No-Reflow Phenomenon and Lesion Morphology in Patients With Acute Myocardial Infarction

Abstract

Background-The no-reflow phenomenon is associated with poor functional and clinical outcomes for patients with acute myocardial infarction (AMI). In the era of primary intervention, accurately identifying lesions at high risk of no reflow is of crucial importance. At present, no study into the relationship between lesion morphology and no reflow has been performed. The aim of this study was to investigate the relationship between preintervention intravascular ultrasound (IVUS) lesion morphology and the no-reflow phenomenon. Methods and Results-This study comprised 100 consecutive patients with AMI who underwent preintervention IVUS and were successfully recanalized with primary balloon angioplasty or stenting. IVUS was again performed to identify and exclude any mechanical vessel obstruction in cases of thrombolysis in myocardial infarction flow grade 0, 1, or 2 after intervention in the absence of angiographic stenosis. Angiographic no reflow was seen in 13 patients (13%). Univariate analysis indicated that hypercholesterolemia, fissure and dissection, lipid pool-like image, lesion, and reference external elastic membrane cross-sectional area correlate with the no-reflow phenomenon. Multivariate logistic regression analysis showed that lipid pool-like image (PϽ0.05; odds ratio 118; 95% CI, 1.28 to 11 008) and lesion elastic membrane cross-sectional area (PϽ0.05; odds ratio 1.55; 95% CI 1.01 to 2.38) are independent predictive factors of no-reflow phenomenon after reperfusion for AMI. Conclusions-Large vessels with lipid pool-like image are at high risk for no reflow after primary intervention for AMI.Also, plaque content may play a role in damage to the microcirculation after primary intervention for AMI.

Coronary Flow Velocity Pattern Immediately After Percutaneous Coronary Intervention as a Predictor of Complications and In-Hospital Survival After Acute Myocardial Infarction

“…However, it was reported that reperfusion therapy resulted in insufficient coronary microcirculation attributable to reperfusion injury, such as oxygen-free radical injury, 28,29 calcium overload, microvascular spasm, 10 neutrophil plugging of the microvessels, 30 and tissue edema 8 or embolization of the coronary microvasculature attributable to dissemination of thrombi and the contents of the disintegrated atheroma in the lesion to distal parts of the coronary vasculature. 31,32 In the present study, in 75% of the patients with severe microvascular injury, an ST-segment reelevation was observed in the absence of epicardial mechanical obstruction immediately after PCI. Therefore, microvascular injury is not only determined by the size of the infarction associated with myocardial ischemia but also by reperfusion injury and interventioninduced release of the thrombi and the contents of the disintegrated atheroma.…”

Effect of Adjunctive Tirofiban Therapy on Angiographic and Clinical Outcomes in Patients With ST-segment Elevated Acute Myocardial Infarction Undergoing Primary Stenting

“…Impact of thrombus burden on myocardial reperfusion: In the present study, we found that an RLD of the IRA ≥ 3.5 mm and a lesion length ≥ 3.5 mm were the independent predictors of unsuccessful reperfusion. Our finding was consistent with recent studies 22,23) which demonstrated that large vessels usually contain large amounts of plaque burden and high-burden thrombus formation. Furthermore, our clinical observations led us understand that the longer the lesion length, the greater the plaque burden.…”

“…During coronary intervention, the thrombus is crushed and the plaque is artificially ruptured, which in turn, cause a release of macro-and microthrombus, and lipid pool-like contents. 22,23) These materials subsequently cause macro-and microembolism, and microvascular dysfunction. 22,23) The dislodged thrombi further activate more platelets and therefore, the thrombosis cascade, and this ultimately yields slow-flow or no-reflow in the IRA.…”

“…22,23) These materials subsequently cause macro-and microembolism, and microvascular dysfunction. 22,23) The dislodged thrombi further activate more platelets and therefore, the thrombosis cascade, and this ultimately yields slow-flow or no-reflow in the IRA. Therefore, the large IRA and the longer lesion length had a mutual interaction which appeared to be a determinant for unsuccessful reperfusion.…”

Coronary Blood Flow Assessment After Successful Angioplasty for Acute Myocardial Infarction Predicts the Risk of Long-Term Cardiac Events

“…However, microvascular injury is determined not only by the size of the infarct but also by reperfusion injury, 16 PTCA-induced thrombus, and atheroma fragmentation. 17 Indeed, patients with severe microvascular injury immediately after PTCA have a higher frequency of ST-segment re-elevation 11 or incomplete ST-segment resolution, 18 and a continuously declining post-PTCA velocity has been linked to vessel reocclusion. 19 Several studies have shown that patients with no reflow on myocardial contrast echocardiography 20 or Doppler guidewire assessment 9,11,12 have poor functional LV recovery and a high frequency of complications such as CHF, pericardial effusion, cardiac tamponade, and cardiac rupture.…”