Abstract

After a myocardial infarction (MI), despite the resolution of the coronary occlusion, the deterioration of myocardial perfusion persists in a considerable number of patients. This phenomenon is known as microvascular obstruction (MVO). Initially, the focus was placed on re-establishing blood flow in the epicardial artery. Then, the observation that MVO has profound negative structural and prognostic repercussions revived interest in microcirculation. In the near future, the availability of co-adjuvant therapies (beyond timely coronary reperfusion) aimed at preventing, minimizing, and repairing MVOs and finding convincing answers to questions regarding what, when, how, and where to administer these therapies will be of utmost importance. The objective of this work is to review the state-of-the-art concepts on pathophysiology, diagnostic methods, and structural and clinical implications of MVOs in patients with ST-segment elevation MIs. Based on this knowledge we discuss previously-tested and future opportunities for the prevention and repair of MVO.

Highlights

  • IntroductionHerrick reported the first human evidence regarding the role of thrombotic obstruction of coronary arteries in the pathophysiology of myocardial infarction (MI), including the observation that this syndrome did not necessarily imply the immediate death of patients [1]

  • microvascular obstruction (MVO) plays a major role in the pathophysiology of segment elevation MIs (STEMIs)

  • Late gadolinium-enhancement cardiovascular magnetic resonance (CMR) has become the gold standard of non-invasive imaging techniques for the detection and quantification of microvascular damage after STEMI

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Summary

Introduction

Herrick reported the first human evidence regarding the role of thrombotic obstruction of coronary arteries in the pathophysiology of myocardial infarction (MI), including the observation that this syndrome did not necessarily imply the immediate death of patients [1]. Despite successful reperfusion at the epicardial level, the deterioration of myocardial perfusion persists in a considerable number of patients. This phenomenon is known as microvascular obstruction (MVO) and can occur in 50% to 60% of cases [3] and has been associated with adverse ventricular remodeling and a heightened risk of future cardiovascular events [4,5]. 50 years after these contributions, MVO remains an unresolved problem that continues to have deleterious structural and prognostic consequences [5,7,8]

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