SCAD (Spontaneous coronary artery dissection) will also screw you up by David Carr.
Carr’s Clinic is back but this time – with the man himself. David Carr walks us through a case which had him spooked (and for good reason).
A 33 year old female comes into the Emergency Room with crushing chest pain.
She has terrible pain radiating down her arm and it has only been 36 hours since she gave birth to her fifth kid.
Her ECG showed a STEMI. But, 33 year old women who just gave birth don’t have MI’s. Do they?
Turns out, she has SCAD – Spontaneous coronary artery dissection.
SCAD represents 1 to 4% of all ACS angiograms.
30% of the time it presents as a STEMI and 70% of the time as a non-STEMI.
The kicker? SCAD looks like STEMI. It has the same story, the same ECG, the same biomarker that is positive… it just depends on who is getting it.
91% of people with SCAD are less than the age of 25 and 85-94% are women.
It also represents 43% of MIs in women under the age of 50.
So how do we catch it? Think about the plus ones.
ACS plus young woman with no risk factors.
ACS plus pregnant or postpartum.
ACS plus some significant stressor.
Spontaneous coronary artery dissection is something we need to remember and we need to consider. SCAD will also screw you up.
For more like this, head to our podcast page. #CodaPodcast
– (David) I’m super excited. I’m super excited about the release of Carr’s Coda Clinic. I had the absolute pleasure of interviewing Sara, Tarlan and Swami. I can’t wait for you to hear the sections for those who missed it. What I’m even more excited about is that Coda22 is back. Now, I’m hoping to have a haircut by then and I’m hoping I’m going to see you in Melbourne, on 3-6 April 2022. Book off your time. We’re working on the program. It’s coming together. It’s going to be an unbelievable time. It’s a reunion. We all need this. We all need you to be there. So take a look at codachange.org for details but I can’t wait to see you down under in just under a year. See ya soon.
– (Swami) All right, CodaZero, this is Carr’s Clinics. Carr’s Clinics is amazing. You guys all know it, you love it, you’ve seen a couple of these already. Now we’re going to turn the tables because we’re all tired of getting asked all the questions and having to be the experts, when we know that we have the expert, David Carr. So David, we’re going to turn it around, I’m going to ask you questions. You’re going to tell me about a case and we’re going to put you on the spot with this diagnosis. So why don’t you go ahead and start us off with this amazing case.
– (David) Awesome case. Thanks for the introduction. I saw a case that really spooked me. You know I love cardiovascular killers that make people afraid. So I saw this 33 year old female, she came in with crushing chest pain, a very classic, she just looked like a STEMI. She had terrible pain radiating down her arm. It had been about 36 hours since she just gave birth to her fifth kid. So I’m kind of thinking to myself, this trooper has five kids. She’s in the emergency department, this is the last place that she wants to be but she just looks terrible and I was nervous.
– (Swami) So the first thing I know is that 33 year old women who just gave birth, David, they don’t have MIs. So I can go ahead and take MI off the table, right? So we’re not thinking about that. We’re thinking about, let’s be honest, this is just like the case that we had before, we’re jumping right to pulmonary embolism. 33 year old, postpartum, that’s a PE?
– (David) Yeah. That’s my thought and I’ve given talks on this and I’ve listened to your talks. Here’s the problem, her ECG showed tombstones anteriorly. I’m thinking to myself, okay, she doesn’t use cocaine, she’s not Marfanoid, there’s just no way she has a STEMI, but her ECG showed a STEMI and I was pretty freaked out.
– (Swami) Okay. So let’s go back and I’m going to take back what I said before, 33 year old women clearly can have STEMIs. This sounds like a STEMI. I mean, you know, it walks like a duck, it sounds like a duck. It’s a duck. Except that we’re only like four minutes in, David, so it’s got to be something else. So she’s got a STEMI on ECG, she’s got chest pain, she’s postpartum. Put this all together, tell me what I’m missing here?
– (David) So, my differential was PE and maybe dissection but she had SCAD. SCAD, spontaneous coronary artery dissection. Now, if you Google search it, it will be the Savannah College Art of Design. This barely even hits Google. SCAD, much like an aortic dissection is an intimal tear in your coronary artery. This is a diagnosis that is made angiographically. So if you don’t follow up on your angiograms, you actually might not realise that you’ve seen SCAD.
– (Swami) This is kind of an interesting diagnosis, not one that I’m very familiar with. Now, I did do a little reading before we got online, otherwise, I’m not sure how much I know about SCAD and you’re right, I don’t follow up my angios. Patient has a STEMI, I send them to the lab, wipe my hands, go see the next patient, I’m done with that. So you’re right, I probably have missed this. You know, what do we need to know about SCAD as a diagnosis? Are we really going to see this? Is this something that is common? Or are you just bringing up a zebra here?
– (David) I like zebras but you’ve missed it. You’ve seen it, I guarantee it. This represents 1 to 4% of all ACS angiogram. That number’s significantly higher if you include young women. Now, as I said before, SCAD is an intimal tear, or it can lead to an intramural hematoma. It represents and it presents 30% of the time as a STEMI and 70% as a non-STEMI. The LAD, that important vessel, is the culprit in about 32 to 45% of the time. But what you have to realise about this, and you said it best, it looks like a duck and it walks like a duck. SCAD looks like STEMI. It has the same story. It has the same ECG. It has the same biomarker that’s positive. It’s just who’s getting it doesn’t seem to fit the phenotype.
