الفهرس 
Patients and methodsOnly 14 pages are availabe for public view
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Abstract
Summary
SUMMARY
_ In a study for evaluating the effect of elevated serum lipoprotein (a) as
a risk factor for left atrial thrombus in patients with chronic AF. We
investigated 50 patients in the National heart institute and Benha
University Hospital between Feb. 2001 and November 2002.
_ where tranthroacic and TEE studies was done searching for SEC,
LAA peak flow velocity and left atrial thrombus.
_ Also the serum level of fibrinogen concentration, plasminogen Ddiamers
and total cholesterol was meased by laboratory assays.
_ All the echo and lab data were collected tabulated and statistically
analysed. Patients was divided into 2 groups of patients.
• Patients with and without LA thrombus group.
• Patients with high and low Lp(a) group [Lp(a) ~ 30 considered high
Lp(a)).
In our study we found that Lp(a) was higher in patients with left
atrial thrombus. LA thrombus were present in 23 of 30 subjects with
Lp(a) level ~ 30 mg/dL.
Lp(a) may promote thrombus formation in the left atrium in
patients with chronic AF by inhibiting the fibrinolytic system left atrial
appendage is the most common site of left atrial thrombus formation it is
presumed that blood stasis is most pronounced in the left atrial
appendage.
In the present study the left atrial thrombus and all patients with
left atrial thrombus had left atrial appendage peak flow velocity < 25
em/sec.
”’”140 -8t
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Summary
In addition to Lp(a) level and LAA dysfunction an elevated
fibrinogen concentrations was an independent predictor of
thromboembolism in the present study we could not show any significant
relation between Lp(a) level and the level of Dsdiemers or plasminogen
concentration and D-diamers showed no significant difference between
groups.
On the other hand there was significant correlation between the
level ofLp(a) and total cholesterol.
The striking homology of a poprotein (a) to plasminogen suggests
that Lp(a) has prothrombotic properties. Lp(a) competes with
plasminogen for binding to endothelial and mononuclear cells as well as
to platelets. Thereby reducing the conversion of plasminogen to plasmin
and inhibiting fibrinolysis.
Lp(a) further interferes with plasminogen activation on the surface
of a thrombus by competitively inhibiting the binding of plasminogen and
tissue-type plasminogen activator to fibrin. In conclusion this group of
patients with chronic atrial fibrilation the serum level of Lp(a) was
significantly higher in patients with left atrial thrombus than in patients
without left atrial thrombus and Lp(a) must be considered as a new risk
factor for left atrial thrombus in patients with chronic atrial fibrilation.·
&0 141 e40
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