oct findings in patients with recanalization of organized...

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OCT Findings in Patients With Recanalization ofOrganized Thrombi in Coronary Arteries

Soo-Jin Kang, MD, PHD,* Masataka Nakano, MD,† Renu Virmani, MD,†Hae-Geun Song, MD,* Jung-Min Ahn, MD,* Won-Jang Kim, MD,* Jong-Young Lee, MD,*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,* Seung-Jung Park, MD, PHD*

Seoul, Korea; and Gaithersburg, Maryland

O B J E C T I V E S The purpose of this study was to determine the angiographic and optical coherence

tomographic (OCT) characteristics of coronary lesions with recanalized thrombi.

B A C K G R O U N D Although spontaneous recanalization of thrombi has been reported pathologi-

cally, it is rarely recognized in clinical practice.

M E T H O D S Based on histopathologic features, recanalization of thrombi was defined by character-

istics on OCT.

R E S U L T S Recanalization of thrombi was identified in 6 patients (3 male, 3 female; median age 63

years; age range 54 to 72 years). Based on symptoms, 3 patients were diagnosed with unstable angina;

2 were diagnosed with stable angina; and 1, who had mitral stenosis and huge left atrial thrombi, was

diagnosed with post-infarct angina. All had normal serum concentrations of cardiac markers at

admission. Angiography showed irregular linear filling defects and haziness. Two patients with near total

occlusion had Thrombolysis In Myocardial Infarction (TIMI) flow grade 1 and collaterals, whereas 4

patients had TIMI flow grade 3 and no collaterals. All patients showed OCT findings consistent with

recanalized thrombi, which consisted of signal-rich, high backscattered septa that divided the lumen

into multiple small cavities communicating with each other. These structures, which had smooth inner

borders, created a “Swiss cheese” appearance. Percutaneous coronary intervention was performed in 5

patients with angiographic slow flow or inducible-ischemia as documented by invasive or noninvasive

stress tests. The remaining 1 patient with restored coronary flow underwent mitral valve surgery and left

atrial thrombectomy.

C O N C L U S I O N S OCT provided details on the characteristics of the organization of thrombi in both

chronic total occlusion and subtotal narrowing. Coronary lesions containing recanalized thrombi were

characterized by multiple small channels, with most showing functional significance. (J Am Coll Cardiol

Img 2012;5:725–32) © 2012 by the American College of Cardiology Foundation

From the *Department of Cardiology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea; and the†CVPath Institute, Inc., Gaithersburg, Maryland. This study was supported by a grant of the Korea Healthcare TechnologyR&D Project, Ministry of Health and Welfare, Republic of Korea (A102065). Dr. Virmani has served on the Speakers’ Bureauand has received research support from Terumo Corporation and St. Jude Medical. All other authors have reported they haveno relationships relevant to the contents of this paper to disclose. Neil J. Weissman, MD, served as Guest Editor for this paper.

Manuscript received December 9, 2011; revised manuscript received February 29, 2012, accepted March 19, 2012.

http://dx.doi.org/10.1016/j.jcmg.2012.03.012

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Kang et al.

OCT in Recanalized Thrombi

726

lthough recanalization of coronary thrombihas been characterized pathologically, it israrely recognized in real clinical practice

(1–5). Because angiographic hazinessand filling defects are common but nonspecificfindings, it is speculated that a recanalized throm-bus is often misdiagnosed as other pathologicalconditions such as fresh thrombosis by plaquerupture/erosion, spontaneous dissection, aneurysm,or heavy calcification. Despite several case reportsaddressing neovascularization within thrombi (6–9), itsincidence and functional significance remain un-clear.

Advances in high-resolution imaging modalities,such as intravascular ultrasound (IVUS) and opticalcoherence tomography (OCT), have provided newinsights into evolving thrombotic lesions (6–9). Asangiographic haziness does not always signify afresh thrombus, intravascular imaging is necessaryto differentiate the causative mechanisms in vivoand may provide information allowing an appropri-ate treatment approach specific to the underlyingetiology. We have assessed the morphological charac-

teristics on angiography, IVUS, and OCTof coronary lesions with spontaneous recan-alization of thrombi.

