Complications of coronary intervention

Acute Stent Thrombosis: Technical Complication or Inadequate Antithrombotic Therapy? An Optical Coherence Tomography Study

Sammy Elmariah, MD, MPH

Ik-Kyung Jang, MD, PhD

A 68-year-old woman was admitted to the hospital with non–ST-segment elevation myocardial infarction. Coronary angiography showed a 95% mid stenosis in the left anterior descending artery ( Fig. 2.1 A). The lesion was treated with a 2.50 × 18 mm Xience drug-eluting stent (Abbott Vascular, Santa Clara, California) during bivalirudin infusion ( Fig. 2.1 B). At the end of the procedure, the patient received a 600-mg loading dose of clopidogrel and bivalirudin was discontinued. Seventy minutes later, the patient experienced chest pain with anterior ST-segment elevations. Repeat angiography demonstrated acute stent thrombosis (AST) ( Fig. 2.2 A). While the patient was on heparin and eptifibatide, low-pressure angioplasty was performed. Optical coherence tomography imaging showed an intravascular mass consistent with platelet-rich thrombus within the stent ( Fig. 2.2 B).

Technical factors or inadequate antithrombotic therapies are responsible for AST. ^, In this case, mechanical complications, such as dissection, underexpansion, or significant malapposition were ruled out. Review of the timing of antithrombotic therapy revealed possible gaps in therapy. Bivalirudin was discontinued simultaneous to the administration of clopidogrel. Clinical effects of bivalirudin continue for 1 hour after its discontinuation, whereas the anticipated onset of clopidogrel (600 mg) effect is 2 hours after its administration. Consequently, antithrombotic therapy in our patient was insufficient for approximately 1 hour, during which the AST occurred ( Fig. 2.3 ).

Our case highlights the usefulness of optical coherence tomography in evaluating underlying mechanisms for AST and in characterizing thrombus composition (platelets). Additionally, it emphasizes the significant increase in ischemic events with bivalirudin in subjects not pretreated with clopidogrel. ^, Care is needed to ensure sufficient antithrombotic therapy in these patients with the use of rapidly acting antithrombotic agents, prolongation of bivalirudin infusion, or earlier administration of the clopidogrel loading dose.

An Unusual Case of Stent-in-Stent Thrombosis

Jiang Ming Fam, MBBS

W. den Dekker, MD

Paul de Graaf, BSC

Evelyn Regar, MD, PhD

A 71-year-old man was admitted for acute coronary syndrome. Six weeks earlier he had a Promus Premier 3.0 × 12 mm (Boston Scientific, Natick, Massachusetts) drug-eluting stent (DES) implanted in the obtuse marginal artery for unstable angina. On repeat coronary angiography, haziness ( Fig. 2.4 A, Online Video 2.1 ) in the ostial stented region was observed; however Thrombolysis In Myocardial Infarction grade flow was good. Optical coherence tomography (OCT) revealed a nonexpanded stent (star with struts marked with +) within and protruding out of the implanted stent. The stent appeared well expanded and apposed to the vessel wall (implanted stent with struts marked with asterisk [ Fig. 2.4 C–D, Online Video 2.2 ]). There was lumen compromise secondary to a large amount of thrombus formation seen around the unexpanded stent struts together with incomplete lesion coverage proximally. Attempts to rewire or retrieve the unexpanded stent were unsuccessful. On the basis of the OCT findings, the decision was made to crush the unexpanded stent and implant a Promus Premier 3.5 × 12-mm drug-eluting stent (Boston Scientific, Natick, Massachusetts) proximally with good results (angiography shown in Fig. 2.4 B, Online Video 2.3 ). Multiple layers of struts (OCT) (white arrows in Fig. 2.4 D-3; Online Video 2.4 ) from the two overlapping implanted stents as well as the previously unexpanded stent can be seen in Fig. 2.4 D–E. Fig. 2.4 F shows the three-dimensional reconstruction (QAngio OCT software, Medis Specials, Leiden, Netherlands) of the vessel before and after procedure showing the crushed stent in stent.

We describe a rare cause of stent thrombosis, emphasizing that mechanical stent-related causes should always be ruled out, especially if stent thrombosis occurs soon after implantation. In our case, an unexpanded stent formed the nidus of thrombus formation. The unexpanded stent was likely due to loss or embolization during attempts at device delivery in a challenging procedure owing to significant calcification, severe tortuosity, and suboptimal guide catheter backup. Of note, this complication was previously undetected on angiography. This is a rare case of stent-in-stent thrombosis in which OCT demonstrates the potential to improve clinical diagnosis and procedural outcome.

