BACKGROUND : Strokes are commonly preceded by transient ischemic attacks (TIAs). TIA is often associated with
metabolic syndrome (causing chronic inflammation), resulting in a proinflammatory- and procoagulantenvironment.
The aim of this study was to determine whether platelet- and fibrin network-morphology or
coagulation profiles of individuals that suffered a TIA in the presence of metabolic syndrome was altered when
compared to healthy individuals.
MATERIALS AND METHODS : The study consisted of 40 voluntary participants. Twenty individuals that suffered a TIA in
the previous 48 h with at least two metabolic syndrome risk factors present and twenty healthy age-matched
controls. Scanning electron- and atomic force microscopy was used to study platelet- and fibrin-morphology,
atomic force microscopy was used to study platelet- and fibrin fiber-elasticity and thromboelastography® for the
study of coagulation profiles. Statistical analysis was performed to compare the two groups. In all cases a p-value of
less than 0.05 was considered statistically significant.
RESULTS : Platelets of the control group appeared spherical with few pseudopodia present while the platelets of the
TIA individuals presented with numerous pseudopodia and spreading, indicating activation. Platelet aggregation
was also present. The fibrin networks of the healthy individuals consist of thick and thin fibers that form an
organized network of fibers. The fibrin networks of the TIA individuals appeared less organized with less taut fibers.
Fibrin fiber thickness was found to be significantly increased in the TIA group (p-value <0.001) when compared to
healthy controls. The thicker fibers formed irregular networks with thick masses of fibrin fibers. Platelet and fibrin
fiber elasticity was found to be significantly lower in the experimental group (p-value 0.0042 and p-value 0.0007
respectively). The hemostatic profiles of the diseased individuals did not differ significantly (p-value > 0.05) from the
healthy controls, indicating a normal functioning coagulation cascade.
CONCLUSION : The findings indicate that pathological clot formation is not caused by alterations in the coagulation
cascade but rather by the premature activation of platelets (as a result of chronic inflammation) that in turn causes
altered fibrin formation.