M E T H O D S

Angiographic analysis. From July 2010 toSeptember 2011, OCT was performed in

71 patients. Recanalization of organized thrombias found in 6 patients on the basis of OCTndings. Qualitative and quantitative angiographiceasurements were performed using standard tech-

iques with automated edge-detection algorithmsCAAS-5, Pie-Medical, Maastricht, the Nether-ands) at the angiographic analysis center of theardioVascular Research Foundation, Seoul, Korea

10,11).OCT imaging and analysis. Before February 2011,OCT images were acquired by an occlusive tech-nique using a commercially available system forintracoronary imaging and a 0.019-in ImageWire(LightLab Imaging, Westford, Massachusetts) be-fore IVUS imaging. The artery was cleared of bloodby continuous flushing with iodixanol 370 (Visi-paque, GE Health Care, Cork, Ireland) at a flowrate of 3.0 ml/s (12). Since March 2011, OCTimages were acquired by a nonocclusive techniquewith a C7XR system (DragonFly catheter andC7XR, LightLab Imaging). Based on previous

und

histopathologic studies, recanalization or neovascu- m

larization of thrombi was defined as multiple chan-nels divided by thin septa with or without commu-nication with each other (3–8). Calcification wasdefined as a well-delineated, signal-poor regionwith sharp borders (13). Fresh thrombi were de-fined as masses �250 �m in diameter protrudingnto the vessel lumen and discontinuous from theurface of the vessel wall. Red thrombi were defineds high-backscattering protrusions with signal-freehadowing, and white thrombi as signal-rich, lowackscattering projections into the lumen (14–17).he OCT analysis was performed by 2 independentbservers (S.J.K. and H.G.S.).

IVUS imaging and analysis. IVUS imaging was per-ormed after OCT imaging and after intracoronarydministration of 0.2 mg nitroglycerin using motor-zed transducer pullback (0.5 mm/s) and a commercialcanner (Boston Scientific/SCIMED, Minneapolis,

innesota), consisting of a rotating 40 MHz trans-ucer within a 3.2-F imaging sheath. Using comput-rized planimetry (EchoPlaque 3.0, Indec Systems,

ountain View, California), off-line quantitativeVUS analysis was performed in a core laboratory athe Asan Medical Center. External elastic membranend minimal lumen areas were measured at the lesionite and reference segments (18).

R E S U L T S

Clinical characteristics. Based on the OCT findings,ecanalization of organized thrombi was identifiedn 6 patients. The median age of the patients was 63ears (range 54 to 72 years) and 3 were female. Fiveatients had no history of previous percutaneousoronary intervention or coronary bypass surgery.nly 1 patient (Patient #6) showed in-stent reste-

osis after drug-eluting stent implantation 4 yearsarlier.

Table 1 summarizes the history and clinicalresentation of the 6 patients. Three patients, withecently developed or aggravated angina symptomsor 1 to 8 weeks before admission, were diagnosedith unstable angina. Two patients presented with

table angina, and 1 patient (Patient #4) with mitraltenosis and huge left atrial thrombi 5 weeks afteron–ST-segment elevation myocardial infarctionas diagnosed with post-infarct angina. All 6 pa-

ients were admitted through the out-patient de-artment. At admission, none had resting chestain or presented with acute myocardial infarction.heir serum concentrations of creatine kinase-

A B B R E V I A T I O N S

A N D A C R O N YM S

IVUS � intravascular ultraso

OCT � optical coherence

yocardial band and troponin were normal.


