Microvascular Obstruction and the No-Reflow Phenomenon After Percutaneous Coronary Intervention

Platelet MEKK3 regulates arterial thrombosis and myocardial infarct expansion in mice

“…11 Microthrombosis is a common cause of the no-reflow phenomenon, which leads to defective myocardial reperfusion after reperfusion therapy, including thrombolytic or mechanical interventions. 37 Patients with myocardial infarct expansion have poorer exercise tolerance, more symptoms of congestive heart failure, and greater early and late mortality than those without expansion. 38,39 Excitingly, using a chronic MI model, we found that MEKK3 deficiency significantly impaired microthrombosis at the edge of the infarct area, alleviated infarct expansion from the ischemic region, and improved heart function post-MI.…”

Establishment and Characterization of an Experimental Model of Coronary Thrombotic Microembolism in Rats

“…Atherosclerotic embolization in the microvasculature is associated with adverse prognosis. [1][2][3][4] Research results derived from suitable experimental models of coronary microembolism would help clinicians to understand the underlying pathological mechanisms and to develop effective therapies of coronary microembolism induced by atherosclerotic embolization in the microvasculature.5 Until now, plastic microspheres ranging from 20 to 900 m in diameter were injected into the coronary microcirculation to establish the coronary microembolism models in dog, swine and sheep.6 -11 Experimental models were also made by injecting adenosine-diphosphate or catecholamine to induce platelet aggregation in coronary microcirculation in pigs.12-13 However, injecting microspheres with unique sizing would only occlude respective vessels with comparable sizes, while thrombotic debris in patients might vary greatly in sizing and affect vessels with different diameters. Models using adenosine diphosphate or catecholamine could mimic the platelet aggregation process during coronary microthrombosis but could not reflect the influences of various embolism components of atherosclerotic plaques.…”

“…Atherosclerotic embolization in the microvasculature is associated with adverse prognosis. [1][2][3][4] Research results derived from suitable experimental models of coronary microembolism would help clinicians to understand the underlying pathological mechanisms and to develop effective therapies of coronary microembolism induced by atherosclerotic embolization in the microvasculature. 5 Until now, plastic microspheres ranging from 20 to 900 m in diameter were injected into the coronary microcirculation to establish the coronary microembolism models in dog, swine and sheep.…”

Cardioprotective effect of liposomal prostaglandin E1 on a porcine model of myocardial infarction reperfusion no-reflow

“…Infarct size and microvascular hypoperfusion may increase at the time of coronary reperfusion, beyond that observed during the ischemic period. Endothelial injury is induced by an acute inflammatory response, generation of reactive oxygen species, intracellular calcium overload, and opening of the mitochondrial permeability transition pore (Jaffe et al, 2008). …”

“…"Reperfusion no-reflow" occurs after primary PCI for reperfusion of an infarct-related artery in AMI, which may be asymptomatic or present with continued chest pain and ST-segment elevation. Reperfusion no-reflow is preceded by ischemic cell injury, is confined to the irreversibly damaged necrotic zone, and may be exacerbated at the time of reperfusion (Jaffe et al, 2008), which is an independent predictor of adverse clinical outcome after AMI regardless of infarct size and which is associated with heart failure and increased mortality (Morishima et al, 2000).…”