Journal of Cardiology 62 (2013) 138–139
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Editorial
What imaging modality do you want to select for prediction of the no-reflow phenomenon?
Keywords: No reflow Intravascular ultrasound Optical coherence tomography
No-reflow after percutaneous coronary intervention (PCI) has been shown to predict larger myocardial infarct size and as a result, poor clinical outcomes. Thus, accurately detecting high-risk lesions of no-reflow phenomenon is warranted for interventional cardiologists. No-reflow phenomenon is caused by multiple factors including endothelial dysfunction, myocyte edema, neutrophil infiltration, microvascular spasm, oxygen-free radicals, and distal embolization of plaque and/or thrombus at culprit coronary lesion. Among these factors, distal embolization of the contents of the plaque and/or thrombus might be prevented, therefore several distal protection devices have been developed, and the interventional cardiologists realized their clinical usefulness. However, there are few articles to elucidate the usefulness of the distal protection devices. Incidence of no-reflow phenomenon is around 11–15% after PCI in acute coronary syndrome (ACS) [1,2]. Namely, because the majority of patients do not require distal protection devices, we cannot prove the effectiveness on the premise to use distal protection devices for all cases. If a randomized clinical trial were to be conducted in patients who are at high risk of no-reflow phenomenon during PCI, the effectiveness of the distal protection devices might be demonstrated. Based on this way of thinking, various researches to investigate the predictors of no-reflow phenomenon using imaging modalities have been actively carried out. In imaging modality used for predictive factor identification of no-reflow phenomenon, at first, intravascular ultrasound (IVUS) was the main constituent. Tanaka et al. showed that lipid poollike image and large vessels were independent predictive factors of no-reflow phenomenon after reperfusion of acute myocardial infarction (AMI) [3]. Watanabe et al. also showed that positively remodeled vessels with lipid-rich plaques as characterized by IVUS before PCI predicted the occurrence of angiographic no-reflow [4]. Their observation suggested that large amounts of plaque and
DOI of original article: http://dx.doi.org/10.1016/j.jjcc.2013.03.005.
lipid-like images estimated by IVUS might be associated with the occurrence of no-reflow phenomenon. However, lipid-like image estimated by IVUS is not a major predictor of no-reflow phenomenon in the real-world clinical setting, whereas, attenuated plaque is an important predictor in clinical practice. Okura et al. showed attenuated plaques might be related to a transient deterioration in coronary flow and result in larger infarct size and higher incidence of fatal arrhythmia following PCI in patients with ACS [5]. Yamada et al. evaluated the histological characteristics of plaques and revealed that attenuated plaques contained more fibrofatty tissue and necrotic core compared to non-attenuated plaques [6]. In this way, several studies have been done, however they were unfortunately not enough to be convincing because of small sample size. Although it is not an article to make specific mention of no-reflow phenomenon, Mehran et al. investigated 2256 cases by using IVUS and demonstrated that extensive atherosclerotic plaque burden both at the lesion and reference segment were independent predictors of creatine kinase-MB elevation after PCI [7]. Wu et al. analyzed clinical, angiographic, and IVUS data from 364 patients (n = 364 infarct-related arteries) enrolled in the randomized HORIZONSAMI trial. They concluded that the amount of attenuated plaque strongly correlated with no-reflow phenomenon [8]. In the clinical setting, many Japanese interventional cardiologists determine the indication of distal protection devices according to plaque volume and presence of attenuated plaque. This judgment is simple and quick, therefore this decision-making manner is widely accepted. Recently, Shibuya et al. reported that although tissue characterization of integrated backscatter (IB)-IVUS might provide additional information for distal embolization, plaque volume was the only significant predictor of distal embolization during PCI [9]. As seen from the above, IVUS derived-plaque volume is an important factor to predict no-reflow