American Society of Hirudotherapy

Antithrombotic effects of saratin on human atherosclerotic plaques

Research article published in Thromb Haemost (2004)

Last Updated: June 18, 2026Reviewed by: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Research reportSalivary PharmacologyDrug DevelopmentVilahur G et al. · Thromb Haemost, 2004

Abstract

Platelets play a primary role in thrombus formation after plaque rupture. Platelets recognize the exposed collagen via Von Willebrand factor (VWF) and become activated. Saratin, an inhibitor of the VWF-dependent binding of platelets to collagen, may reduce the thrombotic risk associated to atherosclerosis. Our objective was to evaluate the antithrombotic effects of local treatment with saratin on human atherosclerotic lesions. Thrombus formation was assessed by the deposition of (111)In-platelets on different human atherosclerotic lesions under three local shear conditions (800,1700 and 3400/s) with blood derived from catheterized pigs. Human atherosclerotic lesions were locally treated with saratin (30 microg/ml) at 37 degrees C for 5 min and placed in the chamber. Under stenotic shear conditions of 800/s, saratin significantly (p<0.05) reduced platelet deposition triggered by human denuded vessel wall (44%), fatty streaks (47%), severely damaged vessel (50%) and atherosclerotic plaque (57%). Thrombus characterization by immunohistochemistry showed also a reduction in fibrin deposition in treat-ed vessels. These results suggest that the local site-specific treatment with saratin inhibits atherosclerotic plaque thrombogenicity at haemodynamic conditions typical of moderately stenotic coronary arteries.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal ArticleResearch Support, Non-U.S. Gov't
Indexed MeSH termsAnimalsArteriosclerosisBlood PlateletsCollagenFibrinolytic AgentsHumansIn Vitro TechniquesIndium RadioisotopesPlatelet AdhesivenessSalivary Proteins and PeptidesSus scrofaThrombosis

Summary

Platelets play a primary role in thrombus formation after plaque rupture. Platelets recognize the exposed collagen via Von Willebrand factor (VWF) and become activated.

Why This Matters for Hirudotherapy

This ex-vivo study evaluated saratin, described as an inhibitor of von Willebrand factor-dependent platelet binding to collagen, as a local treatment to reduce thrombus formation on human atherosclerotic lesions. Using blood from catheterized pigs perfused over treated plaques, saratin (30 microg/ml) significantly reduced platelet deposition on denuded vessel wall, fatty streaks, severely damaged vessel, and atherosclerotic plaque at 800/s shear, and also reduced fibrin deposition. The abstract does not identify saratin's biological origin and makes no mention of leeches, the leech secretome, or hirudotherapy. There is no defensible connection to ASH's domain based on this abstract. The study used pig blood perfused over human tissue with no clinical data.

Citation

Antithrombotic effects of saratin on human atherosclerotic plaques.

Vilahur G et al. · Thromb Haemost, 2004

DOI

Added to ASH library: May 27, 2026 · Site last updated: June 18, 2026

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