Delayed Healing of a Coronary Stent Graft

Masamichi Takano, MD

Masanori Yamamoto, MD

Toru Inami, MD

Daisuke Murakami, MD

Yoshihiko Seino, MD

Kyoichi Mizuno, MD

A polytetrafluoroethylene (PTFE)-covered stent composed of 2 metallic stents and sandwiched PTFE membrane is used especially for bailout of percutaneous intervention complicated with coronary perforation and treatment of aneurysms to prevent subsequent rupture. Detailed features within coronary stent grafts have not yet been reported in living patients. A 65-year-old man underwent implantation of a PTFE-covered stent (3.5/19 mm) to seal a giant aneurysm in the right coronary artery. Follow-up angiography at 32 months showed patency and a slightly irregular contour of the stent segment. Coronary angioscopy showed sufficient neointimal growth at the stent proximal edge. Several struts in the mid portion were regarded as exposed struts lacking neointimal coverage. Red thrombi were found in the distal portion despite continuous oral anticoagulation and dual-antiplatelet therapies ( Fig. 2.5 , Online Video 2.5 ). Optical coherence tomography confirmed the presence of uncovered struts as well as thrombus formation ( Fig. 2.6 ). Pathologic validation using light and electron microscopy has demonstrated incomplete endothelialization and accumulation of fibrin clots within endovascular stent grafts implanted for aortic aneurysms. The images for this case suggest that delayed healing and thrombogenicity of coronary stent graft persists for an extended period.

Multivessel Honeycomb-Like Structure Finding in Optical Coherence Tomography

Mio Musashi, MD

Norio Tada, MD

Naoki Uemura, MD

Osamu Kawashima, MD

Tatsushi Ootomo, MD

Naoto Inoue, MD

Hideki Abe, MD

Taiichiro Meguro, MD, PhD

A 66-year-old man with a history of chronic atrial fibrillation was referred to our hospital for a preoperative cardiac evaluation for intestinal stenosis. An electrocardiogram showed negative T wave in leads II, III, aVF, and V ₃ to V ₅ , and an echocardiogram showed moderate hypokinesis in the anteroseptal left ventricular wall. Coronary angiography revealed multiple linear filling defects with haziness in the right coronary artery and left anterior descending artery ( Fig. 2.7 A–B). After surgery for intestinal stenosis, we performed a staged percutaneous coronary intervention for right coronary artery and left anterior descending artery stenosis. In both lesions, optical coherence tomography revealed multiple channels of various sizes communicating with each other with smooth septa, so-called honeycomb-like structures ( Fig. 2.7 C–J, Online Videos 2.6 and 2.7 ). The septa were composed of high signal intensity and low-signal attenuation, suggesting that the structure consisted of fibrous material. We implanted Xience Prime stents (Abbott Vascular, Santa Clara, California) for both lesions, resulting in successful revascularization. Although anticoagulation therapy with warfarin in addition to dual-antiplatelet therapy was started after percutaneous coronary intervention, renal infarction occurred 3 months after percutaneous coronary intervention. Emergent angiography revealed a filling defect with thrombus in the left renal artery, and it was successfully removed with percutaneous thrombectomy. Under intensive anticoagulation therapy after the renal infarction, transesophageal echocardiography revealed no evidence of thrombus; however, spontaneous echocardiographic contrast was observed in the left atrium including an appendage.

A honeycomb-like structure finding during optical computed tomography has been reported previously. Authors of the studies reported a honeycomb-like structure that represented recanalization of an organized thrombus. However, its etiology is still controversial. To our knowledge, there has been no report of a honeycomb-like structure at multiple vessels. The patient had received no anticoagulation therapy on the first visit. From the history of atrial fibrillation and renal thromboembolic infarction, we speculated that, in our case, the honeycomb-like structure represented recanalization of cardiogenic embolism.

