Response to Letter Regarding Article, “Optical Coherence Tomographic Analysis of In-Stent Neoatherosclerosis After Drug-Eluting Stent Implantation”
We appreciate Nakano et al's interest and concern regarding the inconsistent frequency of in-stent neoatherosclerosis between the pathological and optical coherence tomography (OCT) data. In their autopsy study, Nakazawa et al reported the frequency of neoatherosclerosis in 41% of drug-eluting stent (DES) lesions with a follow-up time of 2–6 years.1 To the contrary, our recent OCT data showed lipid-containing and thin-cap fibroatheroma-containing neointima in 90% and 52% of DES lesions with in-stent restenosis at median follow-up of 32 months.2 With regard to this discrepancy, we fully agree with the plausible explanations based on the comparison between histological and OCT methodologies suggested by Nakano et al. Although foamy macrophage accumulation on the luminal border of neointima possibly suggests intimal vulnerability, the incidence of thin-cap fibroatheroma-containing neointima might have been overestimated in the OCT study.
In a clinical aspect, we would like to emphasize the remarkable difference in the population characteristics of the two studies. In the autopsy cases with DES, more than 70% of deaths were not stent-related. Stent thrombosis was observed in 20%, and restenosis was shown in only 6% overall. Conversely, our OCT study included selected patients with DES in-stent restenosis (30 stable and 20 unstable angina as clinical presentations) in which intimal hyperplasia was a predominant restenosis mechanism, excluding stented lesions showing underexpansion with little neointima. Moreover, all but 1 patient underwent clinically driven target lesion revascularization. In patients presenting with acute coronary syndrome, the frequency of thin-cap fibroatheroma-containing neointima (75% versus 37%), intimal rupture (75% versus 47%), and intraluminal thrombi (80% versus 43%) was much higher than in stable angina, which suggests a relationship between clinical presentation and intimal vulnerability. Thus, we assume that the higher incidence of major OCT findings, such as thin-cap fibroatheroma-containing neointima and intimal rupture, may be related to more advanced neoatheroslcerosis in the selected lesion subset with clinically significant restenosis. In our current OCT study, the overall incidence of neoatherosclerosis in the general DES population remains unclear. Nevertheless, the data strongly support that de novo atherosclerotic process of neointima is a frequent and important mechanism of late DES in-stent restenosis.
As Nakano et al mentioned in their letter, OCT findings of intimal tissue should be interpreted with caution and totally validated. Furthermore, the presence of stent failure, clinical presentation, and stent duration in a studied cohort should be considered for better understanding.
Seung-Jung Park, MD, PhD
Soo-Jin Kang, MD, PhD
Duk-Woo Park, MD, PhD
Jong-Young Lee, MD
Won-Jang Kim, MD
Seung-Whan Lee, MD, PhD
Young-Hak Kim, MD, PhD
Cheol Whan Lee, MD, PhD
Seong-Wook Park, MD, PhD
Department of Cardiology
University of Ulsan College of Medicine
Asan Medical Center
Gary S. Mintz, MD
Cardiovascular Research Foundation
New York, New York
Takashi Akasaka, MD, PhD
Division of Cardiovascular Medicine
Wakayama Medical University
- © 2011 American Heart Association, Inc.