spontaneous echo contrast in the left atrium, a phenomenon which is almost exclusively diagnosed by TEE, as well as for endocarditis associated vegetations that can be identified by TEE with a sensitivity higher than 90%. Patient foramen ovale is usually diagnosed by precordial contrast echocardiography combined with a Valsalva maneuver; color Doppler or contrast TEE allows to increase the detection rate. In the diagnosis of prosthetic valve attached thrombi and vegetations, TEE is clearly superior compared to the precordial examination, at least concerning prosthetic devices in mitral position. If echocardiography fails to identify a potential cardiac source of embolism, other techniques don't add significant information in most cases. Detection of a potential source of embolism, however, does not necessarily prove that the particular finding represents the true etiology of an embolic event; results of all clinical and technical examinations have to be evaluated in a critical synopsis. In addition, proper therapeutic consequences in quite a number of abnormalities considered as potential cardiac sources of embolism are not yet defined.