after PCI. On the other hand, optical coherence tomography (OCT) is a new imaging modality with unrivaled high resolution of 10–20 m. OCT has higher image resolution than IVUS and is superior in the evaluation of the plaque contents including calcification, thrombus, lipid pool, and thin-cap fibroatheroma (TCFA). However, OCT has several limitations. Because of the limited penetration depth of OCT (2 mm), plaque volume or arterial remodeling of atheromatous plaques cannot be estimated by OCT. In addition, the presence of thrombus, especially red thrombus, at the ACS lesion severely affects imaging analysis by OCT. Because exclusion of the blood is necessary, it may not be applicable for assessment of ostial coronary disease, severe stenotic lesions, and total occluded lesions. There are few articles that investigated the predictors of no-reflow
0914-5087 © 2013 The Author. Published by Elsevier Ltd. Open access under CC BY-NC-ND license. http://dx.doi.org/10.1016/j.jjcc.2013.05.013
Editorial / Journal of Cardiology 62 (2013) 138–139
after PCI by using OCT. Tanaka et al. revealed as follows: TCFA were more frequently observed in the no-reflow group than in the reflow group (50% vs. 16%, p < 0.005). The frequency of the no-reflow phenomenon increases according to the size of the lipid arc in the culprit plaque. A multivariable logistic regression model revealed that lipid arc alone was an independent predictor of no-reflow phenomenon in non-ST-segment elevation acute coronary syndrome [10]. Ozaki et al. also showed that TCFA was a high-risk plaque for microvascular obstruction after PCI in patients with ACS. Their conclusions suggested OCT-derived TCFA was an important predictor of no-reflow phenomenon [11]. As just described, IVUS-derived plaque volume is an important factor to predict no-reflow after PCI. It is necessary to quote the paper of Miyamoto et al. [12], in order to understand this discrepancy. They revealed that the OCT-derived TCFA had larger plaque burden and positive remodeling with predominant lipid component and less fibrous plaque assessed by IB-IVUS. In this way, OCT-derived TCFA is a surrogate marker of large plaque burden. Ikenaga et al. [13] investigated AMI patients using OCT and concluded that length of lipid pool was associated with microvascular no-reflow after primary PCI. Because plaque contents of culprit lesion in AMI include thrombus, evaluation by OCT is difficult due to the nature of this imaging modality. Thrombus hides the microarchitecture of plaque. Therefore, it might be possible that some TCFAs were misdiagnosed as non-TCFA. The authors evaluated longitudinal extent of lipid by multi cross-sectional OCT images to prevent misdiagnosis. At this point, it was thought that there was originality in this study. Unfortunately in the present study, patients with large vessels or less than thrombolysis in myocardial infarction grade 3 flow were excluded. A further study enrolling such patients who were excluded in the present study is needed to make this way of detection more convincing in real-world clinical practice. Despite several limitations of OCT, this innovative tool has various potentials in our field. Future studies using OCT might help us to predict no-reflow phenomenon by more precise imaging of intravascular pathophysiology and might eventually improve clinical outcomes of patients treated with PCI. I strongly hope that OCT provides new knowledge into interventional cardiology. References [1] Muramatsu T, Kozuma K, Tsukahara R, Ito Y, Fujita N, Suwa S, Koyama S, Saitoh M, Kamiya H, Nakamura M. Comparison of myocardial perfusion by distal protection before and after primary stenting for acute myocardial infarction: angiographic and clinical results of a randomized controlled trial. Catheter Cardiovasc Interv 2007;70:677–82. [2] Hong YJ, Jeong MH, Choi YH, Ko JS, Lee MG, Kang WY, Lee SE, Kim SH, Park KH, Sim DS, Yoon NS, Youn HJ, Kim KH, Park HW, Kim JH, et al. Predictors of noreflow after percutaneous coronary intervention for culprit lesion with plaque rupture in infarct-related artery in patients with acute myocardial infarction. J Cardiol 2009;54:36–44.
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Junji Yajima (MD) ∗ Department of Cardiovascular Medicine, The Cardiovascular Institute, 3-2-19, Nishiazabu, Minato-ku, Tokyo 106-0031, Japan ∗ Tel.:
+81 3 3408 2151; fax: +81 3 3408 2159. E-mail address:
[email protected] 14 May 2013
