Rhythm Nation Feb 2020 Answer – Spontaneous Coronary Artery Dissection

Answer from Rhythm Nation- February 2020

Answer: Spontaneous coronary artery dissection (SCAD)

Interpretation:

Rate: 60/min

Rhythm: sinus 

Axis: Normal 

Intervals: Normal 

ST-T-Q: STE in lead III, aVF. STD I, aVL; Wellens type A pattern in V1 and V3, short/symmetric T wave inversions in V2, V4, V5. Biphasic T waves in leads II, III, avF, V1, V6. 

Coronary territories involved: R main coronary artery. Every lead has signs of ischemia in this EKG, which should alert the provider to a proximal coronary occlusion. STE is most notably in the inferior leads, while biphasic T waves are seen most prominently in both inferior and anterior leads, pointing to involvement of the RCA. 

Epidemiology:

Spontaneous coronary artery dissection (SCAD) is a rare presentation of atraumatic, non-iatrogenic, non-atherosclerotic acute coronary syndrome. Although its absolute prevalence is unknown on account of likely underdiagnosis, certain common characteristics have been identified amongst the cases that have been documented. It most commonly affects young-to-middle-aged women with few or no traditional risk factors for occlusion MI. Common risk factors appear to be pregnancy, exercise, connective tissue disorders (fibromuscular dysplasia, Marfan Syndrome, Ehlers Danlos), exogenous hormone use, and certain autoimmune disorders (SLE, rheumatoid arthritis, sarcoidosis).(1) It has been reported to account for ~25% of acute coronary syndromes in women ≤ 50.1 Men with SCAD tend to have more traditional atherosclerotic risk factors than women, and have more cases of isometric exercise-related events.(1,2)

Any vessel can develop SCAD. It is more common for the mid-to-distal segments of the vessels to be involved; less than 10% of cases involve the proximal vessel. Up to 23% of cases present with multivessel SCAD.1 Below is a breakdown of the most common vessels involved in the literature:(1) 

LAD, septal, diagonal branch territory – 45% to 61%.

Circumflex, ramus and obtuse marginal branches – 15% to 45%

Right coronary artery and acute marginal, posterior descending, and posterolateral branches –  10% to 39%

Left main coronary artery –  4% of cases

Pathophysiology and presentation:

As the name suggests, SCAD occurs due to a tear in the intima. A tear of the vaso vasorum leading to an intramedial hemorrhage has also been proposed as a possible mechanism of the disease. As in aortic dissection, they both lead to the formation of a false lumen and an intramural hematoma. An enlarging hematoma can further expand the false lumen, thereby leading to coronary occlusion. Hormonal effects causing weakening of the vessel wall as well as physiologic stresses have been proposed as triggers for SCAD in pregnant or early postpartum women.(1-3)

SCAD patients generally present with signs and symptoms of acute coronary syndrome or sudden cardiac death. This includes chest pain, both typical and atypical, diaphoresis, respiratory distress, syncope, and exertional symptoms. SCAD may evolve slowly after a triggering event and lead up to clinically significant myocardial injury many days later 5.  ECG findings depend on vascular involvement and mirror the myocardial territory affected. 

Figure 1. Frequency of presenting symptoms in SCAD. Image obtained from Luong, et al (7)

ED Management:

For ED clinicians, the most important piece of managing this particular condition is considering SCAD on the differential, particularly in patients with few or no risk factors for ACS. SCAD is presumed to be significantly underdiagnosed as a result of low suspicion of ACS in young women (with or without classic presenting symptoms), limitations of current coronary angiographic techniques, and lack of physician familiarity with the condition.(1,3,4) The patient in this case, for example, presented to an urgent-care with chest pain three months prior to this event, and had been discharged without an ECG. Essentially, think of “typical” symptoms, but in an “atypical” patient. 

PCI is high-risk due to the fragility of the intimal wall, so unless the patient is hemodynamically unstable, has a left main dissection or is actively having an infarct, conservative management is preferred (beta blockers, aspirin, anticoagulation.)(1-6) A prospective study published in AHA concluded that conservative management is associated with spontaneous angiographic healing in a large number of patients.(6) PCI in these patients can have numerous procedural complications, including wire insertion into the false lumen, expansion of the dissection and/or hematoma, and the need for more stents than anticipated.(4) SCAD can spontaneously resolve within days; however, in less than 10% of patients SCAD progression may occur within the first week.(1) Therefore, even stable patients with preserved coronary blood flow should be observed as an inpatient. In addition to PCI, other invasive interventions such as CABG, fibrinolysis, ECMO and cardiac transplant have been reported, but no randomized controlled trial has been performed to suggest an optimal management strategy. The following algorithm for management was proposed by Hayes, et al:(1)

Figure 2. Proposed algorithm for management of SCAD. A: Consider CABG for left main or proximal 2-vessel coronary artery dissection. Obtained from Hayes, et al.1

What about this patient’s presentation suggests SCAD? 

This patient’s ECG, on the first look, shows abnormal ST-T intervals in every lead except aVR, which is a grim sign pointing to either multi-vessel involvement or something that could affect large areas of the myocardium diffusely (i.e. aortic dissection, septic shock, SCAD, acute pulmonary edema). Given that our patient is a young female without a history of coronary artery disease, hyperlipidemia, or diabetes, she fits the demographic for the disease as discussed above. As it is with our younger population, think dissections, drug use, or genetic disorders when presented with something as dramatic as this ECG. 

References:

1. 1. Hayes, S. N., et al.(2018). Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association. Circulation, 137(19), E523–E557
2. 2. Fahmy P, Prakash R, Starovoytov A, et al. (2016). Predisposing and Precipitating Factors in Men With Spontaneous Coronary Artery Dissection. JACC Cardiovascular Interventions; 9:866.
3. 3. Saw J, Aymong E, Mancini GB, et al. (2014) Nonatherosclerotic coronary artery disease in young women. Can J Cardiol; 30:814.
4. 4. Alfonso F, Paulo M, Lennie V, et al. (2012). Spontaneous coronary artery dissection: long-term follow-up of a large series of patients prospectively managed with a “conservative” therapeutic strategy. JACC Cardiovascular Interventions; 5:1062.
5. 5. Tweet MS, Kok SN, Hayes SN. (2018) Spontaneous coronary artery dissection in women: What is known and what is yet to be understood. Clinical Cardiology; 41(2):203–210.
6. 6. Saw, et al. (2014). Spontaneous Coronary Artery Dissection: Association With Predisposing Arteriopathies and Precipitating Stressors and Cardiovascular Outcomes. Circulation: Cardiovascular Interventions; Vol 7:5
7. 7. Luong C, et al. (2017). Clinical presentation of patients with spontaneous coronary artery dissection. Catheter Cardiovasc Interv;89:1149–1154. 

Edited by Robby Allen, PGY-3

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