Biomedical Engineering Reference
In-Depth Information
Fig. 5
Cardiac thromboembolus due to atrial i brillation.
Hematoxylin staining with additional
myeloperoxidase antibody staining of a freshly embolized cell-rich cardiac thrombus in a patient
with paroxysmal atrial i brillation (modii ed at er Hammwöhner
et al.
2008). Note the abundant
inl ammatory cells (darkly stained myeloperoxidase, white arrow) mixed with platelets (small and
lightly stained, black arrow) forming platelet-leukocyte aggregates embedded in a protein matrix
of thrombin, i brin and other proteins of the coagulation cascade. Original magnii cation level
× 200. Microscope: Zeiss Axioskop 50; Camera: Nikon Coolpix 990; contrast enhanced for bet er
dif erentiation of cell groups.
ACE inhibitor, as experiments in animal models showed. h e granulocyte-platelet
conjugates depicted in Figs. 5 and 6 are known to correlate with silent cerebral
ischemia.
Interestingly, soluble ICAM-1 and VCAM-1 levels were also found to be elevated
in patients with silent cerebral infarction (Kawamura
et al.
2006). Of note, soluble
adhesion molecule levels were found to correlate with a high predictive value with
membrane-bound intramyocardial adhesion molecules (Noutsias
et al.
2003).
In line with these study results, we recently demonstrated that systemic plasma
levels of ICAM-1 and VCAM-1 levels were increased in patients with AF, reaching
the highest levels in patients with atrial thrombi. Soluble VCAM-1 levels were
an independent predictor of atrial thrombi in multivariate analysis of variance
(Hammwöhner
et al.
2007b). h us, AF-induced augmentation in endothelial