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The most common finding on electrocardiogra-phy was T-wave inversion, observed in 4 (67%)patients, whereas Q-wave was seen in only 1 pa-tient. Regional wall motion abnormalities of thetarget vessel territory were observed in 4 patients(67%). The results of noninvasive and invasivestress tests are shown in Table 1.Angiographic and grayscale IVUS. The involved ves-sel was the left anterior descending artery in 2patients and the right coronary artery in 4 patients.All lesions presented with multiple speckled stain-ing of contrast or filling defects with irregular

Table 1. Clinical Characteristics, Cases 1 Through 6

Patient # Sex/AgeClinical Presentation

at Admission

1 F/72 Chest pain during exercise8 months previously;aggravated symptomsfor 1 month

Un

2 M/63 5-year history of angina;aggravated chest painfor 1 week

Un

3 F/54 New onset of prolongedchest pain for 4 weeks

Un

4 F/63 Non-STEMI 5 weeksearlier; mitral stenosiswith LA thrombi atrialfibrillation

Ol

5 M/55 Effort-related chest painfor 1 year

Sta

6 M/73 s/p DES implantation4 years earlier;recurrent angina 1 yearearlier

Sta

DES � drug-eluting stent(s); ECG � electrocardiogram; Echo � echocardiograpelevation myocardial infarction.

Table 2. Angiographic Findings

Findings 1 2

Lesion site RCA RCA

Lesion length, mm 29.3 19.5

Diameter stenosis, % 65 42

TIMI flow grade 3 3

Collaterals None None

Visible thrombi � �

Plaque rupture � �

Haziness or filling defect � �

Calcification � �

Dissection � �

Minus symbols indicate negative findings; plus symbols indicate positive findin
LAD � left anterior descending artery; RCA � right coronary artery; TIMI � Throm
lumen border. In each, the lumen included multiplelinear structures mimicking a spontaneous dissec-tion. Three patients showed only a mild degree ofangiographic stenosis (diameter stenosis �50%).Angiography showed irregular linear filling defectand haziness. Two patients with near total occlu-sion had Thrombolysis In Myocardial Infarction(TIMI) flow grade 1 and collateral vessels, whereasthe other 4 patients had TIMI flow grade 3 and nocollateral vessels (Table 2).

Pre-procedural IVUS was performed in 4 of the6 patients and showed multiple cavities of variable

agnosis Risk Factors Noninvas

le angina Hypertension,hyperlipidemia

ECG: Q-wave in II, III,Echo: inferoposteriorThallium: partially revsevere perfusion d

le angina Smoking, hypertension,hyperlipidemia

ECG: T-wave inversioEcho: inferoposteriorFFR at maximal hype

le angina None ECG: T-wave inversiolateral leads

Thallium: partially revdefect in apical sepmid anteroseptum

Echo: akinesia of ante

yocardialrction

Hypertension ECG: T-wave inversioEcho: severe mitral st

(5 � 3 cm), hypokinferior wall, EF 50

angina Hypertension,hyperlipidemia,smoking

Thallium: reversible, lin apical septum a

ECG and Echo: norma

angina Diabetes mellitus ECG: T-wave inversioEcho: normal finding

F � ejection fraction; FFR � fractional flow reserve; LA � left atrial; s/p � status p

Patient #

3 4 5

LAD RCA LAD

65.0 20.4 15.9

36 41 100

3 3 1

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size at the lesion site. There was vigorous bloodspeckling suggesting severe blood stasis in thelumen. The IVUS also revealed free-floating, hugeintraluminal thrombi in 3 patients. All had mark-edly dilated vessels (external elastic membrane di-ameter �5.0 mm) with positive remodeling at thelesion segment and angiographic haziness.OCT findings. On OCT, all patients with recana-lized thrombi showed signal-rich, high backscat-

Figure 1. Histology and OCT Illustrations of Recanalization With

(A) The old lumen is occupied by an organized thrombus (black arwell endothelialized (red asterisks). (B) The signal-poor, darker tissu(OCT) corresponds to a proteoglycan-rich area (red arrows). Converand collagen, as well as being brighter on OCT (black arrow).

