We initially enrolled 178 patients who presented with suspected acute ischemic stroke or TIA and 63 healthy controls in the study. All these patients had at least 1 blood sample drawn for the assessment of plasma D-dimer levels. In 8 of the 178 patients, the initial diagnosis subsequently failed to be confirmed. In 1 patient, the second computed tomographic scan of the brain showed small metastases that were not visible in the previous one performed at the emergency department, and in 7 patients the initial diagnosis of a suspected TIA was subsequently denied (2 patients had convulsions, 2 had vertigo, and 3 had an isolated syncope). Plasma D-dimer levels were within the reference range (<0.50 µg/mL) in 7 patients and slightly abnormal in the patient with malignancy. Exclusion criteria were subsequently identified in 44 patients. An acute infection developed in 29. Ten had malignancy; 7, a recent trauma; 2, a recent acute myocardial infarction; 1, deep vein thrombosis in the hospital; 1, a recent surgical procedure; and 1, a chronic rheumatologic disorder (rheumatoid arthritis). Although the primary end point of the study was the correlation between stroke subtype and D-dimer level measured on admission, patients were also excluded if the criterion was identified during hospitalization to not interfere with the subsequent assays. Of the 126 remaining patients, 40 had a TIA (mean age, 75.6 years; 18 men) and 86 had an acute ischemic stroke (mean age, 75.7 years; 44 men) (Table 1). Among the 63 healthy controls, the mean age was 75.4 years and 31 were men. We initially compared the 3 measures of D-dimer levels among the patients with acute ischemic stroke, those with TIA, and controls (with a single measure). Patients with stroke and TIA had significantly higher D-dimer levels than controls at all 3 measurements, whereas no statistical difference was found in any of the measurements between the patients with stroke and TIA (Table 2). No correlation was found between D-dimer levels and stroke severity as assessed using the Unified Neurological Stroke Scale (r = 0.2284). We subsequently compared D-dimer levels according to stroke subtypes. Among the 126 patients undergoing evaluation, 34 (27%; mean age, 79.9 years) had a cardioembolic event; 34 (27%; mean age, 74.1 years), an atherothrombotic event; 31 (25%; mean age, 74.7 years), a lacunar event; and 27 (21%; mean age, 74.1 years), an unknown mechanism of acute cerebrovascular ischemia (Table 3). Mechanisms for the cardioembolic event were atrial fibrillation in 21 patients receiving aspirin or not receiving any antithrombotic prophylaxis, congestive heart failure in 8, severe mitral valve disease in 3, ischemic heart disease in 1, and heart valve replacement with a mechanical valve in 1 who spontaneously stopped warfarin sodium treatment 1 week before the event. On day 1, D-dimer levels were significantly higher in the groups of patients with a cardioembolic stroke or a TIA (2.96 ± 0.51 µg/mL) than in the groups with an atherothrombotic (1.34 ± 0.21 µg/mL; P<.05) or a lacunar (0.67 ± 0.08 µg/mL; P<.01) event (Table 3). There was also a statistically significant difference between these latter 2 groups (P<.01), whereas no difference was shown between patients with lacunar events and controls. According to these results, the optimal D-dimer level cutoff point for discriminating the presence or absence of a cardioembolic source was determined to be 2.00 µg/mL, with a specificity of 93.2%, a sensitivity of 59.3%, a positive predictive value of 72.7%, and a negative predictive value of 88.2% (Table 4 and Figure 1). On the other hand, the optimal cutoff point for discriminating a lacunar event was determined to be 0.54 µg/mL, with a specificity of 96.2%, a sensitivity of 61.3%, a positive predictive value of 86.4, and a negative predictive value of 86.2% (Table 4 and Figure 2). After 6 ± 1 days, D-dimer levels were substantially stable in all 3 groups, whereas after 12 ± 1 days, we found a clear increase in the cardioembolic and atherothrombotic groups, but no change in the lacunar group (Table 3).