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Table of Contents
Year : 2023  |  Volume : 24  |  Issue : 2  |  Page : 119-121  

Role of optical coherence tomography in chronic spontaneous coronary artery dissection-diagnosis and management

1 Department of Interventional Cardiology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK; Department of Cardiology, Faculty of Medicine, Al Balqa Applied University, Amman, Jordan
2 Department of Interventional Cardiology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
3 Department of Interventional Cardiology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust; Institute of Cardiovascular Sciences, University of Birmingham, Birmingham, UK

Date of Submission29-Oct-2022
Date of Acceptance16-Feb-2023
Date of Web Publication24-Mar-2023

Correspondence Address:
Dr. Sohail Q Khan
Queen Elizabeth Hospital, Mindelsohn Way, B15 2TH
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/heartviews.heartviews_101_22

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Spontaneous coronary artery dissection is an underdiagnosed cause of acute coronary syndrome, often occurring in younger females. Such a diagnosis should always be considered in this demographic. In this case report, we focus on the importance of optical coherence tomography in the diagnosis and management of this condition in the elective setting.

Keywords: Acute coronary syndrome, coronary angiogram, optical coherence tomography, spontaneous coronary artery dissection

How to cite this article:
Maqableh GM, Khan KA, Shahid F, Khan SQ. Role of optical coherence tomography in chronic spontaneous coronary artery dissection-diagnosis and management. Heart Views 2023;24:119-21

How to cite this URL:
Maqableh GM, Khan KA, Shahid F, Khan SQ. Role of optical coherence tomography in chronic spontaneous coronary artery dissection-diagnosis and management. Heart Views [serial online] 2023 [cited 2023 Jun 2];24:119-21. Available from: https://www.heartviews.org/text.asp?2023/24/2/119/372457

   Introduction Top

This is a case of chronic SCAD with unhealed distal LAD. The SCAD was originally diagnosed 5 years ago and treated with a bioabsorbable stent.

   Case Presentation Top

A 53-year-old female presented to the cardiology clinic with a 3-month history of substernal chest pain exacerbated by exertion. She was well with a regular pulse rate of 70bpm and a blood pressure of 120/70 mmHg. Cardiac examination was unremarkable with regular rhythm; there were no murmurs, rubs, or gallops. Electrocardiogram in the clinic showed normal sinus rhythm with no ischemic changes. The patient's medical history is significant for dyslipidemia and Coronary artery disease (CAD) for which she had undergone percutaneous coronary intervention (PCI) and stenting of the mid-left anterior descending (LAD) 5 years ago. Due to her symptoms, Bruce protocol was used to induce stress through exercise which achieved 100% of the predicted heart rate with no chest pain. She did however display ST segment depression in the inferior leads and V2-V6. Subsequent myocardial perfusion imaging revealed reversible ischemia affecting 2/17 myocardial segments. The differential diagnosis for her chest pain included CAD due to atherosclerosis or in-stent restenosis. Thus, elective coronary angiography was arranged for her.


The patient was admitted for an elective diagnostic coronary angiogram study. The procedure was performed from the right radial artery approach. The angiogram showed an unobstructed left main stem and circumflex coronary artery. There was evidence of mild atheroma in the mid-LAD with visible markers from the previously deployed bioresorbable vascular scaffold. A “hinge point” was evident after the previously deployed absorb stent. The very distal LAD was a “fishtail” in its appearance with a distal atheroma. The right coronary artery was dominant and unobstructed [Video 1].

[Additional file 1]

We proceeded to interrogate the LAD through a Voda left 3.5 guide catheter. A Terumo Run through the wire was passed into the distal vessel. Optical coherence tomography (OCT) revealed a unique appearance of a chronic distal LAD dissection with evidence of fenestration at three separate points [Figure 1] and [Video 2].
Figure 1: OCT confirming mid-LAD atheroma (yellow arrow) (a), with chronic SCAD distally (b). There are three pointes of connection between the true (*) and false lumen (#). In addition, the OCT showed a potential cause of SCAD in this case by the presence of prominent vasa vasorum (white arrow) just below the elastic membrane of tunica intima. SCAD: Spontaneous coronary artery dissection. OCT: Optical coherence tomography, LAD: Left anterior descending

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[Additional file 2]

The subsequent resting full-cycle ratio of the LAD was resoundingly negative at 0.94.


