Case Study

Intravascular Ultrasound to Aid in the Diagnosis of Spontaneous Coronary Artery Dissection

Charles F. Sineri, DO, MHA; Vikram Raje, DO; Vincent Varghese, DO 

Deborah Heart and Lung Center, Department of Interventional Cardiology, Browns Mills, New Jersey

Charles F. Sineri, DO, MHA; Vikram Raje, DO; Vincent Varghese, DO 

Deborah Heart and Lung Center, Department of Interventional Cardiology, Browns Mills, New Jersey


Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome. Intravascular imaging with intravascular ultrasound (IVUS) has a pivotal role in the diagnosis and management of SCAD. IVUS is used to identify the extension of the intramural hematoma, examine intimal tears, and differentiate the true and false lumen. We present a case in which the diagnosis of SCAD to the distal left anterior descending artery was ambiguous on coronary angiography, with subsequent IVUS imaging demonstrating the correct pathology. 


SCAD is an epicardial coronary artery dissection that is not iatrogenically induced or associated with atherosclerosis. SCAD is diagnosed on coronary angiography in 1-4% of all acute coronary syndromes and is rarely the etiology of sudden cardiac death.1 SCAD primarily occurs in women without any cardiovascular risk factors.2 Fibromuscular dysplasia is the most common associated condition with SCAD, having a prevalence of 72-86%.3 SCAD is the most common etiology of myocardial infarction among pregnant and post-partum women, with a prevalence of 1.8 events per 100,000 pregnancies.4 It is thought to be secondary to hormonal influences on the arterial media causing weakening of the architecture. In addition to metabolic effects, hemodynamic changes can increase sheer stress, further weakening the arterial wall.5 The majority of dissections occur in the mid to distal left anterior descending artery (LAD).6 

Case Presentation

A 50-year-old male with no known prior coronary artery disease initially presented with angina and dyspnea on exertion. An electrocardiogram revealed non-specific ST-T wave changes with troponin of 0.01 ng/ml. Inpatient nuclear stress imaging revealed severe anterior wall ischemia. Coronary angiography was pursued and demonstrated a severe 90% tubular diameter stenosis in the mid LAD (TIMI-2 flow) with concomitant distal LAD spontaneous dissection suspicious for type 3 SCAD (Figure 1). Subsequently, a Prowater coronary guidewire (Asahi-Intecc) with a 1.5 mm over-the-wire balloon was advanced into the distal LAD. Prior to advancing additional equipment, a distal contrast injection through the coronary balloon confirmed an intraluminal position within the distal LAD. The balloon was removed and an IVUS catheter was delivered to the distal LAD. IVUS revealed eccentric, non-obstructive plaque with a lumen area of 2.4 mm2 (proximal reference of 6.3 mm2) and lesion length of 19.8 mm, within the lumen and without evidence of vessel dissection (Figure 2A). 

After defining the lesions in the mid and distal LAD, standard IVUS-guided revascularization to the mid LAD was performed (Figure 2B). Percutaneous coronary intervention (PCI) proceeded with a 2.75 x 38 mm Resolute Onyx drug-eluting stent (Medtronic) deployed to the mid LAD. The angiographic result was acceptable, with TIMI-3 flow (Figure 3). The patient had an uncomplicated post procedure course and was discharged home the following day. 


The mechanism of SCAD is thought to be secondary to a disruption of the intimal wall, causing an intramural hematoma and leading to the formation of a false coronary lumen.7 A false lumen and subsequent intramural hematoma can cause compression of the true arterial lumen, with clinical manifestations of myocardial ischemia or infarction. Moreover, SCAD can appear different on angiography between patients, and an angiographic classification system has been developed to further guide diagnosis and management.8 Type 1 SCAD results in contrast dye staining of the arterial wall, with multiple radiolucent lumens. Type 2 SCAD involves an abrupt change in arterial diameter from normal to diffusely narrowed, involving the mid to distal segments of the artery. Type 3 SCAD mimics atherosclerosis and is challenging to discern on angiography.9 Type 3 SCAD requires intravascular imaging to confirm diagnosis, with visualization of a double lumen or intramural hematoma. IVUS is used to differentiate the morphology and extent of the dissection. 

Optimal coherence tomography (OCT) offers greater spatial resolution compared to IVUS, especially in smaller coronary arteries. OCT’s spatial resolution allows for greater detail discrimination between the various layers of the arterial wall. However, in larger coronary arteries, the detail is diminished due to the inferior depth penetration of OCT compared to IVUS. For this patient, an EagleEye 20 megahertz (MHz) catheter (Philips Volcano) was used. The axial resolution is about 40 microns. Current coronary IVUS catheters range from 20 MHz to 60 MHz. The OptiCross HD system (60 MHz) (Boston Scientific) has an IVUS resolution of 22 microns, which is similar to OCT.10 For this case, a 60 MHz catheter may have helped to provide a definitive diagnosis of type 3 SCAD. 