Optical Coherence Tomography Assessment of Late Intrascaffold Dissection: A New Challenge of Bioresorbable Scaffolds

Yohei Ohno, MD

Andrea Mangiameli, MD

Guilherme F. Attizzani, MD

Davide Capodanno, MD, PhD

Corrado Tamburino, MD, PhD

A 48-year-old man was admitted because of a non–ST-segment elevation myocardial infarction. Fifteen months earlier, a 3.0 × 28 mm bioresorbable vascular scaffold (BVS) (Absorb, Abbott Vascular, Santa Clara, California) was implanted in the mid left anterior descending coronary artery for stable angina. Coronary angiography showed a focal in-scaffold restenosis ( Fig. 2.8 A). Optical coherence tomography (Ilumien, St. Jude Medical, St. Paul, Minnesota) revealed a heterogeneous pattern consisting of neointimal hyperplasia ( Fig. 2.8 C), mural white thrombus ( Fig. 2.8 C), and lipidic plaque with attenuation ( Fig. 2.8 D). Optical coherence tomography after predilation with a 2.0 × 15 mm semicompliant balloon showed outer migration of scaffold struts ( Fig. 2.8 E, G, and H) visible in several frames leading to intrascaffold dissection ( Fig. 2.8 E–H) extending behind the disrupted scaffolds. Good angiographic result was obtained after a 3.0 × 15 mm noncompliant balloon was dilated and administration of an abciximab infusion ( Fig. 2.8 B); no further intervention was performed.

Although a BVS promotes acute vessel scaffolding similar to metallic stents, it carries a unique feature of complete resorption approximately 3 years after implantation. It is known that 6 months after the implantation, a BVS loses radial strength and structural continuity; therefore it no longer functions as a scaffold, which was likely the potential mechanism that favored in-scaffold dissection after balloon dilation in our case. Although clinicians should be aware that in-scaffold dissections might occur after performing in-BVS balloon dilation for late BVS failure (i.e., theoretically after 6 months), as herewith presented, the best management of BVS restenosis (i.e., implanting another BVS in BVS or balloon dilation only) remains to be determined.

Phantom Stent Thrombosis Intracoronary Imaging Insights

Fernando Rivero, MD

Javier Cuesta, MD

Amparo Benedicto, MD

Teresa Bastante, MD

Daniel Rodriguez-Alcudia, MD

M. Cruz Aguilera, MD

Fernando Alfonso, MD

A 72-old-year-man was admitted for an inferior ST-segment elevation acute myocardial infarction. Seven years earlier, a 2.75 × 15 mm bare-metal stent was successfully implanted in the posterolateral branch of the right coronary artery at another institution. Emergent coronary angiography showed a thrombotic occlusion at the mid segment of the right coronary artery ( Fig. 2.9 ). After multiple unsuccessful attempts to cross the occlusion, eventually a hydrophilic guidewire was advanced across the occluded segment. Thromboaspiration was unsuccessful despite the use of two different aspiration devices that were unable to cross the lesion. Optical coherence tomography (OCT) was performed to clarify the underlying substrate. A large intracoronary red thrombus with intense posterior shadowing that prevented an adequate visualization of the underlying vessel wall was revealed with OCT. At this point, the use of intravascular ultrasonography (IVUS) was considered to further clarify the anatomy of this challenging lesion. IVUS revealed the presence of a metal structure embedded within the thrombus, highly suggestive of the presence of an “abandoned,” underexpanded intracoronary stent at this coronary segment. The abandoned stent was eventually crushed to the arterial wall with a new bare-metal stent. Subsequent hospitalization was uneventful.

Intracoronary loss of unexpanded stents is an infrequent but potentially serious complication that may occur unnoticed during the procedure. ^, Despite its unique axial resolution, OCT may have major problems in identifying the culprit “phantom” underlying stent in the setting of a large thrombus burden. In this scenario, IVUS, despite its lower spatial resolution, readily visualizes structures behind thrombus content and fully delineates the complete vessel wall and the outer vessel contour, even without any coronary flow. Our findings demonstrate that IVUS may be especially useful for revealing the presence and disclosing the characteristics of an underlying phantom stent, even in the presence of a large thrombus burden.

Two Cases of Coronary Stent Thrombosis Very Late After Bare-Metal Stenting

Masamichi Takano, MD

Masanori Yamamoto, MD

Kyoichi Mizuno, MD

The medical literature has recently focused on very late stent thrombosis (VLST) after drug-eluting stent implantation, while its mechanistic issue was not fully explored in the bare-metal stent (BMS) era. The first case is that of a 59-year-old man with inferior non–ST-segment elevation myocardial infarction 4 years after BMS implantation (NIR 3.5/18 mm, Boston Scientific, Galway, Ireland) for a long-term total occlusion lesion in the proximal right coronary artery. Coronary angiograms showed Thrombolysis In Myocardial Infarction (TIMI) grade flow 1 and filling defects in the BMS previously implanted, and massive red thrombi attaching to uncovered stent struts were found by angioscope ( Fig. 2.10 , Online Video 2.8 ). Thrombectomy and adjunctive balloon angioplasty were performed based on the angioscopic findings, and TIMI grade flow 3 was obtained.

