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Spontaneous cervical artery dissection is accompanied by a hypercoagulable state and simultaneous inflammatory
Johann Otto Pelz1, Kristian Harms2, Michael Metze3
1Department of Neurology, University of Leipzig, Leipzig, Germany. johann.pelz@medizin.uni-leipzig.de.
Background:
Spontaneous cervical artery dissections (sCAD) are often preceded by infections. However, existing data about inflammatory parameters remained inconsistent. Remarkably, concurrent information about the coagulation system, whose affection seems also reasonable to cause ischaemic events, are still lacking in sCAD patients. Thus, this study explores the association between the inflammatory and coagulation system in patients with sCAD.
Methods:
The parameters leukocyte and thrombocyte count, C-reactive protein, fibrinogen, D-dimer, activated partial thromboplastin time (aPTT) and prothrombin time were extracted from hospital-based medical records of patients (n = 60) with sCAD and compared with those of a control group (n = 97) from a prospective observational stroke study. Univariate analyses were added by multiple regression analyses.
Results:
As compared with the control group, patients with sCAD had an increased leucocyte count (9.2 ± 3.2 vs. 7.9 ± 2.2 × 109/l; p = 0.003), an increased thrombocyte count (252 ± 52 vs. 229 ± 64 × 109/l; p = 0.021), a shortened aPTT 28.0 ± 3.5 vs. 29.9 ± 3.6 s; p = 0.001) and decreased D-dimer values (0.44 ± 0.29 vs. 0.76 ± 0.73 mg/l; p = 0.002). However, in multiple regression analyses adjusted for age, sex, initial stroke severity, arterial hypertension, diabetes mellitus and smoking only the shortened aPTT remained statistically significant (p = 0.045) between groups, while differences on leucocyte count (p = 0.087), thrombocyte count (p = 0.234) and D-dimer (p = 0.321) failed statistical significance.
Conclusion:
We found evidence for a hypercoagulable state in patients with sCAD as indicated by a shortened aPTT, which was associated with a trend to an increased leucocyte count at the same time. Our findings first strengthen the hypothesis that inflammation critically impacts on the occurrence of sCAD, and second linked this condition with a marked affection of the coagulation system.
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