Thromb Haemost 1987; 58(01): 317
DOI: 10.1055/s-0038-1643952
Abstracts
PLATELET THROMBUS IMAGING
Schattauer GmbH Stuttgart

PROSTAGLANDIN E1 REDUCES ENDOCARDIAL PLATELET DEPOSITION AND INCREASES LEFT VENTRICULAR EJECTION FRACTION (LVEF) IN PATIENTS WITH CARDIOMYOPATHY (CMP)

H Sinzinger
Depts. Nuclear Medicine, Cardiology and Internal Medicine, University of Vienna, Austria
,
H Glogar
Depts. Nuclear Medicine, Cardiology and Internal Medicine, University of Vienna, Austria
,
H Weidinger
Depts. Nuclear Medicine, Cardiology and Internal Medicine, University of Vienna, Austria
,
H Sochor
Depts. Nuclear Medicine, Cardiology and Internal Medicine, University of Vienna, Austria
,
H Auinger
Depts. Nuclear Medicine, Cardiology and Internal Medicine, University of Vienna, Austria
,
M Weissel
Depts. Nuclear Medicine, Cardiology and Internal Medicine, University of Vienna, Austria
,
P Fitscha
Depts. Nuclear Medicine, Cardiology and Internal Medicine, University of Vienna, Austria
,
H Bergmann
Depts. Nuclear Medicine, Cardiology and Internal Medicine, University of Vienna, Austria
,
Susanne Granegger
Depts. Nuclear Medicine, Cardiology and Internal Medicine, University of Vienna, Austria
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Publikationsverlauf

Publikationsdatum:
23. August 2018 (online)

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It is well known, that patients suffering from CMP exhibit a significantly enhanced thromboembolic risk. Thus, we examined in these patients platelet function (f3TG, PF4, TXB2-serum and plasma) and kinetics after 111-In-oxine sulphate (100μCi) labelling. In a total of 67 patients (50o,17g; 29-66a with a LVEF of < 30%) the following findings have been obtained.

During γ-camera imaging and by engymetric monitoring using a portable detector system (Novo Int. Danmark) CMP-patients show an enhanced platelet deposition over the heart. Platelet half-life (1: 100-115h) is extremely shortened (< 50hrs). Prostaglandin (PG) E1 (prostavasin; α1-cyclodextrin PGE1; Sanol-Schwarz GmbH, Monheim, FRG) administered i.v. in a dose range of 5-50 ng/kg/min causes a significant (p< 0,01) increase in LVEF of 20-95% dose-dependently as measured by means of radioisotope technique.

Furthermore, a diminution in the local platelet uptake over the heart starting at the 2nd day of continuous PGE1-infusion can be monitored.

It is hypothetized, that PGE1 renders the endocardium less thrombogenic and increases LVEF by vasodilatation and decreasing the afterload. As PGE1 is metabo-lically degraded to a major extent during the first lung passage, the data after i.v. application are at least suggestive, that more stable PGE1-derivatives may contribute to this effect.

It is therefore concluded, that PGE1 in a safe dose of 25ng/kg/min may appear in the future as an optimal long-term therapeutic agent in CMP-patients offering the benefit of significantly enhanced LVEF and decreased platelet deposition, which should result in a decreased thromboembolic risk in these patients.