Introduction:
It is well known that elevation of fibrinolytic markers reflects thrombus formation in the left atrial appendage (LAA) that is identified as a fibrin-rich thrombus. On the other hand, it is sometimes difficult to remove LAA thrombus by the treatment of anti-coagulants alone.
Hypothesis:
Circulating platelet activation is also responsible for the thrombus formation in the LAA in patients with cardioembolic stroke.
Methods:
In 98 consecutive patients with cerebral infarction (mean age, 71±12 years old), we performed trans-esophageal echocardiography within 7 days after the onset, and at the same time, measured circulating platelet-derived microparticles (PDMP, as a marker of platelet activation, < 20 U/ml), and serum levels of D-dimer (DD, as a marker of fibrinolytic activity, normal level < 1.0 μg/ml). Patients with LAA peak emptying flow velocity < 20 cm/s were classified as having LAA dysfunction.
Results:
In patients without warfarin treatment, both PDMP and DD levels were significantly higher in LAA thrombus positive (n=12) than in negative group (n=70) (PDMP, 113.5±80.4 vs. 65.5±30.7 U/ml, P<0.001; DD, 7.3±10.4 vs. 2.9±3.7 μg/ml, p < 0.01). In patients with warfarin treatment (PT-INR 1.64±0.35), PDMP, but not DD levels, was markedly higher in LAA thrombus positive (n=6) than in negative group (n=10) (PDMP, 113.4±84.5 vs. 49.7±23.9 U/ml, P<0.05; DD, 2.1±1.8 vs. 1.6±1.3 μg/ml, NS), because DD were effectively suppressed by the anti-coagulant therapy. Furthermore, in LAA thrombus negative patients, there were no significant differences in PDMP between cases with and without LAA dysfunction (LAA dysfunction, n=13, 70.2±26.5 vs. No dysfunction, n=67, 63.3±31.1 U/ml).
Conclusions
: PDMP plays an important role in the LAA thrombus formation that is resistant to anti-coagulant treatment, and may be a useful predictor for the cardioembolic stroke occurrence.