Figure 2. Angiographic and OCT Findings in Patient #1 and Pat

In both Patient #1 (A to C) and Patient #2 (D to F), angiography (Aof the right coronary artery (black arrows). Intravascular ultrasonog(red asterisks). Optical coherence tomography (OCT) (C, F) showed
central lumen (white asterisk). The “Swiss cheese” appearance suggest
tered septa dividing the lumen into multiple smallcavities that communicated with each other (Fig. 1).The thin septa had smooth inner borders, and themultiple holes had a “Swiss cheese” appearance.The deeper portion contained signal-poor, darkertissue, corresponding to a proteoglycans-rich areawith or without neovascularization on histology. Incontrast, the areas near the lumen tended to bebrighter, suggesting a relatively higher content of

hrombi

heads). The surface of septa of recanalized spaces are smooth andthe deeper portion observed on optical coherence tomography, the areas near the lumen tend to be rich in smooth muscle cells

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smooth muscle cells and collagen. The angio-graphic, IVUS, and OCT findings of the 6 patientsare shown in Figures 2 to 5. Fresh or organizinghrombi with signal attenuation were present in thereas adjacent to the lesion in 3 patients, whereasCT-defined calcification was not observed. Thereas no definitive evidence of plaque rupture orissection as a nidus of thrombotic occlusion.

Revascularization. Treatment strategy was based onhe functional significance of stenosis. All 3 patientsho underwent thallium scans (Patients #1, #3, and5) showed reversible or partially reversible perfu-ion defects in the corresponding territories, and 1Patient #2) showed a reduced fractional flow re-erve of 0.65. These 4 patients with documentednducible ischemia underwent percutaneous coro-ary intervention, with drug-eluting stents success-ully implanted. In addition, a drug-eluting stentas implanted in Patient 6, who was diagnosedith total in-stent restenosis and angiographic slowow. There was symptomatic improvement in allatients after treatment. The remaining patientPatient #4) with restored coronary flow underwentitral valve surgery and left atrial thrombectomy.

Figure 3. Angiographic and OCT Findings in Patient #3

(A) Intraluminal filling defects accompanied by a long flaplike strucicking a spontaneous dissection. (B, C) On optical coherence tomogdeeper portion (white arrows), represent neovascularization within
(D) The lesion was successfully treated by placement of Nobori stents.
D I S C U S S I O N

Three major findings were observed in coronarylesions with recanalization of organized thrombi:1) common angiographic findings such as multipleirregular filling defects and intraluminal hazinesswere not specific for recanalization; 2) on OCT, therecanalization of organized thrombi was character-ized by multiple small channels divided by thinsepta communicating with each other; and 3) de-spite the neovascularization process, most of theselesions were functionally significant.

Previous histopathologic studies found thatolder coronary thrombi undergo organization orrecanalization to form a few large or several smalllumens. Neovascularization is of variable sizes,endothelium-lined vascular channels within thethrombus, supported by a small amount of con-nective tissue (1–5). One-third of patients withthrombotic occlusion were reported to have somedegree of recanalization, as confirmed by pathol-ogy (3,19). Although recanalization of thrombiwas not infrequent in histopathologic studies(1,3,19), it was reported to be rare when assessed

in the entire left anterior descending artery (black arrows), mim-hy (OCT), multiple channels (red asterisks), with darker tissue in aanized thrombi. A disrupted septum is visible (white arrowhead).

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angiographically (4). Because of poor resolution,oronary “luminography” has been unable to dif-erentiate multiple vascular channels from moreommon pathological conditions causing angio-raphic haziness (3,9,20). Although IVUS pro-ides cross-sectional images of atheroscleroticlaque and vessel walls, its relatively low resolu-ion limits proper diagnosis and accurate tissueharacterization. Because of its better resolution,CT can clarify the etiology of angiographic

mbiguity and potentially guide an optimal ther-peutic approach.

