%0 Journal Article
%T Spontaneous and Procedural Plaque Embolisation in Native Coronary Arteries: Pathophysiology, Diagnosis, and Prevention
%A Giovanni Luigi De Maria
%A Niket Patel
%A George Kassimis
%A Adrian P. Banning
%J Scientifica
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/364247
%X The detachment of atherothrombotic material from the atherosclerotic coronary plaque and downstream embolisation is an underrecognized phenomenon and it causes different degrees of impairment of the coronary microcirculation. During treatment of obstructive atherosclerotic plaque by percutaneous coronary intervention (PCI) distal embolisation (DE) is considered to be inevitable and it is associated with potential clinical and prognostic implications. This review aims to assess the main aspects of both spontaneous and procedural DE, analyze their different pathophysiology, provide specific insights on the main diagnostic tools for their identification, and finally focus on the main strategies for their treatment and prevention. 1. Introduction Atherogenesis is the cause of ischemic heart disease and knowledge about its pathophysiology is progressively increasing. Progression of plaque within a vessel is not merely a consequence of cholesterol accumulation but a dynamic process related to a complex interaction of several risk factors [1]. Intermittent plaque erosion and healing are probably a common event but clinically occult unless protuberant thrombus either dislodges causing flow disturbance downstream or plaque volume increases during healing reducing the luminal volume. This reduced luminal volume may be too small and produces myocardial ischemia in the dependant territory during exertion, manifesting clinically as anginal chest pain. Treatment of obstructive atheroma by coronary balloon angioplasty was originally described by Gruentzig in 1977. Since then progressive and remarkable innovations in techniques and materials have made percutaneous coronary intervention (PCI) a cornerstone for the treatment of obstructive coronary artery disease (CAD) in many clinical settings [2]. However, achievement of epicardial coronary artery patency does not always translate into a complete and effective myocardial perfusion [3]. This phenomenon known as no reflow (NR) is caused by functional and mechanical impairment of coronary microcirculation and can be described as a condition of ¡°open artery with closed myocardium¡± (Figure 1). Figure 1: No reflow versus normal myocardial perfusion after revascularization. Individual susceptibility, ischemic-reperfusion, injury and distal embolisation (DE) are the main mechanisms leading to NR [4]. Among these three factors, DE of atherothrombotic debris downstream the coronary circulation with consequent microvascular obstruction (MVO) is the most relevant to the procedure of PCI. Its occurrence may prelude to a failure in
%U http://www.hindawi.com/journals/scientifica/2013/364247/