No-reflow in native coronaries and vein grafts: the role of drugs and distal protection
Restoration of normal coronary bloodflow and relieving myocardial ischaemia is the main goal of percutaneous coronary intervention (PCI). However, whilst reducing an epicardial coronary stenosis by balloon dilatation may appear to be a relatively easy task, subsequent detrimental changes in bloodflow can paradoxically result in reduced/impaired myocardial perfusion. This condition of mismatch between post-PCI epicardial coronary patency and impaired myocardial reperfusion is defined as slow-flow or no-reflow. It is typically caused by and related to the presence of a damaged, dysfunctional, and/or obstructed coronary microvasculature. When no-reflow occurs, it has an adverse effect on the subsequent mid- and long-term prognosis as it is associated with a higher risk of reinfarction, arrhythmias, heart failure, and a higher in-hospital and long-term cardiac mortality. Frustratingly, nearly four decades after the first PCI, there is still uncertainty about the pathophysiology of no-reflow and a need to define successful prevention and treatment strategies.