All 6 of our patients showed multiple linearfilling defects on coronary angiography mimickingspontaneous dissection. Although neovasculariza-tion is based on pathological diagnosis, OCTclearly demonstrated the unique features of recana-lized thrombi in vivo, described as a Swiss cheese–like or spider web–like appearance. These findingssuggest that the organization of thrombi is eithercomplete or ongoing (7–9). Figure 1 illustrates the

athological findings of recanalized thrombi thatere similar to the OCT findings.Although the functional significance of recanali-

ation of organized thrombi has been unclear,revious studies have reported that blood flowhrough recanalized channels is insufficient. Be-ause the growth of vascular channels takes several

Figure 4. Angiographic and OCT Findings in Patient #4 and Pat

In both patients, (A to C) Patient #4 and (D to F) Patient #5, (A, D)with luminal haziness. (B, C, E, F) Optical coherence tomography (Osepta, as well as protruding intraluminal thrombi with attenuation

eeks or months (5,21,22), the role of recanaliza-

ion in the restoration of blood flow may bensignificant, especially soon after infarction. Weound that angiographic diameter stenosis variedrom 36% to 100%. Irrespective of the degree ofngiographic stenosis, all patients who underwentnvasive or noninvasive functional tests had induc-ble ischemia revealed. Despite the recanalization,he stenosis remained functionally significant inost of our patients, and it is also suggested by an

utopsy study that recanalized thrombi may beesponsible for terminal coronary events (2). How-ver, it remains unclear how recanalization affectsarly and long-term prognosis after myocardialnfarction; therefore, more investigations are defi-itely needed in this matter.

Study limitations. As a limitation of retrospectiveobservation, the general incidence of thrombus withrecanalization or the accuracy of angiographic find-ings was not shown. Also, the accuracies of gray-scale IVUS with 40 MHz and 20 MHz catheters inidentifying thrombi were not compared in thestudy. Because the sample size of this study wassmall and there was no histological confirmation,our observations cannot be generalized. More-over, we could not determine the possible causesof initial thrombotic occlusion, such as plaquerupture or spontaneous dissection, as a nidus for

#5

iography showed multiple irregular filling defects (black arrows)showed many channels with smooth inner border of multiplete arrows).

ient

angCT)

thrombus formation. The presence of clinical


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plaque rupture or focal dissection may be ob-scured by organized thrombi or other structures.In addition, the entry site of a dissection isusually small and may not show re-entry into thetrue lumen. Finally, the composition of the extra-cellular matrix including its collagen/proteoglycancontent depends on duration of thrombus, location,and other factors, and this small study did notaddress the various stages of evolving thrombi over

Figure 5. Angiographic and OCT Findings in Patient #6

(A) In-stent restenosis with total occlusion (black arrows) in Patientities (red asterisks) and suspicious thrombi (white arrows). (C, D) Owithin huge thrombi (red asterisks).

ized coronary stenoses: histopatho-6. Cho JM, Raffel O

CJ, Jang IK. Spont

C O N C L U S I O N S

An OCT evaluation provided details on the charac-teristics of the evolution of thrombi. Recanalization ofthese thrombi was characterized by multiple smallchannels, with most showing functional significance.

Reprint requests and correspondence: Dr. Seung-JungPark, Professor of Medicine, Asan Medical Center,388-1 Poongnap-dong, Songpa-gu, Seoul 138-736,

(B) Grayscale intravascular ultrasonography showing multiple cav-al coherence tomography (OCT) showing neovascularization

time. South Korea. E-mail: [email protected].

R E F E R E N C E S

1. Friedman M. The coronary thrombus:its origin and fate. Hum Pathol 1971;2:81–128.

2. Friedman M. The coronary canalizedthrombus: provenance, structure,function and relationship to death dueto coronary artery disease. Br J ExpPathol 1967;48:556–67.

3. Levin DC, Fallon JT. Significance ofthe angiographic morphology of local-

logic correlations. Circulation 1982;66:316–20.

4. Spring DA, Thomsen JH. Recanalizationin a coronary artery thrombus. Case reportwith cineangiographic and hemodynamicfindings. JAMA 1973;224:1152–5.

5. Ridolfi RL, Hutchins GM. The rela-tionship between coronary artery lesionsand myocardial infarcts: ulceration ofatherosclerotic plaques precipitatingcoronary thrombosis. Am Heart J1977;93:468–86.

