By post-mortem angiography and histology in patients who had died from an acute coronary event, typical features of coronary microembolization were identified: intraluminal microthrombi, consisting of platelets, fibrin, atherosclerotic material including cholesterol crystals, and hyalin [1,3,29,30]. These microthrombi were associated with typical microinfarcts in their vicinity, and these microinfarcts were characterized by a pronounced inflammatory reaction. The morphological features in experimental models of coronary microembolization are remarkably similar, supporting the use of such models for the study of coronary microembolization and its pathophysiology: microinfarcts in close vicinity to embolizing particles with a marked infiltration of polymorphonuclear leukocytes, macrophages and monocytes [15,31,32], but also apoptosis [19,32] are typically seen in dogs and pigs within hours after intracoronary infusion of microspheres (Figure 1).

Pathophysiology

The intracoronary infusion of microspheres in dogs immediately reduces coronary blood flow, and this blood flow reduction is quickly followed by a reactive hyperemia response within minutes [33,34]. The reactive hyperemia response is mediated through endogenous adenosine [33]. The coronary blood flood reserve in response to exogenous adenosine is reduced [34]. An increase in postprocedural baseline coronary blood flow velocity along with a reduced coronary blood flow velocity reserve and an increased creatine kinase release are also typically seen in patients undergoing PCI [35,36], again supporting the use of the above models in the study of coronary microembolization´s pathophysiology. Regional contractile function in the microembolized coronary artery perfusion territory is immediately reduced along with coronary blood flow, but then- different from coronary blood flow which recovers fully or even exceeds baseline blood flow- does not recover completely [34], and repeated bouts of coronary microspheres infusion add up to a cumulative contractile deficit (Figure 2). In fact, the immediate contractile impairment after infusion of microspheres into the coronary circulation is followed by a further progressive decline of regional contractile function [15], and eventual full recovery- if it occurs- requires a week [37]. The inotropic reserve in response to dobutamine is reduced in microembolized myocardium [34].