Coronary microvascular reperfusion injury and no-reflow in acute myocardial infarction

Abstract

Purpose: To review (1) the mechanisms of coronary microvascular reperfusion injury, particularly in the relationships between microvascular endothelium dysfunction, microstructure damage, microemboli and no-reflow phenomena; (2) the no-reflow presentation and management at ischemia-reperfusion to suggest future direction for noreflow therapy in acute myocardial infarction. Sources: Original articles and reviews published between 1997 and 2007 and focusing on the no-reflow phenomenon in MEDLINE and PubMed. The search terms used were "no-reflow", "microvascular injury", "acute myocardial infarction" and "reperfusion injury". All papers identified were English-language, full text papers. In addition, the reference lists of identified relevant articles were also searched. Conclusions:The no-reflow phenomenon is characterised by damage to microvascular function and microstructure at ischaemia-reperfusion. Microemboli contribute to noreflow. Clinical myocardial contrast echocardiography (MCE), scintigraphic and magnetic resonance imaging (MRI) have shown evidence of microvascular damage, eg, perfusion defects are closely related to lack of contractile recovery and irreversible myocyte damage. Clinical agents and devices targeting microvascular injury (especially protection of endothelium and reduction of microemboli) after acute myocardial infarction may be key points to improve no-reflow.

Postconditioning of the Lower Limb—Protection Against the Reperfusion Syndrome

“…An early change in the microcirculation after reperfusion is the reduction of the capillary blood flow, the so-called capillary noreflow [14]. This phenomenon seems to be related to an obstruction in the small (capillary) vessels without manifest thrombus formation, endothelial cell swelling and necrosis, loss of the tissue structure, leukocyte activation, accumulation and plugging, generation of soluble mediators and ROS, and the concomitant tissue edema [15]. The significantly higher flow rates detected in the PostC group clearly indicate a reduction in the capillary no-reflow and delineates that PostC must have had a positive effect on the endothelial IR-injury and local inflammatory mechanisms.…”

Coronary no‐reflow phenomenon: From the experimental laboratory to the cardiac catheterization laboratory

“…The event encountered in the clinical setting where no-reflow plays a significant role is acute myocardial infarction [3], and prognosis consequential to an untreated noreflow event is guarded [4].…”

Evaluation of continuous and intermittent myocardial topical negative pressure

“…The treatment of established no-reflow is mainly pharmacological, as the obstruction occurs at the microvasculature level. Compared with patients in whom no-reflow is transient, refractory no-reflow is associated with a markedly increased risk of 30-day mortality [34,35]. To apply TNP at those areas in the acute phase, with for example a transthoracic device, might be useful for those patients.…”