C, Stone JR, Kimaneous recanaliza-

tion of a coronary artery after throm-botic occlusion: in vivo demonstrationwith optical coherence tomography.J Am Coll Cardiol 2010;55:1274.

7. Davlouros PA, Karantalis V, Mavrona-siou E, Damelou A, Alexopoulos D.Optical coherence tomography featuresof late-stage recanalised coronary thrombi.EuroIntervention 2011;6:1022–3.

8. Zakhem B, Fernandez-Ortiz A, Al-fonso F. Optical coherence tomogra-phy findings during “evolving” stentthrombosis. J Invasive Cardiol 2011;

#6.ptic

23:E222–5.

mailto:[email protected]

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1

1

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J U L Y 2 0 1 2 : 7 2 5 – 3 2

Kang et al.


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9. Zollikofer CL, Vlodaver Z, Nath HP,et al. Angiographic findings in recan-alization of coronary arterial thrombi.Radiology 1980;134:303–7.

0. Mehran R, Dangas G, Abizaid AS, etal. Angiographic patterns of in-stentrestenosis: classification and implica-tions for long-term outcome. Circula-tion 1999;100:1872–8.

1. Ryan TJ, Faxon DP, Gunnar RM, etal. Guidelines for percutaneous translu-minal coronary angioplasty. A report ofthe American College of Cardiology/American Heart Association TaskForce on Assessment of Diagnosticand Therapeutic Cardiovascular Pro-cedures (Subcommittee on Percutane-ous Transluminal Coronary Angio-plasty). J Am Coll Cardiol 1988;12:529–45.

2. Gonzalo N, Garcia-Garcia HM, Re-gar E, et al. In vivo assessment ofhigh-risk coronary plaques at bifurca-tions with combined intravascular ul-trasound virtual histology and opticalcoherence tomography. J Am CollCardiol Img 2009;2:473–82.

3. Yabushita H, Bouma BE, Houser SL,et al. Characterization of human ath-
erosclerosis by optical coherence to-
mography. Circulation 2002;106:1640–5.

4. Takano M, Yamamoto M, Inami S, etal. Appearance of lipid-laden intimaand neovascularization after implanta-tion of bare-metal stents extendedlate-phase observation by intracoro-nary optical coherence tomography.J Am Coll Cardiol 2009;55:26–32.

5. Kume T, Akasaka T, Kawamoto T, etal. Assessment of coronary arterialplaque by optical coherence tomogra-phy. Am J Cardiol 2006;97:1172–5.

6. Jang IK, Tearney GJ, MacNeill B, etal. In vivo characterization of coronaryatherosclerotic plaque by use of opticalcoherence tomography. Circulation2005;111:1551–5.

7. Kume T, Akasaka T, Kawamoto T, etal. Assessment of coronary arterialthrombus by optical coherence to-mography. Am J Cardiol 2006;97:1713–7.

8. Mintz GS, Nissen SE, Anderson WD,et al. American College of Cardiologyclinical expert consensus document onstandards for acquisition, measurementand reporting of intravascular ultra-sound studies (IVUS). A report of the
American College of Cardiology Task t
Force on Clinical Expert ConsensusDocuments. J Am Coll Cardiol 2001;37:1478–92.

9. Friedman M, Van den BovenkampGJ. Pathogenesis of a coronary throm-bus. Am J Pathol 1966;48:19.

0. Jaffe R, Irfan A, Hong T, et al. In-traluminal filling defects on coronaryangiography: more than meets the eye.Clin Cardiol 2007;30:480–4.

1. Weisse AB, Lehan PH, Ettinger PO,Moschos CB, Regan TJ. The fate ofexperimentally induced coronary ar-tery thrombosis. Am J Cardiol 1969;23:229–37.

2. Srivatsa SS, Edwards WD, Boos CM,et al. Histologic correlates of angio-graphic chronic total coronary arteryocclusions: influence of occlusion du-ration on neovascular channel patternsand intimal plaque composition. J AmColl Cardiol 1997;29:955–63.

Key Words: angiographichaziness y optical coherencetomography y recanalized
hrombi.