The second case is that of a 71-year-old man who was admitted for a diagnosis of inferior non–ST-segment elevation myocardial infarction 10 years after a treatment with BMS (gfx 3.0/18 mm, Applied Vascular Engineering, Santa Rosa, California) for the culprit lesion of stable angina pectoris in the distal right coronary artery. Angiographic haziness in the BMS segment was seen despite TIMI grade flow 3. Any progressive lesions on angiography were not seen in other segments. Angioscopic observation for the stent segment demonstrated absence of the uncovered struts. Remarkably, ruptured yellow plaque accompanied by thrombi occupied the lumen ( Fig. 2.10 , Online Video 2.9 ). Direct stenting was consequently performed for sealing the ruptured plaque. Although both cases were definite VLST standardized by the Academic Research Consortium, the lumen appearance of direct visualization by angioscope was quite different. Previous autopsy studies showed that plaque disruption outside the BMS with extensive prolapse could lead to thrombosis. For the first time, angioscopic findings in the second case propose strong evidence that atherosclerotic plaque disruption inside the BMS may be one potential trigger of thrombosis. However, persistent uncovered struts in the first case may lead to VLST, as well as those of the drug-eluting stent. The images presented cannot generalize VLST to all cases. However, contrastive angioscopic images suggest that various pathogeneses may contribute to the occurrence of definite VLST after BMS implantation, and different interventional strategies for VLST may be chosen.

Very Late Stent Thrombosis 5 Years After Implantation of a Sirolimus-Eluting Stent Observed by Angioscopy and Optical Coherence Tomography

Takayuki Ishihara, MD

Masaki Awata, MD, PhD

Masashi Fujita, MD, PhD

Tetsuya Watanabe, MD, PhD

Osamu Iida, MD

Yoshio Ishida, MD, PhD

Shinsuke Nanto, MD, PhD

Masaaki Uematsu, MD, PhD

Drug-eluting stents have dramatically reduced the rate of in-stent restenosis. However, very late stent thrombosis (VLST) is one of the clinical issues with regard to the safety of drug-eluting stents. ^, To date there are no articles that report VLST evaluated by both angioscopy and optical coherence tomography (OCT). A 50-year-old man came to the emergency department with chest pain. Five years earlier a 3.0 × 13 mm sirolimus-eluting stent (SES) was implanted in the left anterior descending artery. Coronary angiography revealed severe stenosis with a contrast filling defect at the SES site ( Fig. 2.11 A) that was attributed to VLST. The OCT demonstrated the presence of a massive thrombus ( Fig. 2.11 B). Thrombus aspiration resulted in disappearance of the filling defect ( Fig. 2.11 C). The OCT demonstrated dramatic reduction of the thrombus ( Fig. 2.11 D). On pathologic evaluation the aspirated contents contained thrombi but no plaque or eosinophil ( Fig. 2.12 ). Coronary angiography 12 days after the procedure showed patency of the SES without peri-stent contrast staining ( Fig. 2.13 A). Angioscopic observation showed presence of fully visible struts with red thrombus ( Fig. 2.13 B, Online Video 2.10 ). The OCT also revealed uncovered struts ( Fig. 2.13 C). It has been reported that the main cause of early stent thrombosis is usually a procedure-related issue, whereas the cause of late stent thrombosis is delayed arterial healing, and the cause of VLST is an abnormal vascular response. However, an abnormal vascular response was thought to be less relevant as a cause of VLST in this case because strut malapposition was not severe, and the material aspirated from the strut did not contain eosinophils. In contrast, judging from the fully visible struts observed by angioscopy without neointima formation and the presence of uncovered struts observed by OCT, delayed arterial healing was thought to be the main cause of VLST in this case.

