Coronary microembolization and microvascular dysfunction

Abstract

Plaque erosion, fissuring or rupture occurs spontaneously or during coronary interventions. At some residual blood flow, the atherothrombotic debris is washed into the coronary microcirculation, causing physical obstruction, vasoconstriction, inflammation and ultimately microinfarction. Coronary microembolization also contributes to microvascular obstruction in reperfused acute myocardial infarction. Patients with microvascular obstruction after reperfused myocardial infarction have worse prognosis. Cardioprotective strategies to avoid acute coronary microembolization and rescue myocardium from microvascular obstruction have not yet been established in clinical practice. Subclinical coronary microembolization together with release of thrombogenic, vasoconstrictor and inflammatory substances from a culprit lesion can sensitize the coronary microcirculation and contribute to angina in the absence of major epicardial coronary obstruction. Repetitive coronary microembolization can induce progressive loss of functional cardiomyocytes and induce heart failure in the absence of overt myocardial infarction.