– (Swami) Well, let’s hit that point right there. So we started with a 33 year old woman who just gave birth and you know, we were kind of kidding around, 33 year old women don’t get STEMIs. Do they get SCAD? Is that like what happens to them? Is that the group that we should be looking for it in?
– (David) Yeah. If you had to choose the poster people for SCAD, it’s young women. The mean age of SCAD is 43, which is crazy.
– (Swami) David, I’m 43. I’m 43.
– (David) Yeah and I’m 46. I know, it sucks when we start to have people with diseases younger than us because then we start to get nervous. So mean age is 43. 91% of people with SCAD are less than the age of 25. But the kicker here, is 85 to 94% of these patients are women. It represents up to 43% of MIs in women under the age of 50. So, really this is a disease of young women who otherwise don’t have risk factors.
– (Swami) I think you’re going to miss these patients because first of all, maybe you don’t get the EKG. Now, granted if the patient doesn’t look well and she’s got chest pain, you’re probably going to get the EKG and hopefully you’re going to see a STEMI and it’s going to tip you off. But David, I can imagine seeing this and being like, “No, that’s early repol.” I know there are reciprocal changes, but come on, it’s a 33 year old woman who just gave birth, she’s not having a STEMI. So I can see us trying to sell this away as something normal, as opposed to what it is. Or even David, if we pick it up, maybe our consultants don’t and they don’t know about it, so they miss it. So now we know what group it is, it’s typically younger women. You said the mean age is around 40, most of the patients are women, but why? We got to have a why, I need to know why are they getting it or why is this happening at all?
– (David) Yeah, it’s interesting pathol phys. I think you have to realise there’s two types of SCAD, there’s pregnancy-associated SCAD, which clearly this woman was part of. That represents about 8% of SCAD and occurs in about 200,000 pregnancies and 75% of those times, that is postpartum. So this is exactly who you’re going to see. It really is more likely to occur in grand multips, like this young woman. What you have to realise, is that the coronary arteries have oestrogen and progesterone receptors that weaken as the gestation goes along, much like it does in an aortic dissection. It weakens and that’s why you’ll see it in third trimester. So you certainly can see that hormones play a role. Apart from pregnancy-associated SCAD, which is a much worse SCAD, which they tend to have long segments of the LAD, they tend to be more likely to have STEMIs. You also see the contribution to hormones in non-pregnant women. Typically in about 10 to 13% of non-pregnant women, you will see SCAD related to hormones. That may be a woman starting the pill. That may be a postpartum woman who actually has just stopped breastfeeding at 13 months and therefore has that dramatic change in her hormones. Or lastly, you might even see what’s called, menstrual angina, which is as bad as it sounds. The drop in progesterone will cause women to have anginal symptoms. So hormones seem to play a key role, and that seems to be critical of why women are affected.
– (Swami) All right, so clearly we picked this topic because we wanted to make the endocrinologist happy. The endocrinologists are all celebrating, hormones are important. But it can’t be just that group. You said 85% of these patients are women. You said a lot of them are postpartum but there’s got to be other groups that I have to worry about this in.
– (David) Yeah, the other reason and you keep using, “Blow it off,” and I love it because 60% of people with SCAD will have a significant stressor. 40% will be a significant emotional stressor, you got laid off work, you lost your relationship, you lost a loved one. 20% will have a physical stressor, you completed your first tri, you were doing some isometric exercises. So there is that component of stress that seems to be affected. If you see a young person who’s 35 years old and he or she, or mostly a she, says, “I just had this fight with my partner and now I’m having chest pain.” These are the people you blow off. You don’t trop them, you reassure them, hold their hand, send them out. You have to be really careful.
– (Swami) David, I’ve seen a number of your talks. I’ve seen Endocarditis Will F You Up. I’ve seen Aortic Dissection Will F You Up. The thing that you see in all of those of your talks, is it’s plus one, right? It’s a plus one syndrome, you got to make this one fit too. What’s the plus one?
– (David) Yeah, I’m a big plus one, simple person. When you see ACS, think about plus one. ACS plus a young woman with no risk factors. ACS in a woman who’s postpartum or pregnant. ACS in someone with significant emotional or physical stressor. Those are my three plus ones.
– (Swami) All right, David. So, you know, again, I’m a simple emergency doc, just like you are. Patient comes in with chest pain, I get an EKG, she’s got a STEMI, I send her to the cath lab, I can wash my hands now. If the management isn’t going to change for me, why do I have to worry about this? I only have so much space up in this head, David, if I put SCAD in, something like my anniversary’s going to fall out.
