Coronary microembolization vs. coronary microvascular dysfunction - a perspective
Coronary microembolization is only one of several pathomechanisms which contribute to coronary microvascular obstruction after reperfused acute myocardial infarction [65,78,79]. The physical obstruction of coronary microvessels with particulate debris causes sustained myocardial ischemia without eventual reperfusion; as such it is most likely not amenable to cardioprotective interventions after it has occurred. In contrast, the soluble thrombogenic, vasoconstrictor and inflammatory molecules which are released with PCI are potentially amenable to specific inhibitory approaches. However, the evidence for such specific protection of the coronary microcirculation by ischemic conditioning or vasodilators (adenosine, sodium nitrite, nitroprusside, verapamil) is not really convincing at this point [11,64,71,80]. More research is needed here (Figure 4). At this point, microvascular obstruction after reperfused acute myocardial infarction carries an adverse prognosis.[81,82] In clinical practice, during elective coronary interventions, coronary microembolization is inferred from periprocedural increases in biomarker enzymes such as creatine kinase and/or troponin. These periprocedural increases in biomarkers of cardiac injury are mostly transient and only minor, and they are rarely associated with overt clinical events. While we have become aware of coronary microembolization mostly from acute and interventional coronary settings, its routine prevention in such settings appears to not improve clinical outcome, and it therefore may not be of too great importance here. However, we have learned a lot about coronary microembolization and also about the release of soluble substances from such acute and interventional scenarios.
