Intravascular Ultrasound Observation of the Mechanism of No-Reflow Phenomenon in Acute Myocardial Infarction

Abstract

ObjectiveTo study the mechanism of the no-reflow phenomenon using coronary angiography (CAG) and intravascular ultrasound (IVUS).MethodsA total of 120 patients with acute myocardial infarction (AMI) who successfully underwent indwelling intracoronary stent placement by percutaneous coronary intervention (PCI). All patients underwent pre- and post-PCI CAG and pre-IVUS. No-reflow was defined as post-PCI thrombolysis in myocardial infarction (TIMI) grade 0, 1, or 2 flow in the absence of mechanical obstruction. Normal reflow was defined as TIMI grade 3 flow. The pre-operation reference vascular area, minimal luminal cross-sectional area, plaque cross-sectional area, lesion length, plaque volume and plaque traits were measured by IVUS.ResultsThe no-reflow group was observed in 14 cases (11.6%) and normal blood-flow group in 106 cases (89.4%) based on CAG results. There was no statistically significant difference in the patients’ medical history, reference vascular area (no-flow vs. normal-flow; 15.5 ± 3.2 vs. 16.2 ± 3.3, p> 0.05) and lesion length (21.9 ± 5.1 vs. 19.5 ± 4.8, p> 0.05) between the two groups. No-reflow patients had a longer symptom onset to reperfusion time compared to normal blood-flow group [(6.6 ± 3.1) h vs (4.3 ± 2.7) h; p< 0.05] and higher incidence of TIMI flow grade< 3 (71.4% vs 49.0%, p< 0.05). By IVUS examination, the no-reflow group had a significantly increased coronary plaque area and plaque volume compared to normal blood-flow group [(13.7 ± 3.0) mm2 vs (10.2 ± 2.9) mm2; (285.4 ± 99.8) mm3 vs (189.7 ± 86.4) mm3; p< 0.01]. The presence of IVUS-detected soft plaque (57.1% vs. 24.0%, p< 0.01), eccentric plaque (64.2% vs. 33.7%, p< 0.05), plaque rupture (50.0% vs. 21.2%, p< 0.01), and thrombosis (42.8% vs. 15.3%) were significantly more common in no-reflow group.ConclusionThere was no obvious relationship between the coronary risk factors and no-reflow phenomenon. The symptom onset to reperfusion time, TIMI flow grade before stent deployment, plaque area, soft plaques, eccentric plaques, plaque rupture and thrombosis may be risk factors for the no-reflow phenomenon after PCI.

Risk Factors for No-Reflow Phenomenon after Percutaneous Coronary Intervention in Patients with Acute Coronary Syndrome

“…During balloon dilation, the thrombi easily fracture and flow to downstream smaller arteries with the recanalization of blood flow, resulting in adverse events such as distal coronary embolization and secondary embolism after recanalization. Moreover, prolonged reperfusion time can also lead to organization of a large number of intracoronary thrombi and form fibrous tissues, further increasing the difficulty of recanalization as well as the risk of PCI distal embolization [17][18][19][20] .…”

Prognostic Association of Circulating Neutrophil Count with No-Reflow in Patients with ST-Segment Elevation Myocardial Infarction following Successful Primary Percutaneous Intervention

“…ACS is a group of clinical syndromes characterized by rupture or erosion of coronary atherosclerotic plaques and subsequent complete or incomplete thrombotic occlusion [ 22 ]. Lipid-rich plaques are correlated with impaired reperfusion after restoration of the epicardial artery [ 23 ]. Noncalcified plaque burden is correlated with the neutrophil/lymphocyte ratio [ 24 ].…”

Clinic Predictive Factors for Insufficient Myocardial Reperfusion in ST-Segment Elevation Myocardial Infarction Patients Treated with Selective Aspiration Thrombectomy during Primary Percutaneous Coronary Intervention

“…Mechanical resistance at the occlusion has a potential role of prevention of passage of the aspiration device through the IRA segment. In some STEMI patients, a high-grade, nonthrombotic, unstable atherosclerotic plaque causes the coronary obstruction [28]. Postaspiration cTFC value in these patients was often >40.…”