It was apparent that this patient had a chronic dissection in her distal LAD which was not flow limiting with mild mid-LAD atheroma. Thus, the patient's symptoms were managed medically by antianginal medications.

   Discussion Top

Spontaneous coronary artery dissection (SCAD) is an uncommon nonatherosclerotic, nontraumatic, and noniatrogenic etiology of acute coronary syndrome (ACS) seen mostly in young women. It is caused by the sudden disruption of the coronary artery wall, resulting in the separation of the inner intimal lining from the outer vessel wall. The trigger is thought to be either an intimal tear or bleeding from the vasa vasorum which results in intramural hematoma and myocardial injury [Figure 2].[1] The frequency of predisposing and precipitating conditions and cardiovascular outcomes remains poorly described.
Figure 2: Mechanism of SCAD. SCAD can result from intimal tear (a) or bleeding from vasa vasorum (b) resulting in separation of the inner intimal lining from the outer vessel wall. SCAD: Spontaneous coronary artery dissection, *: intimal tear

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The diagnosis of SCAD is made usually at the time of coronary angiography. Angiographic characteristics can be graded into three types [Table 1].[2] Evidence of arterial wall staining (type 1 angiographic SCAD) and an abrupt caliber change (type 2 angiographic SCAD) are features that should raise suspicion of a diagnosis of SCAD. However, these pathognomonic features are only observed in less than one-third of SCAD cases. The use of intracoronary imaging, particularly OCT, plays an important role in the diagnosis of SCAD. In cases where the angiographic features are unclear, OCT can visualize intimal disruption, intramural hematoma, and false lumen for SCAD diagnosis.[3] In addition to early recognition of SCAD, OCT allows a tailored treatment option to avoid unnecessary harmful intervention. However, there are also potential limitations with OCT in the setting of SCAD. This includes difficulties with blood clearance in a lesion with the complete collapse of the lumen and challenges with image interpretation due to the appearance of high- and low-attenuating regions within the “false lumen” zone.
Table 1: Saw classification of spontaneous coronary artery dissection

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Treatment options depend on hemodynamic stability and the location of the dissection. More distal lesions are treated more conservatively as opposed to proximal lesions which are treated with PCI or coronary artery bypass graft, depending on clinical presentation. Conservative medical management is the mainstay of therapy in treating stable patients with SCAD.

In this case, blood flow was preserved, prompting the continuation of medical management. A third coronary angiogram on her final hospitalization confirmed that the LAD SCAD was healing well. The timeline for the resolution of the LAD SCAD was as expected further justifying the decision to pursue conservative management in the absence of flow limitations.

PCI in such circumstances has been found to be associated with high rates of complications including propagation of the dissection flap, intramural hematoma formation, and technical challenges limiting the placement of the wire into the true lumen.

The patient was reviewed in the cardiology clinic 3 months after her angiogram where she reported a significant improvement in her chest pain.

   Conclusions Top

SCAD is a rare but important cause of CAD, especially in young women. Its diagnosis in the elective setting can be even more challenging. When patients present with chest pain and presumed unobstructed coronary arteries, the physician must have a high index of suspicion to consider and diagnose SCAD. In the correct setting, OCT can be extremely beneficial to clarify any ambiguity in the final diagnosis. This, however, must be taken into the context of the patient's clinical presentation and cardiovascular stability.

Learning objectives

  1. To emphasize the importance of OCT in providing detailed information about the nature of CAD in SCAD and its safe use in the elective setting
  2. To understand the pathophysiology of SCAD as a cause of ACS.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Mokhberi V, Bagheri B, Navidi S, Amini SM. Spontaneous coronary artery dissection: A case report. J Tehran Heart Cent 2015;10:159-62.  Back to cited text no. 1
Aziz S. Spontaneous coronary artery dissection. E J Cardiol Pract 2017;14. Available from: https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/spontaneous-coronary-artery-dissection” Spontaneous coronary artery dissection (escardio.org). [Last accessed on 2022 Sep 23].  Back to cited text no. 2
Kim Y, Deharo P, Adlam D, Baumbach A, Johnson TW. The role of optical coherence tomography in decision making during the acute phase of spontaneous coronary artery dissection. Int J Cardiol Heart Vasc 2017;14:6-7.  Back to cited text no. 3


  [Figure 1], [Figure 2]

  [Table 1]


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