Though highly effective, warfarin use is associated with a considerable risk of bleeding, including intracranial hemorrhage, which occurs at a rate of 0.5%/year. This may help explain why recent trials have not found control of the dysrhythmia and maintenance of sinus rhythm more effective than rate control and anticoagulation for prevention of adverse clinical outcomes in patients with AF (17,18).Īt present, protection against ischemic stroke due to cardiogenic embolism in high-risk patients involves oral anticoagulation at a dose adjusted to maintain international normalized ratio between 2 and 3. Hypertension may be a key factor linking vascular lesions with the pathogenesis of thrombus in the appendage, and the consistent association of hypertension with stroke in AF patients may be attributed to atrial stasis or to associated disease of the vasculature supplying the brain. There are also strong correlations between reduced LAA flow velocity, thrombus formation, hypertension, and atheromatous disease of the aorta (15,16). ![]() In patients with AF, several risk factors that predict thromboembolism in clinical studies correlate with reduced flow velocity in the LAA, accounting in part for their links to cardiogenic embolism (13,14). In patients with mitral stenosis, stasis is generalized in both the atrium and the LAA, while, in cases of mitral regurgitation, the LAA may be more prone to this phenomenon than the body of the left atrium (12). These thrombi were located in the LAA in 91% of the patients with non-valvular AF, compared with 57% of those with valvular disease (11). In a meta-analysis of 23 studies in which the LAA was examined by TEE, autopsy, or direct intra-operative inspection, intracardiac thrombus was identified in 17% of patients with non-valvular AF and in 13% of cases in which AF was associated with valvular heart disease. Communication with the atrial cavity increases proportionally, hypothetically facilitating the first stage of embolism by allowing a thrombotic mass to cross the orifice more easily. With long-standing AF, the ejection velocity from the LAA often decreases to negligible levels, and the appendage dilates at least as quickly as the rest of the atrium in patients with chronic mitral valve disease, sometimes reaching an area of 12 cm 2. When fibrillating, the LAA undulates at a rate >350 cycles/min, and outflow velocity is considerably reduced. ![]() ![]() ![]() The LAA is seldom imaged clearly by precordial echocardiography, but, through transesophageal echocardiography (TEE), the LAA has been recognized as a prime nidus of thrombus formation in patients with atrial fibrillation (AF) and, indeed, the leading source of cardiogenic stroke (8–10). Receptors in the LAA influence heart rate, and granules secrete atrial natriuretic peptide, contributing to regulation of intravascular pressure and volume in response to stretch (3–7). This accessory chamber extends over an area of 3 to 6 cm 2, is more compliant than the atrium, and is actively contractile in normal hearts-filling and emptying in response to both ventricular and atrial dynamics (2,3). Shaped like a wizard's hat but long considered functionally insignificant, the conical, trabeculated left atrial appendage (LAA) arises from the embryonic left atrium during the third week of gestation and extends superiorly from the anterolateral surface of the left atrium (1).
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