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Pathophysiology of coronary microembolisation
  1. G Heusch,
  2. R Schulz
  1. Institut für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Essen, Germany
  1. Correspondence to:
    Prof Dr med Dr h c Gerd Heusch, Institut für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Hufelandstrasse 55, 45122 Essen, Germany;

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The combination of endothelial damage and severe coronary stenosis induces typical cyclic coronary flow variations, characterised by progressively decreased coronary blood flow over several minutes followed by an abrupt increase in coronary blood flow.1 Such cyclic flow variations are attributed to platelet aggregates2 that progressively plug the stenotic epicardial coronary artery segment and are then suddenly dislodged into the coronary microcirculation; aspirin consistently prevents cyclic coronary blood flow variations.3 Cyclic coronary blood flow variations cause decreased regional contractile function in the dependent myocardium4 and arrhythmias.5

Coronary microembolisation in the absence of coronary stenosis induces a transient decrease in coronary blood flow immediately with the microembolisation followed by a more prolonged increase in coronary blood flow; the hyperaemia is associated with a release of adenosine and prevented by the adenosine receptor antagonist theophylline. Despite the increase in coronary blood flow which most likely results from dilation of the microvessels surrounding the embolised vessel, coronary microembolisation induces myocardial ischaemia, as evidenced by reduced regional contractile function and reduced lactate extraction.6 The destruction of free radicals by superoxide dismutase enhances the release of adenosine and the resulting hyperaemia, and attenuates the decreases in regional contractile function and lactate extraction following coronary microembolisation.7


Focal microinfarcts with leucocyte infiltration were found in human postmortem studies as well as in experimental studies …

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