Stenting of Culprit Lesions in Unstable Angina Leads to a Marked Reduction in Plaque Burden: A Major Role of Plaque Embolization?

Abstract

Background-Intravascular ultrasound (IVUS) studies have shown that a mechanism of plaque compression/embolization contributes toward the poststenting increase in lumen area. The aim of this IVUS study was to compare the mechanisms of lumen enlargement after coronary stenting in 54 consecutive patients with unstable angina (UA) (group 1) and 56 with stable angina (group 2) to verify whether plaque embolization plays a major role in the former. Methods and Results-Both groups underwent the IVUS assessment (speed, 0.5 mm/sec) before the intervention and after stent implantation. The lumen area, the external elastic membrane area, and the plaqueϩmedia area (PA) were measured at 0.5-mm intervals. PA reduction in the lesion site was significantly greater in group 1 (Ϫ2.50Ϯ1.97 versus Ϫ0.53Ϯ1.43 mm 2 , PϽ0.001). After stenting, 47% of the lumen area increase in group 1 was obtained by means of PA reduction, and 53% was attributable to external elastic membrane area increase; the corresponding figures in group 2 were 13% and 87% (PϽ0.05). Decrease in PA after stenting was the only significant predictor of the MB fraction of creatinine kinase (CK-MB) release in a multiple regression model (Pϭ0.047). Conclusions-Serial volumetric IVUS assessment revealed in UA lesions a marked poststenting reduction in plaque volume, which is significantly greater than in stable angina and is associated with postprocedural CK-MB release. The decrease in PA during the procedure predicts CK-MB release in a multiple regression model. These findings suggest that stent deployment is often associated with plaque embolization in patients with UA. (Circulation. 2003;107:2320-2325.)

Target Lesion Thin-Cap Fibroatheroma Defined by Virtual Histology Intravascular Ultrasound Affects Microvascular Injury During Percutaneous Coronary Intervention in Patients With Angina Pectoris

“…[18][19][20][21][22] In addition to the effect of plaque burden, specific plaque characteristics, such as lipid pool-like image, intracoronary mural thrombus, or ultrasonic attenuation (assessed by grayscale IVUS), have been shown to be related to the no-reflow phenomenon during PCI in patients with ACS. 23- 27 Recently, radiofrequency signal-derived IVUS tissue characterization has been developed to provide objective and quantitative information for predicting distal microembolization and slow flow during PCI.…”

Troponin Elevation After Percutaneous Coronary Intervention Directly Represents the Extent of Irreversible Myocardial Injury

“…In general, angiographic appearance of flow, dissection, and mechanical side-branch occlusion were all poorly predictive of new MRI-defined injury, which possibly implies the important role of collateral vessels and of plaque lesion composition in the occurrence of irreversible injury. 22 …”

Plaque Volume and Occurrence and Location of Periprocedural Myocardial Necrosis After Percutaneous Coronary Intervention

“…The net loss of plaque volume was thought to represent a combination of plaque redistribution, compression, and/or embolization. In patients with severe unstable angina (with no glycoprotein IIb/IIIa inhibition or clopidogrel), Prati et al 18 were able to show a PCI-related pronounced reduction in plaque volume, and reduction in plaque area was directly proportional to the rise in CK-MB. In patients undergoing primary PCI, Sato et al 19 demonstrated a decrease in plaque volume that was significantly larger in patients with inadequate reflow than in those with normal reflow and showed that changes in plaque volume were significantly correlated with c-TFC after PCI.…”