Embolization As a Pathological Mechanism

INTRODUCTION Spontaneous plaque rupture is the central event in the pathogenesis of acute coronary syndromes (ACS). Similarly, iatrogenic plaque rupture is induced in the cardiac catheterization laboratory during percutaneous coronary intervention. Plaque rupture leads to superimposed platelet adhesion, aggregation, and thrombus formation. Subsequent embolization of atherothrombotic material rich in platelets can lead to microvascular obstruction and dysfunction, and, ultimately, to myocardial necrosis (Figure 1). The real frequency and clinical significance of such distal embolization has only recently been appreciated. While other etiologies of microvascular obstruction such as tissue inflammation or edema exist, embolization has been increasingly recognized as having a major role in this process. Therapies that prevent embolization or minimize its impact in creating microvasculature obstruction are in evolution. Embolization and microvascular obstruction have a significant impact during both coronary interventional procedures and ACS. However, the impact and importance of distal embolization was first established for percutaneous coronary intervention. Initially, embolization was believed to be of little consequence unless it was manifest angiographically. Accumulating evidence has revealed that embolization is not as benign a process as interventional cardiologists would like to believe. Using an emboli capture device in routine stent and balloon coronary revascularization procedures, Yadav and colleagues have shown that all patients undergoing coronary intervention have evidence of atheroembolic material [1]. This observation provides a basis for interpretation of much of the pivotal data in the field.