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Recent studies suggest that abnormalities of the left atrium in the absence of atrial fibrillation (AF) may increase risk of stroke, either as precursors to AF or as independent risk factors for the development of atrial thrombus and subsequent stroke. Markers for atrial disease, such as left atrial enlargement (LAE) on echocardiogram, evidence of left atrial abnormality demonstrated by increased p-wave terminal force in lead V1 (PTFV1) on ECG, and increased serum levels of a form of brain natriuretic peptide (NT-proBNP), have been associated with increased stroke risk and used to define a new entity known as atrial cardiopathy.1
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