Cardiovascular Intervention and Therapeutics

, Volume 27, Issue 1, pp 47–51

Culprit segments identified by optical coherence tomography in patients with acute myocardial infarction: two case reports

Authors

  • Daisuke Sato
    • Department of Cardiovascular MedicineNagasaki University Hospital
    • Department of Cardiovascular MedicineNagasaki University Hospital
  • Tomohiko Yasunaga
    • Department of Cardiovascular MedicineNagasaki University Hospital
  • Tomoo Nakata
    • Department of Cardiovascular MedicineNagasaki University Hospital
  • Masayoshi Takeno
    • Department of Cardiovascular MedicineNagasaki University Hospital
  • Yuji Koide
    • Department of Cardiovascular MedicineNagasaki University Hospital
  • Satoshi Ikeda
    • Department of Cardiovascular MedicineNagasaki University Hospital
  • Naoto Ashizawa
    • Department of Cardiovascular MedicineNagasaki University Hospital
  • Koji Maemura
    • Department of Cardiovascular MedicineNagasaki University Hospital
Case Report

DOI: 10.1007/s12928-011-0081-0

Cite this article as:
Sato, D., Koga, S., Yasunaga, T. et al. Cardiovasc Interv and Ther (2012) 27: 47. doi:10.1007/s12928-011-0081-0

Abstract

The high resolution of optical coherence tomography (OCT) provides detailed information about coronary plaque morphology, which enables the mechanism of acute myocardial infarction to be evaluated. We describe two patients with acute myocardial infarction in whom culprit segments were identified by OCT, but not by either coronary angiography or intravascular ultrasound.

Keywords

Acute myocardial infarctionOptical coherence tomographyPlaque ruptureThrombusUlcer

Introduction

Optical coherence tomography (OCT) is a new intravascular imaging modality with higher resolution (10–20 μm) than intravascular ultrasound (IVUS).

We describe two patients with acute myocardial infarction in whom OCT provided useful intracoronary information for detecting culprit lesions and understanding the mechanism of onset.

Case 1

A 73-year-old woman with diabetes mellitus and hypertension was admitted to our hospital within 6 h of severe chest pain arising. Electrocardiography revealed ST segment elevation in leads I, aVL, V2–V5, and reciprocal ST segment depression in leads II, III, aVF. Echocardiography revealed severe hypokinesis in the antero-septal and apex wall with an ejection fraction (EF) of 42%. Emergency coronary angiography (CAG) revealed occlusion in the proximal portion of the left anterior descending artery (LAD) (Fig. 1a1, b1). Thrombus was aspirated, and red thrombi were retrieved (data not shown), which achieved thrombolysis in myocardial infarction (TIMI) flow grade 2. Since the recanalized vessel was small and did not reach the apex, we regarded it as the first major septal branch (MSB), rather than as the main vessel of the LAD (Fig. 1a2, b2). Crossing the guide wire into the occluded main vessel of the LAD was complicated because CAG could not discriminate the entry site. We therefore performed IVUS (Atlantis SR Pro 2, Boston Scientific, Natick, MA, USA) and OCT (ImageWire, LightLab Imaging, Westford, MA, USA) to determine the entry site. Images were obtained by pullback from the MSB. Although IVUS generated clear images of the LAD–MSB bifurcation, evidence of either plaque rupture or thrombi was absent (Fig. 2b1, b2). In contrast, OCT revealed ruptured plaque at the LAD–MSB bifurcation, and a flap-like mass protruding into the lumen of the LAD at the LAD–MSB bifurcation (Fig. 2c1, c2) that we regarded as thrombus. Based on these images, we considered that the culprit lesion was located in the LAD side of the LAD–MSB bifurcation. However, we were still unable to cross the guide wire into the occluded LAD. The patient was treated with heparin and aspirin. Two weeks later, a CAG revealed that a recanalized large main vessel of the LAD had reached the apex (Fig. 1a3, b3). Furthermore, severe stenosis was identified a little distal to the LAD–MSB bifurcation. These findings indicated that this stenosis was the culprit lesion.
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Fig. 1

CAG images from the RAO (a) and the LAO (b) cranial views. a1, b1 CAG before thrombus aspiration shows occlusion in proximal portion of LAD (white arrowheads). a2, b2 CAG after thrombus aspiration shows reperfusion of MSB and persistent LAD occlusion (white arrows). a3, b3 CAG images at 2 weeks after onset show recanalized LAD (black arrowheads) with stenosis (black arrows) somewhat distal to LAD–MSB bifurcation. CAG coronary angiography, RAO right anterior oblique, LAO left anterior oblique, LAD left anterior descending artery, MSB first major septal branch

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Fig. 2

a Magnified image of proximal LAD. Black arrowhead occlusion point of LAD. b1, b2, c1, c2 IVUS and OCT images at bifurcation of LAD–MSB. Flap-like thrombus (white arrow) and plaque rupture (white arrowhead) visualized by OCT, but not by IVUS. IVUS intravascular ultrasound, OCT optical coherence tomography. Other abbreviations are as in Fig. 1

