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It’s the call that no healthcare professional wants to get…
“Hi Mate. Sorry to bother you, it’s just Lucy has got some chest pain and doesn’t look great. Do you think I should take her to the hospital?”
Lucy is in her late forties and totally fit and well. She has never smoked, has no family history of cardiac disease and is on no medication.
“We’ve got loads to do today and don’t want to spend hours sitting in Casualty (sic) waiting to be seen if it’s nothing”
Part of your brain is telling you that it is nothing, just a bit of indigestion maybe, after all, she has no risk factors at all, but then there is the key phrase “she doesn’t look great”. You would never forgive yourself if she really did have something wrong, however unlikely that might be.
Now picture you are the doctor working in the Emergency Department that day. The history you get is of two episodes of intrascapular pain with light headedness. They were not brought on by exercise and the pain did not radiate. She is now pain free and her ECG looks like this. She is asking if she can go home…
When she had first arrived she had some blood tests taken, including a high sensitivty troponin and you ask her to wait for that to come back, although you are sure it is nothing to worry about.
An hour later the lab call: her troponin is 2914 ng/l (Normal = <18ng/l). She’s referred to cardiology and admitted to CCU, but you’re perplexed: she’s not yet 50; a non smoker; has no family history at all; is on no medication and is previously fit and well. Is this just an atypical presentation of a myocardial infarction?
Well yes and no, but if you have already worked out what was wrong with Lucy, you are a better clinician than me. Or you read this recent review in the New England Journal of Medicine…
Spontaneous Coronary Artery Dissection (SCAD)
Whilst in the ED we are very aware of, in fact you could say obsessed with, dissection or the aorta, similar pathology of the coronary arteries has gone relatively unrecognised. We are all familiar with the structural changes that can occur with the aortic dissection and the process within the coronary arteries is similar.
It results from the developement of a false lumen, within the outer third of the tunica media. How this occurs is still under debate: it could be a tear between the endothelial and intimal layers (inside-out); or disruption of a microvessel within the vaso vasorum, leading to bleeding within the tunica media (outside-in); or it could be both. Regardless, this causes blood to propagate along this newly formed tract, blocking the true lumen and causing compression of the true lumen and a reduction in oxygen supply to the heart muscle.
Who gets SCAD?
It turns out that Lucy is in the ‘classic’ group who get SCAD. 90% are female between the ages of 47-53 years of age, often with fewer cardiovascular risk factors than those who get atherosclerotic disease. It also accounts for up to a fifth of myocardial infarctions during pregnancy and the peripartum period. Clearly this suggests an association with female sex hormornes, but the exact mechanism for this has not yet been elucidated.
Clinical Signs and Symptoms
A small number of patients with SCAD do not make it to hospital, with ischaemia presumable causing ventricular arrthymias and death. In those that do make it to hospital most manifest themselves with symptoms typical of myocardial infarction and up to half may have STEMI changes on their ECG. Chest pain is the predominant symptom, with various patterns of radiation. However, some may have initial troponin levels that are reported as normal, so a heightened awareness of the condition is necessary to make sure that these patients who are ‘low risk’ for ACS are not discharged inadvertently.
Diagnosis and Treatment
Ultimately, SCAD is diagnosed with angiography, and this should be performed early to see if the lesion is ameneable to stenting. The most frequently involved vessel is the LAD, but it can involve any coronary artery. Coronary CT angiography can also be used, and may visualise flaps, stenoses and haematomas.
If the patient is clinically stable the preferred treatment is medical (not dissimilar to its pathological cousin in the aorta). If we consider the pathophysiology this makes sense: there is no plaque rupture or erosion or intraluminal thrombosis. Percutaneous coronary intervention (PCI) has been associated with worse outcomes in patients with SCAD and in fact the majority of SCAD lesions show evidence of healing over time, with the degree of stenosis lessening and a restoration of blood flow. Treating the acute lesion may also not help to prevent recurrance, as many patients in whom there is a further episode the dissection will occur in a different vessel.
The treatment objectives are to manage chronic chest pain, prevent recurrance and screen for associated extra coronary vascular abnormalities. There is little evidence to guide treatment regimes, and so much is based on registry data and expert consensus. It is of little surprise that the ‘usual’ secondary prevention medications for ACS are often given: beta-blockers; antihypertensives; antianginals and antiplatelet therapy for up to a year following diagnosis.
Life after SCAD
Although mortality is low, the incidence of recurrence is significant, with up to 20% having a further event within 4 years. This is more likely in patients with a history of high blood pressure, fibromuscular dysplasia (which is present in 50% of patients with SCAD), a history of migraine headaches, and tortuous coronary arteries.
There is no evidence of benefit of further extra coronary artery imaging but because the prevalence of co existing disease is so high this is usually undertaken with either CT or MRI.
There is a recognised group of patients who will suffer from a degree of Post Traumatic Stress Disorder following diagnosis and this may be helped by cardiac rehabillitation programmes or contact with peer support groups, such as ‘Beat SCAD‘ in the UK, who also produce leaflets for both patient and healthcare professionals
Lucy stayed in hospital on CCU for three days. She had a few further episodes of pain, but her troponins went down and her electrocardiogram did not change. She was discharged on secondary prevention medication.
It was Lucy’s idea that I write this blog post to try to raise awareness about this unusual, but important condition.
Dr David Carr is a great friend of St Emlyn’s and has delivered some great talks on SCAD at a number of international conferences. He’s your go-to #FOAMed expert on this topic and this talk will change your practice. You can find one of the CODA clinics on SCAD with two of the best educationalists in the world (David Carr and Anand Swaminathan) online and available on the link below. A must listen that will change your practice.
1, Kim, E. Spontaneous Coronary Artery Dissection. N Engl J Med 2020;383:2358-70. DOI: 10.1056/NEJMra2001524
2, Adlam, D et al. European Society of Cardiology, acute cardiovascular care association, SCAD study group: a position paper on spontaneous coronary artery dissection. European Heart Journal, Volume 39, Issue 36, 21 September 2018, Pages 3353–3368. DOI: 10.1083/eurheartj/ehy080