Cross-Sectional and Longitudinal Positive Remodeling After Subintimal Drug-Eluting Stent Implantation: Multiple Late Coronary Aneurysms, Stent Fractures, and a Newly Formed Stent Gap Between Previously Overlapped Stents

Kenichi Tsujita, MD, PhD

Akiko Maehara, MD

Gary S. Mintz, MD

Michael Poon, MD

Giuseppe Maiolino, MD, PhD

Teppei Sugaya, MD

Keiichi Igarashi, MD, PhD

Masahiko Ochiai, MD, PhD

A 50-year-old man with a history of smoking and hyperlipidemia, but no chest pain, was admitted because of an abnormal electrocardiogram and regional wall motion abnormality on echocardiography (mild inferior hypokinesis). Coronary angiography revealed two chronic total occlusions (CTOs): ostial right coronary artery (RCA) and mid left circumflex artery. The long RCA CTO lesion was treated by intentional retrograde creation of a subintimal lumen with a “knuckled” Fielder XT wire (Asahi Intecc, Nagoya, Japan) ( Fig. 2.14 ) followed by deliberate implantation of four overlapping paclitaxel-eluting stents into the subintimal space. Complete stent−vessel wall apposition and overlapping of adjacent stents was confirmed by postprocedural intravascular ultrasonography ( Figs. 2.15 and 2.16 ). The 8-month follow-up coronary angiogram showed multiple aneurysms in the RCA, but not in the mid left circumflex artery, that had been treated using a conventional antegrade CTO approach and single-stent implantation into the true lumen. At the sites of the RCA aneurysms, intravascular ultrasonography showed large areas of late acquired stent malapposition (LSM) as the result of vessel remodeling (an increase in cross-sectional and longitudinal vessel dimensions), changes that were most marked at the sites of subintimal stent implantation ( Fig. 2.15 ). These areas of LSM were accompanied by stent fractures and a newly formed gap between the (previously overlapped) most distal stent and the proximal adjacent partial stent segment ( Fig. 2.16 ). Serial intravascular ultrasound quantitative analysis revealed positive remodeling (increase in mean vessel area from 15.0 to 20.8 mm ² ). The newly formed gap between the previously overlapped stents suggested that positive vessel remodeling occurred in the longitudinal direction and cross-sectionally.

Drug-eluting stents reduce restenosis even after treatment of CTO lesions. However, the frequency of LSM appears to be greater after the implantation of drug-eluting stents versus bare-metal stents, especially in the setting of treatment of CTO lesions. Hong et al. reported that predictors of LSM were total stent length, primary stenting in acute myocardial infarction, and stenting of CTO lesions. Hong et al. ^, found that LSM may be associated with less neointimal hyperplasia, but it has also been implicated in patients with very late stent thrombosis. In our case, large areas of LSM were observed at the sites of angiographic aneurysms that were detected 8 months after treatment of an RCA CTO. The complex procedure included deliberate subintimal passage of the guidewire and implantation of drug-eluting stent into the subintimal space. This technique might have exaggerated injury to the medial and adventitial layers, or the adventitial location of the drug and polymer may have induced a local hypersensitivity to cause cross-sectional and longitudinal vessel remodeling, LSM, and aneurysm formation. Of note, there were no areas of aneurysm formation or LSM 16 months after treatment of the left circumflex artery CTO using a conventional antegrade approach with sirolimus-eluting stent implantation into the true lumen.

In-Stent Protrusion After Implantation of a Drug-Eluting Stent in a Honeycomb-Like Coronary Artery Structure: Complete Resolution Over 6 Months and the Role of Optical Coherence Tomography Imaging in the Diagnosis and Follow-Up

Kohei Koyama, MD

Kihei Yoneyama, MD, PhD

Takanobu Mitarai, MD

Shingo Kuwata, MD

Yuki Ishibashi, MD, PhD

Ken Kongoji, MD, PhD

Yoshihiro J. Akashi, MD, PhD

A 61-year-old woman had chest pain while walking. The patient had positive electrocardiographic findings for ischemia and a slightly elevated troponin level I (0.271 ng/mL), suggesting acute coronary syndrome. Optical coherence tomography (OCT) confirmed a honeycomb-like structure with multiple signal-free channels ( Fig. 2.17 ). A drug-eluting stent (DES) (everolimus-eluting stent 2.5 × 15 mm) was then implanted because of atherosclerosis at the distal culprit lesion. OCT after stent implantation showed thrombi protrusion and the complete resolution over 6 months ( Fig. 2.18 ).

A spontaneous recanalization of thrombi, forming a honeycomb-like structure, is rare in patients undergoing coronary angiography. The primary concerns are stent thrombosis because of malposition after DES stenting on the thrombi lesion, and in-stent restenosis of the atherosclerotic plaque with bare-metal stent implantation. Follow-up OCT at 6 months confirmed the successful DES deployment and its efficacy in acute coronary syndrome.

