Author + information
- Soo-Jin Kang, MD, PhD,
- Mineok Chang, MD,
- Sung-Han Yoon, MD,
- Jung-Min Ahn, MD,
- Seungbong Han, PhD,
- Duk-Woo Park, MD, PhD,
- Seung-Whan Lee, MD, PhD,
- Young-Hak Kim, MD, PhD,
- Cheol Whan Lee, MD, PhD,
- Seong-Wook Park, MD, PhD and
- Seung-Jung Park, MD, PhD∗ ()
- ↵∗Asan Medical Center, 388-1 Poongnap-dong, Songpa-gu, Seoul, 138-736, South Korea
The development of neoatherosclerosis characterized by lipid core, in-stent thin-cap fibroatheroma (TCFA), calcification, and intimal rupture contribute to development of late stent failure (1,2). We assessed the impact of optical coherence tomography (OCT)-detected TCFA and intimal rupture on the occurrence of periprocedural myocardial infarction (MI) and 2-year major adverse cardiac events (MACE).
From August 1, 2008 to June 1, 2012, 518 patients with in-stent restenosis (ISR) underwent target lesion revascularization at the Asan Medical Center, Seoul, Korea. After excluding the patients with hemodynamic instability, inability of the OCT catheter to cross the tight stenosis, the presence of left main or saphenous vein graft lesions, acute MI, vessel size >4 mm, total stent length >40 mm, pre-dilation before OCT examination, or an angiographically visible thrombus, pre-procedural OCT images were available in 152 patients (41 bare-metal stents [BMS] and 111 drug-eluting stents [DES]). Periprocedural MI was defined as post-procedure peak creatine kinase–myocardial band (CK-MB) >15 ng/ml (>3 times the upper limit of normal). OCT image was obtained by occlusive (LightLab Imaging, Westford, Massachusetts) or nonocclusive (DragonFly catheter and C7XR, LightLab Imaging) technique. Calcific or lipidic intima, TCFA, intimal rupture, and thrombi were previously described (2,3).
All values were expressed as the median value (interquartile range [IQR]) or counts and percentages and compared by nonparametric Mann-Whitney or chi-square statistics. Multivariable analysis included the variables (p < 0.2) such as age, male sex, DES, unstable angina, stent duration, in-stent TCFA, intimal rupture, and thrombi.
The patient age was 64.0 (56.3 to 69.0) years, and 80% were men. Clinical presentation was stable angina in 77% and unstable angina in 23%. The stent duration was 52.8 (17.5 to 86.9) months (46.2 [IQR: 14.0 to 70.0] months in DES vs. 116.4 [IQR: 58.6 to 148.7] months in BMS; p < 0001). Peak CK-MB level before the procedure was normal in all patients. Table 1 summarizes pre-procedural OCT findings.
ISR was treated with DES in 62%, cutting balloon in 26%, and other types of balloon in 12%. The patients with (vs. without) in-stent TCFA had a higher post-procedural peak CK-MB (2.0 [IQR: 1.0 to 5.0] vs. 1.4 [IQR: 0.8 to 2.2] ng/ml; p = 0.012) and more frequent periprocedural MI (13% vs. 2%; p = 0.010). Moreover, the patients with (vs. without) intimal rupture showed a higher post-procedural peak CK-MB (2.0 [IQR: 0.9 to 4.1] vs. 1.3 [IQR: 0.9 to 2.4] ng/ml; p = 0.017) and more frequent periprocedural MI (13% vs. 3%; p = 0.015). Stent duration (r = −0.360), fibrous cap thickness (r = −0.176), and length of in-stent TCFA (r = 0.331) significantly correlated with post-procedural peak CK-MB (all p < 0.05). On receiver-operating characteristic curve analysis, fibrous cap thickness ≤60 μm predicted periprocedural MI (sensitivity = 91%, specificity = 58%, area under curve = 0.744). In 11 patients with periprocedural MI, the mechanism was distal embolization in 5 (45%) patients, side-branch occlusion in 5 (45%) patients, and undetermined mechanism in 1 (10%) patient. Old age (estimated coefficient = 0.024), unstable angina (0.610), DES (−0.422), and intimal rupture (0.431) were independently associated with post-procedural peak CK-MB (all p < 0.05).
With a follow-up time of 32.1 (25.7 to 37.3) months, MACE occurred in 13.8% (cardiac death 1.3%, MI 0.7%, target lesion revascularization 5.3%, and periprocedural MI 7.2%). The MACE rate was significantly higher in the patients with and without in-stent TCFA (20.6% vs. 8.3%; p = 0.026) or intimal rupture (19.7% vs. 8.6%; p = 0.041). However, there was no significant difference in the rates of MACE excluding periprocedural MI between the patients with and without in-stent TCFA (7.4% vs. 6.0%) or intimal rupture (7.0% vs. 6.2%; all p > 0.05).
This current study demonstrates the impact of neoatherosclerosis with high-risk features on the occurrence of periprocedural MI after target lesion revascularization. Although in-stent neoatherosclerosis may have diverse features, the presence of intimal rupture, TCFA or thrombi was significantly associated with the high risk of periprocedural MI. Fibrous cap thickness ≤60 μm predicted periprocedural MI, and intimal rupture independently affected post-procedural CK-MB elevation. However, in the majority, the elevation of CK-MB was only modest and the underlying mechanism of periprocedural MI was side-branch occlusion (not a large dissection or no reflow), which partly account for the lack of association with 2-year MACE excluding periprocedural MI.
Because of the relatively small sample size, low event rate and selection bias, the results cannot be applied to the general population. Also, the study did not compare the risk of periprocedural MI among various methods of ISR treatment. Second, with different stent duration, this study could not compare the frequency and implication of neoatherosclerosis between DES and BMS. Finally, the definition and clinical impact of periprocedural MI according to the magnitude of cardiac enzyme remain uncertain.
In conclusion, vulnerable intimal characteristics in restenotic tissue within previously implanted stents were associated with the occurrence of periprocedural MI, but rarely affected long-term clinical outcomes after target lesion revascularization.
Please note: This study was supported by a grant from the Korea Health 21 R&D Project, Ministry of Health and Welfare, South Korea (A090264). All authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation
- Nakazawa G.,
- Otsuka F.,
- Nakano M.,
- et al.
- Kang S.J.,
- Mintz G.S.,
- Akasaka T.,
- et al.
- Yabushita H.,
- Bouma B.E.,
- Houser S.L.,
- et al.