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Coronary microembolization
Gerd Heusch1, Rainer Schulz, Michael Haude
1Institut für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Hufelandstrasse 55, Essen 45122, Germany.
Insights
Atherosclerotic plaque rupture can cause coronary microembolization, leading to arrhythmias and microinfarcts. This review explores evidence and prevention strategies for this condition in acute coronary syndromes.
Area of Science:
- Cardiovascular Medicine
- Pathophysiology
- Interventional Cardiology
Background:
- Atherosclerotic plaque rupture is central to acute coronary syndromes and interventions.
- Rupture can lead to microembolization of debris into the coronary microcirculation, not always complete occlusion.
Purpose of the Study:
- To review morphological, experimental, and clinical evidence of coronary microembolization.
- To detail its pathophysiology, clinical features, and prevention.
Main Methods:
- Review of morphological evidence in deceased patients with coronary artery disease.
- Analysis of experimental pathophysiology in animal models.
- Synthesis of clinical evidence in patients with acute coronary syndromes.
Main Results:
- Morphological evidence supports microembolization in coronary artery disease.
- Experimental models elucidate pathophysiology.
- Clinical features include arrhythmias, contractile dysfunction, microinfarcts, and reduced coronary reserve.
Conclusions:
- Coronary microembolization is a significant consequence of plaque rupture.
- Clinical features in patients mirror experimental findings.
- Prevention strategies involve mechanical devices and glycoprotein IIb/IIIa antagonism.
Abstract:
Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndromes and during coronary interventions. Atherosclerotic plaque rupture does not always result in complete thrombotic occlusion of the entire epicardial coronary artery with subsequent acute myocardial infarction, but may in milder forms result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation. This review summarizes the available morphological evidence for coronary microembolization in patients who died from coronary artery disease, most notably from sudden death. Then the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes is detailed. Finally, the review presents the available clinical evidence for coronary microembolization in patients, highlights its key features--arrhythmias, contractile dysfunction, microinfarcts and reduced coronary reserve--, compares these features to those of the experimental model and addresses its prevention by mechanical protection devices and glycoprotein IIb/IIIa antagonism.
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