(Circulation. 2009;120:1822-1836.)
© 2009 American Heart Association, Inc.
Contemporary Reviews in Cardiovascular Medicine |
From the Institut für Pathophysiologie (G.H., P.K., B.L., R.S.) and Klinik für Kardiologie (D.B., R.E.), Universitätsklinikum Essen, Essen, Germany; and Städtische Kliniken Neuss (M.H.), Lukaskrankenhaus GmbH, Neuss, Germany.
Correspondence to Prof Dr med Dr hc Gerd Heusch, FRCP, Direktor des Instituts für Pathophysiologie, Universitätsklinikum Essen, Hufelandstraße 55, 45122 Essen, Germany. E-mail gerd.heusch{at}uk-essen.de
Coronary microembolization from the erosion or rupture of a vulnerable atherosclerotic plaque occurs spontaneously in acute coronary syndromes and iatrogenically during percutaneous coronary interventions. Typical consequences of coronary microembolization are microinfarcts with an inflammatory response, contractile dysfunction, and reduced coronary reserve. Apart from transient elevations of creatine kinase and troponin, microemboli can be visualized by intracoronary Doppler and the resulting microinfarcts by late-enhancement nuclear magnetic resonance. Statins, antiplatelet agents, and coronary vasodilators protect against microembolization and microinfarction when started before percutaneous coronary interventions. Distal protection devices can retrieve atherothrombotic debris and prevent its embolization into the microcirculation, but their effect on clinical outcome has been disappointing so far, except for saphenous vein bypass grafts. Devices for aspiration of thrombi and thrombus-derived vasoconstrictor, thrombogenic, and inflammatory substances, however, reduce thrombus burden, improve perfusion, and provide protection in patients with acute myocardial infarction.
Key Words: coronary disease imaging infarction inflammation reperfusion statins vasoconstriction
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