Background and Purpose-Aortic arch atheromatosis (AAA) is a common cause of cerebral embolism. Transesophageal echocardiography (TEE) shows not only the extension of atherosclerotic plaques but also the mobility of superimposed thrombi. In most cases AAA is only detected after the embolic event. This study was therefore designed to identify predictive factors for AAA. Methods-One hundred seven consecutive patients referred for routine TEE were included in the study. Patients on warfarin therapy, with a history of recent surgery, or with any signs of infectious, immunological, or malignant diseases were excluded. Results-Diabetes mellitus carried the highest risk for AAA (odds ratio, 3.0), followed by hyperlipidemia (2.5) and arterial hypertension (2.3). Age Ͼ70 years was accompanied with a 1.8-fold increased risk. Patients with aortic calcifications on standard chest x-ray had a 4.6-fold higher prevalence. Severe AAA was associated with higher levels of C-reactive protein (

No abstract

No abstract

In patients with cerebral ischemia, a frequent finding is atheromatous plaques in the ascending aorta and the aortic arch. Since we were able to demonstrate that patients with atrial fibrillation have an increased coagulatory activity, we wanted to evaluate a potential systemic activation of the coagulatory system in patients with aortic arch atheromatosis (Aortic AA). In 134 consecutive patients, we determined several parameters of the coagulatory and fibrinolytic systems as well as several thrombophilia risk factors and compared the results with 134 age- and sex-matched healthy controls. In 90 of the 134 patients, transesophageal echocardiography showed Aortic AA, and in the remaining 44 patients, there were no aortic findings. The Aortic AA group showed higher concentrations of thrombin-antithrombin (TAT) and plasmin-antiplasmin complexes (PAP). Further division into 4 subgroups of different severity (grade I: no plaques; grade II: plaques 2-5 mm, grade III: plaques > 5 mm, grade IV: mobile plaques), revealed increasing concentrations of fibrinogen, D-dimers and tissue-type plasminogen activator. The grade IV-group displayed the highest values in comparison to all other groups. In conclusion, Aortic AA as such is a risk factor for cerebral ischemia. It causes a systemically detectable activation of coagulation which substantially exceeds the values for controls. This observation is in accordance with our findings in patients with atrial fibrillation.