Prevention and Treatment of Microvascular Obstruction-Related Myocardial Injury and Coronary No-Reflow Following Percutaneous Coronary Intervention

Abstract

Microvascular obstruction (MVO) commonly occurs following percutaneous coronary interventions (PCI), may lead to myocardial injury, and is an independent predictor of adverse outcome. Severe MVO may manifest angiographically as reduced flow in the patent upstream epicardial arteries, a situation that is termed "no-reflow." Microvascular obstruction can be broadly categorized according to the duration of myocardial ischemia preceding PCI. In "interventional MVO" (e.g., elective PCI), obstruction typically involves myocardium that was not exposed to acute ischemia before PCI. Conversely "reperfusion MVO" (e.g., primary PCI for acute myocardial infarction) occurs within a myocardial territory that was ischemic before the coronary intervention. Interventional and reperfusion MVO have distinct pathophysiological mechanisms and may require individualized therapeutic approaches. Interventional MVO is triggered predominantly by downstream embolization of atherosclerotic material from the epicardial vessel wall into the distal microvasculature. Reperfusion MVO results from both distal embolization and ischemia-reperfusion injury within the subtended ischemic tissue. Management of MVO and no-reflow may be targeted at different levels: the epicardial artery, microvasculature, and tissue. The aim of the present report is to advocate a systematic approach to prevention and treatment of MVO in different clinical settings. Randomized clinical trials have studied strategies for prevention of MVO and no-reflow; however, the efficacy of measures for reversing MVO once no-reflow has been demonstrated angiographically is unclear. New approaches for prevention and treatment of MVO will require a better understanding of intracellular cardioprotective pathways such as the blockade of the mitochondrial permeability transition pore.

Impact of Coronary Plaque Burden and Composition on Periprocedural Myocardial Infarction and Coronary Flow Reserve After Percutaneous Coronary Intervention

“…25) Bahrmann, et al demonstrated that a large amount of embolic particles could reduce the post-PCI CFR. 10) In the present study, we excluded patients with side-branch occlusion after PCI, which could lead to low post-PCI CFR.…”

Monitoring of Monocyte Recruitment in Reperfused Myocardial Infarction With Intramyocardial Hemorrhage and Microvascular Obstruction by Combined Fluorine 19 and Proton Cardiac Magnetic Resonance Imaging

“…4,5,10 Various approaches have been explored to reverse MVO in clinical trials, but their efficacy is unclear. 26 MVO regions are composed primarily of necrotic tissue; therefore, reversal of MVO is not expected to rescue viable myocardium but instead to optimize healing and achieve better long-term outcomes. The present results showed that the impaired infiltration of monocytes/macrophages in MVO regions was associated with worse functional outcomes in rats.…”

No-Reflow Phenomenon

“…29,30 The poor prognosis with no-reflow is due to larger infarct sizes and reduced systolic function left ventricule. 30 The clinical trials tested a number of treatment strategies for no-reflow have been conflicting and there is no definitive treatment of no-reflow once it has occurred.…”

“…29,30 The poor prognosis with no-reflow is due to larger infarct sizes and reduced systolic function left ventricule. 30 The clinical trials tested a number of treatment strategies for no-reflow have been conflicting and there is no definitive treatment of no-reflow once it has occurred. [31][32][33][34][35] In the absence of an effective treatment strategy, it is crucial to prevent no- reflow by knowing the predictors or risk factors of no-reflow.…”