– (David) It may but it needs to. This is why, you have to realise, much like aortic dissection, if you work in a centre that doesn’t have a cath lab, you might be thrombolysing patients. You can imagine that, just as an aorta that’s tearing doesn’t want to be thrombolysed, neither does a coronary artery. So standard cocktails, preprinted ACS order sets, don’t fly here. This is a time where you need to plant the seed. You need to talk to the people who take care of sick, cardiac patients in your shop and say, look, “I have a young female, she has no risk factors. She’s postpartum, or she’s super young and just fits the part, what do you want me to do? She may have had aspirin already, do you want her to go right to the cath lab?” Whereas in the old days we might drip and ship. This would be something where we’re just going to ship when we have that phone call, when we plant that seed.
– (Swami) So planting the seed is important here, and I agree with you, you know. We don’t do a lot of thrombolysis for STEMI in my shop but it happens. If you don’t work in a cath centre, it happens quite a bit. So we have to be thinking, maybe don’t load them up. It’s very similar to the dissection where you get the dissecting vessel back into the coronary vessels, and you’re like, I really don’t want to load this patient up on every antiplatelet agent that I can think of. So maybe that’s not the best idea here. But what about on the table? So I talk to my consultant, I plant the seed, maybe this could be SCAD, so they say, “You know what, that’s great. Hold off on all the antiplatelets, all the anticoagulants. We’ll start them up here.” Does it change what my cardiologist is doing in the lab?
– (David) It does, because firstly, giving them that seed makes them open their eyes. This is above the scope of this discussion, but it angiographically isn’t always simple. About a quarter of the time you can make that diagnosis, other times it requires more cognitive thoughts. So planting the seed helps. They might not start that heparin. You know, they might have the dual antiplatelets or they might have the aspirin started but the other stuff’s not going to go. The key about PCI here, is you actually don’t want to do it. You actually want to do nothing. When the interventionist looks through those arteries, they notice, “Huh, they look pretty clean. I don’t see hot-clot.” 70 to 90% of SCAD heals spontaneously. The reason you don’t want to stent these people is that fact, plus they’re 15 times more increased risk of an iatrogenic dissection, that’s when you hear that code blue in the cath lab. 27 to 53% of the time, there’s technical failure. Cath is not good, and even the 12% of people who get cath that go on to have CABG, they don’t do well either because those vessels aren’t spared from future and subsequent episodes of SCAD.
– (Swami) Clearly some important points here, a good diagnosis for us to have in our heads. David, let’s wrap this all up. Let’s bring it all together. What do we need to know about SCAD? How can we keep our eyes out for it? How can we catch it?
– (David) The most important thing, is you need to think about the plus ones, in my opinion. You need to think whenever you see someone with ACS and they don’t fit. ACS plus young woman with no risk factors. ACS plus pregnant or postpartum. Or ACS plus some significant stressor, you have to think SCAD. You have to plant the seed. You can’t just use standard ACS therapies. This needs shared decision-making and a discussion. The complexity of that discussion probably is dependent on the proximity of your hospital to the cath lab. If it’s upstairs and it’s Thursday at 9:00 AM, this is a simple discussion. But if it’s Saturday and you’re six hours away, you have to make therapeutic decisions based on a balance of probability. You need to offload that to the emergency cardiology services that you work out. Lastly, if you don’t look up cath results, you’ve missed SCAD. Make sure you check things out. Learn, listen, follow up, and please be safe, because SCAD will also screw you up.
– (Swami) I love this, David. SCAD is out there, we have to be thinking about it. If we don’t know about it, we’re not going to make the diagnosis. This is a great reminder, if you’ve heard about SCAD before. For those of us who haven’t, it’s a great first lesson. I love this case. It’s absolutely fantastic. It’s a good way to kind of wrap up Carr’s Clinic. Thank you guys all at CodaZero for having us. This was a wonderful time, really fun. Wish we could be there with you guys sharing a drink and hopefully next year, we’ll all be together again.
– (David) Awesome. See you soon.
David Carr is an Associate Professor in the Division of Emergency Medicine at the University of Toronto. He is an Emergency Physician and Clinical Investigator at the University Health Network and Mackenzie Health Hospital. He has been the recipients of multiple Undergraduate and Post Graduate Clinical Teaching awards. During the Baseball season, he works at the Roger’s Centre as the Medical director of Stadium Medicine for the Toronto Blue Jays. In 2010, he pursued his passions serving as an ER physician in the Athletes Village for the Winter Olympics in Vancouver. Since 2010, He has co- authored the chapter on Occlusive Arterial Disease in the 7-9th editions of Tintinalli’s Emergency Medicine.
Anand Swaminathan is a core faculty member of the St. Joseph’s Regional Medical Center Emergency Department in Paterson, NJ. He is an assistant professor of Emergency Medicine at the Hackensack Meridian School of Medicine and the Medical Education Fellowship Director at St. Joseph’s Hospital. His main interests are in resident education, faculty development, resuscitation and knowledge translation. Anand is the managing editor and conference chair for EM: RAP and the managing editor for EM Abstracts. He is a big believer in and contributor to the Free Open Access Medical Education (FOAM) movement. Anand is an associate editor for REBEL EM and REBELCast and a regular contributor to the EM Cases Quick Hits podcast. When not working, Anand enjoys long distance running and building Legos with his kids (Matt 12, Maya 9 and Luke 5).