Patients with myocardial infarction, stroke and renal disease are at increased risk of future cardiovascular thrombotic events, through increased platelet reactivity, usually due to high shear. Patients affected by these conditions also demonstrate impairment of endogenous thrombolysis. In atrial fibrillation (AF), patients are at increased risk of left atrial thrombus formation, but in a low shear environment.Methods
Blood samples were tested from healthy volunteers (n = 82), patients with AF (n = 44), stable coronary artery disease (CAD, n = 31). The patients with AF and CAD were taking aspirin, whereas the healthy volunteers were on no antithrombotic treatment.Thrombotic status was assessed using the near-patient automated Global Thrombosis Test (GTT). This allows assessment of thrombogenicity (platelet reactivity) and endogenous thrombolysis. The GTT measures the time (in seconds) required for thrombus formation (occlusion time, OT) and the time required for spontaneous lysis of that thrombus (lysis time, LT). The test is performed on native blood without external agonists no chemical additivesResults
In AF patients, median OT was 447s (25th–75th % ile 347–555) and LT was 1472s (1145–2121). In CAD patients OT was 353s (300–441) and LT 1654s (1138–2247) and OT in healthy volunteers was 363s (307–418) with LT of 1052s (896–1256). OT was similar in CAD and healthy volunteers (P = 0.468). In AF patients, OT was prolonged in comparison to normal volunteers (P = 0.004) and CAD patients (P = 0.005). LT was similar in CAD and AF patients (P = 0.598) but prolonged in comparison to healthy volunteers (P < 0.0001).Conclusions
Platelet reactivity in healthy volunteers was similar to the profile in CAD patients on aspirin treatment, suggesting that aspirin normalisesthe enhanced platelet reactivity to high sheer in CAD patients.Conclusions
In comparison, patients with AF demonstrate reduced platelet reactivity but markedly impaired endogenous thrombolysis. Thus, AF and CAD patients have differing platelet reactivity, but both demonstrate impairment of endogenous thrombolysis.