Case 2

A 53-year-old man with coronary risk factors including hyperlipidemia and cigarette smoking was admitted to our hospital within 48 h of the onset of chest pain. Electrocardiography demonstrated ST segment elevation in leads I, aVL, V2–V5, and a negative T wave in leads I, aVL, V4–V6. Echocardiography indicated severe hypokinesis in the antero-lateral wall with an EF of 50%. CAG revealed TIMI flow grade 3 in the LAD, but the first diagonal branch (DB) was occluded (Fig. 3a). Mild stenosis with an ulcer-like formation in the LAD was identified at the origin of the DB (Fig. 3b). Mainly red thrombi were aspirated (Fig. 3c). Low-echo plaque and an ulcer were demonstrated by IVUS at a site opposite the DB, but there were no thrombi (Fig. 4b1–b4). On the other hand, OCT revealed lipid rich plaque and thrombus in the LAD at the origin of the DB (Fig. 4c1–c4), and an ulcer formation with microvessels (diameter <100 μm) just proximal to the LAD–DB bifurcation (Fig. 4c2). These findings indicated that the thrombosis in the LAD had spontaneously resolved but the DB remained occluded. We were unable to cross the guide wire into the occluded DB. Since the main vessel of the LAD was TIMI grade 3, the patient was medically treated with heparin and aspirin.
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Fig. 3

a CAG in LAO-cranial view and b magnified image of proximal LAD. Occluded DB and mild stenosis with ulcer in LAD at DB origin. c Gross findings of red thrombi removed from proximal LAD. DB first diagonal branch. Other abbreviations are as in Fig. 1

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Fig. 4

Magnified image of proximal LAD after thrombus aspiration (a), IVUS (b1b4) and OCT (c1c4) images. Unlike IVUS, OCT shows lipid-rich plaque (asterisk), ulcer (star), white (arrows) and red (arrowhead) thrombi. d Magnified OCT image of ulcerated plaque shows microvessel (small arrowhead). Abbreviations are as in Figs. 1 and 2

Discussion

Optical coherence tomography is a novel invasive imaging method that can assess coronary plaque morphology at a resolution of 10–20 μm, which is about tenfold higher than that of IVUS. This method has emerged as a promising tool for assessing patients with acute coronary syndrome and for detecting key features of plaques including thin-cap fibroatheroma, plaque rupture and thrombus in such patients [1].

In case 1, OCT revealed ruptured plaque at the LAD–MSB bifurcation and a flap-like mass in the LAD side of the LAD–MSB bifurcation. We regarded this flap-like mass as thrombus. Thrombi on OCT are defined as masses protruding into a vessel lumen discontinuously from the surface of the vessel wall [2]. Intracoronary thrombi can be accurately identified by OCT [3]. Thrombus detected by OCT can present in various forms, but flap-like thrombi such as those in the present case are rare. Prati et al. [2] also described a flap-like thrombus, but the present case was unusual as the flap was rather large. The features of thrombi can be distinguished by OCT. Red thrombi consist mainly of red blood cells and OCT images are characterized by high-backscattering protrusions with signal-free shadowing [4]. White thrombi consist mainly of platelets and white blood cells, and are characterized by signal-rich, low backscattering billowing projections that protrude into the lumen [4]. In reality, thrombi are rarely all white or all red and mixed thrombi are common. Whether the flap-like thrombus in the present case was red or white thrombus was unclear. When ulcerated or ruptured plaques present with thrombus on OCT, the lesion can generally be defined as being culprit [2]. Thus, OCT was helpful in locating the culprit lesion in the LAD side of the LAD–MSB bifurcation during the acute phase of the disease in this patient. In fact, this notion was supported by CAG findings during the chronic phase.

An occlusion of the DB and TIMI-3 grade flow in the main vessel of the LAD was confirmed by CAG in case 2. These findings indicated that the DB was the culprit vessel whereas OCT confirmed an ulcer with thrombi in the LAD at the origin of the DB. Thus, the OCT findings indicated that the culprit lesion was in fact ulcerated plaque in the LAD, not the DB. Furthermore, microvessel formation in the inner plaque near the ulcer was also detected by OCT. Neovascularization in atherosclerotic plaques is associated with plaque vulnerability [5] and the high resolution of OCT allows direct visualization of plaque neovascularization in vivo [6]. Microvessels in plaque are generally considered to appear on OCT as thin black holes with a diameter of 50–100 mm in at least 3–4 consecutive frames in pull-back images [2]. The presence of such microvessels in the inner plaque near the ulcer also supported our conclusion that the culprit lesion was ulcerated plaque in the LAD.

Thus, OCT in addition to CAG and IVUS can provide detailed intracoronary information. Combinations of these imaging modalities would be more helpful and increase reliability for detecting culprit lesions, and for understanding the mechanisms of acute coronary syndrome onset.

Copyright information

© Japanese Association of Cardiovascular Intervention and Therapeutics 2011