Intramural Hematoma Appearing as a New Lesion After Coronary Stenting

Jennifer A. Tremmel, MD, SM

Tomomi Koizumi, MD, PhD

Aiden O’Loughlin, MBBS, BSc, MB

Alan C. Yeung, MD

A 51-year-old man with hypertension and hyperlipidemia had exertional chest pain and underwent a stress echocardiogram that showed anterior and lateral ischemia. Coronary angiography revealed a 70% stenosis of the mid left circumflex artery and an 80% stenosis of the proximal left anterior descending artery ( Fig. 2.19 A). The left circumflex artery was directly stented with a 2.5 × 12 mm drug-eluting stent (DES). The left anterior descending artery stenosis was predilated with a 3.0 × 9 mm balloon and a 3.5 × 16 mm DES was placed, with a maximal inflation pressure of 16 atm. After stent placement there appeared to be a new lesion at the distal end of the stent ( Fig. 2.19 B). The angiographic abnormality was not relieved by intracoronary nitroglycerin or verapamil. The patient remained hemodynamically stable without electrocardiographic changes or chest pain.

Intravascular ultrasonography was used to determine the etiology of this new lesion and showed an intramural hematoma originating at the distal end of the stent ( Fig. 2.20 ). There was no identifiable entry point. The intramural hematoma was treated with an overlapping 3.0 × 20 mm DES implanted at a maximal pressure of 12 atm. The stent length was chosen to cover beyond the distal extent of the intramural hematoma. Final intravascular ultrasonography showed resolution of the intramural hematoma, and angiography demonstrated no residual stenosis and Thrombolysis In Myocardial Infarction grade flow 3. The creatinine kinase-myocardial band the next morning was normal.

Intramural hematomas after percutaneous coronary intervention are defined as an accumulation of blood within the media that displaces the internal elastic membrane inward and the external elastic membrane outward, with or without identifiable entry and exit points. They have been demonstrated in up to 7% of all percutaneous coronary interventions and are most common in patients with diabetes and those with less-diseased coronary arteries. The angiographic appearance of an intramural hematoma is generally a dissection (60% of cases), but in 11% it appears as spasm or a new lesion, and in 29% there is no significant angiographic abnormality. Intramural hematomas can occur at both the distal (55%) and proximal stent edges (45%). Up to 26% are complicated by a non–Q-wave myocardial infarction. The proper management of intramural hematomas remains poorly defined.

Ruptured Neoatherosclerosis Presenting as a Large Intrastent Neointimal Dissection

Fernando Rivero, MD

Javier Cuesta, MD

Amparo Benedicto, MD

Teresa Bastante, MD

Fernando Alfonso, MD

A 77-year-old man was admitted for a prolonged chest pain. Nine years earlier he required implantation of a bare-metal stent in the proximal left anterior descending coronary artery for stable angina. In the emergency department, the electrocardiogram showed dynamic ST-segment depression on the anterior leads. A significant increase in cardiac biomarkers was subsequently confirmed. Coronary angiography showed no significant coronary stenosis, although a faint, linear haziness was visualized within the stent ( Fig. 2.21 A). Optical coherence tomography revealed a typical pattern of nonocclusive intrastent neoatherosclerosis (NA) ( Fig. 2.21 B). However, at the mid segment of the stent, a clear rupture of a bright, glistening neointima was readily demonstrated ( Fig. 2.21 C). Interestingly, this tear induced a relatively large intrastent dissection (up to 5 mm in length) and a striking double-lumen morphology ( Fig. 2.21 D–F). The mean dissection thickness was 340 mm. The minimal lumen area of the true lumen was 1.7 mm ² , and the maximal area of the false lumen was 3.6 mm ² . No residual intracoronary thrombi were recognized. An excellent result was obtained with the implantation of an everolimus-eluting stent.

NA is a well-defined cause of very late in-stent restenosis and stent thrombosis. Because of its unsurpassed resolution, optical coherence tomography provides a unique tool in the diagnosis of NA. Characteristic findings include infiltrated neointima, lipid pools, thin-cap fibroatheroma, calcification, and even macrophage accumulation. ^, Complicated NA is characterized by relatively confined neointimal ruptures with associated intracoronary thrombus. ^, However, our unique findings suggest that complicated NA may also present as a relatively large, angiographically silent, intrastent coronary dissection.