Precise diagnosis of SCAD is crucial in order to guide appropriate management strategies in a variety of clinical presentations. When flow into the intramural hematoma is minimal, angiographic evidence of a dissection may not be visible.11 In order to accurately diagnose with angiography alone, SCAD requires the presence of an intimal tear. IVUS can provide insights into unique morphological features of SCAD, such as double lumen morphology, intramural hematoma, or an associated thrombus.12 The optimal treatment for SCAD has not been clearly defined. It can be difficult to decide which patients would benefit from a conservative versus an invasive management strategy. Several factors are evaluated in a SCAD management strategy, including the site of dissection, number of vessels involved, distal coronary blood flow, and hemodynamic status of the patient.13 Early angiographic recognition of SCAD is imperative, as it may prevent potentially harmful therapies such as fibrinolysis or unnecessary percutaneous coronary intervention.9 Therapies should be guided by the clinical presentation, ischemic burden, and severity of symptoms. As per American College of Cardiology/American Heart Association guidelines, clinical presentations of SCAD with ongoing or recurrent ischemic symptoms, hemodynamic instability, or left main dissection should receive revascularization.14 A conservative approach can be utilized in clinically stable patients with less ischemic burden, as the majority of cases spontaneously resolve over time.

A Mayo Clinic pilot study revealed that an initial conservative management strategy in SCAD patients led to an uncomplicated hospital course without any worsening long-term morbidity or mortality.15 As part of the study protocol, repeat angiography was conducted on SCAD patients treated with a conservative approach, and 71% had full resolution of the dissection, 18% had partial resolution (one patient required PCI 60 days later for ongoing chest pain), and 11% had persistent dissection (3 patients required PCI after 24 days for ongoing chest pain). Not only was conservative management safe, but there was a potential harm with mechanical revascularization in stable SCAD patients. A quarter of the coronary interventions for SCAD were complicated with unanticipated propagation of the dissection flap, requiring placement of multiple stents.15 

We recognize a few limitations in our case report. First, there is a possibility of angiographic artifact in the distal LAD. Contrast linear defects distal to a severe stenosis could correspond to an angiographic artifact caused by a jet of collateral flow arising from another artery. For example, collateral flow from the right coronary artery or the left circumflex artery could enter into the distal LAD through a septal or marginal branch, respectively, partially washing the lumen filled with contrast and generating a linear defect. After review of the coronary angiogram, there appeared to be no collateral flow to the distal LAD (Figure 3). Additionally, in certain cases, the 20 MHz resolution of the IVUS catheter could be inadequate to show the intimal dissection flap, especially when the intima is thin and healthy, as in a young woman.  


Herein, we present a case of unstable angina with angiographically suspected SCAD. IVUS confirmed the absence of a distal LAD dissection and identified non-obstructive atherosclerotic plaque that was ambiguous on coronary angiography. This case report further supports the use of IVUS, especially in situations of diagnostic uncertainty. 

Disclosures: The authors report no conflicts of interest regarding the content herein.

The authors can be contacted via Charles Sineri, DO, MHA, at

  1. Nishiguchi T, Tanaka A, Ozaki Y, et al. Prevalence of spontaneous coronary artery dissection in patients with acute coronary syndrome. Eur Heart J Acute Cardiovasc Care. 2016; 5: 263-270. 
  2. Rogowski S, Maeder MT, Weilenmann D, et al. Spontaneous coronary artery dissection: angiographic follow-up and long-term clinical outcome in a pre- dominantly medically treated population. Catheter Cardiovasc Interv. 2017; 89: 59-68. 
  3. Saw J, Ricci D, Starovoytov A, et al. Spontaneous coronary artery dissection: prevalence of predisposing conditions including fibromuscular dysplasia in a tertiary center cohort. JACC Cardiovasc Interv. 2013; 6: 44-52. 
  4. Faden MS, Bottega N, Benjamin A, Brown RN. A nationwide evaluation of spontaneous coronary artery dissection in pregnancy and the puerperium. Heart. 2016; 102: 1974-1979.
  5. Manalo-Estrella P, Barker AE. Histopathologic findings in human aortic media associated with pregnancy. Arch Pathol. 1967; 83: 336-341.
  6. Saw J, Aymong E, Sedlak T, et al. Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes. Circ Cardiovasc Interv. 2014; 7:645-655. 
  7. Hayes SN, Kim ES, Saw J, et al. Spontaneous coronary artery dissection: current state of the science: a scientific statement from the American Heart Association. Circulation. 2018; 137(19): e523-e557.
  8. Saw J, Humphries K, Aymong E, et al. Spontaneous coronary artery dissection: clinical outcomes and risk of recurrence. J Am Coll Cardiol. 2017 Aug 29; 70(9): 1148-1158.
  9. Saw J. Coronary angiogram classification of spontaneous coronary artery dissection. Catheter Cardiovasc Interv. 2014; 84(7): 1115-1122.
  10. OPTICROSS™ HD, 60MHz Coronary Imaging Catheters. Boston Scientific. Available online at Accessed Oct. 20, 2020.
  11. Maehara A, Mintz GS, Castagna MT, et al. Intravascular ultrasound assessment of spontaneous coronary artery dissection. Am J Cardiol. 2002; 89(4): 466-468.
  12. Mintz GS, Nissen SE, Anderson WD, et al. American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound Studies (IVUS). A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. J Am Coll Cardiol. 2001 Apr; 37(5): 1478-1492.
  13. Arnold JR, West NE, van Gaal WJ, et al. The role of intravascular ultrasound in the management of spontaneous coronary artery dissection. Cardiovasc Ultrasound. 2008 May; 6: 24.
  14. Alfonso F, Paulo M, Lennie V, et al. Spontaneous coronary artery dissection: long-term follow-up of a large series of patients prospectively managed with a “conservative” therapeutic strategy. JACC Cardiovasc Interv. 2012; 5: 1062-1070.
  15. Tweet MS, Hayes SN, Pitta SR, et al. Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation. 2012 Jul 31; 126(5): 579-588.