A 30 years old patient healthy, smoker come 3hours after chest pain radiating to left arm.
Dr. Haytham Serhan (HS)
Dr. Antoine Sarkis (AS)
Dr. Samer Mansour (SM)
Dr. Nagi Azzi (NA)
Dr. Abdel-Razzak Nakouzi (AN)
Dr. Marcel Sokhn (MS)
HS: 30 years old patient healthy, smoker come 3hours after chest pain radiating to left arm. Her ECG showed:
HS: WhatsApp Video 2018-01-06 at 11.15.08 AM
Should we stent it?
AN: Another view? You have FFR?
If no FFR and symptomatic, yes for stent
NA: Another view? Because it seems hazy from this view. Also doing hs tropo at 3hours would enforce the indication
HS: Negative. So direct stenting or predilatation?
AN: Direct seems to work
HS: WhatsApp Video 2018-01-06 at 11.30.41 AM
NA: Can we see the RCA also plz? For the sake of completeness
WhatsApp Video 2018-01-06 at 11.37.52 AM
NA: Your stent is a bit long and the positioning a bit proximal if you finally inflated it in that position
HS: With NC balloon. Its 3.0×26 mm. If shorter maybe will not be in the lesion. And I took if we will do the bifurcation if needed
NA: I’d have put my stent in that fashion. Not all the plaque was covered distally. Post dilatation with short 3.5 mandatory, in prox stent
HS: It’s like this. 15mm NC
WhatsApp Video 2018-01-06 at 11.49.47 AM
WhatsApp Video 2018-01-06 at 12.04.10 PM
HS: After 10min
WhatsApp Video 2018-01-06 at 12.04.39 PM
MS: You should consider in this set-up spontaneous coronary artery direction (SCAD) described lately after the use of intra vascular imaging. Unfortunately imaging not available to all of us. The treatment totally differ conservative no stenting. No PY12 inhibitor. In other words if the intima is intact by imaging no stent because flow is TIMI 3.
HS: You leave it without stenting? What if you will have a thromb migration? Because fluttering.
WhatsApp Video 2018-01-06 at 12.28.46 PM After stenting of proximal edge
MS: Guessing isn’t an answer confirmation comes only with intra vascular imaging. If no thrombus and intima intact only subintimal hematoma you can leave it without stenting and it will heal spontaneously. What was done is perfect in case of dissected coronary plus thrombus. But I have evoqued this differential diagnosis cause young 31 y old and probably not much risks factors.
NA: It we’re still in the same case of direct stenting then post-dilatation we can’t talk of spontaneous CA dissection. And even not a dissection because in my sense it’s a minor thrombus at the prox edge of the stent. Aggrastat is the answer and may be low pressure inflation with the NC ballon (4-6atm)
MS: Not at all. Starting the first injection this differential diagnosis is to be considered in patients with low probability of atherosclerotic disease. After intra-vascular imaging you can consider the management of your patient. And only conservative management if the intima is intact no dissection.
NA: Also R/O:
– Suboptimal heparin dosage per procedure
– Patient on fondaparinux before procedure not relayed with heparin
HS: Heparine 7500u iv and brilinta loading dose
AS: For the sake of complete discussion. The initial lesion might be a spontaneous type 2 dissection. Only OCT or IVUS can differentiate from atherosclerotic plaque rupture. When you put a stent on a type 2 SCAD you may cause extension of the hematoma
Very interesting review
NA: Dear Dr Sarkis. Don’t you think we are enough sure on the initial lesion+ the context that we were in front of an atherosclerotic plaque rupture?
AS: Not at all. It may be from the beginning type 2 SCAD
AS: SCAD is often under-recognized and incorrectly classified as due to atherosclerosis if diagnosis is reliant upon visualization of the classic dissection flap. Type 2 SCAD is the most common, resulting in compression of the lumen due to intramural haematoma with no intimal flap (67% of cases). Type 1 SCAD with classic dissection flap occurs in 29%, and Type 3 SCAD mimicking atherosclerosis is relatively uncommon, occurring in 4% of cases
AN: Not to forget P-SCAD. Which overlooked as well
AS: If Claude Semaan can read this. She presented once a lesion on RCA with extension of hematoma proximally after placement of each stent
NA: Don’t you think it’s more like a type 1 SCAD if we want to assume that was the diagnosis? I think type 2 SCAD is remote from the index lesion
HS: Is thromboaspirarion effective in this case? Is it risky to leave it only on aggrastat; because we don’t have abxicimab?
NA: Small thrombus at the stent prox edge. It’s futile to do thromboaspiration. Aggrastat with adapted LMWH dose+DAPT is largely enough in my sense
AN: It is type one
SM: Hi to all. Thanks for adding me to the group. I looked on the last interesting case
Few questions / comments:
What the patient was doing at the beginning of the chest pain? Is the patient a drug user?
Regarding the angiopraphical aspect and taking into account the patient age SCAD should be considered. Angiographically can look as type 1. Entry point is just before 1st diagonal and exits close to third diagonal. OCT is the test of choice for diagnosis confirmation (ffr not for any help)
If stenting decided ( should take long stent) the one used is a bit short and small in diameter (proximally the vessel is at least 4,0) will take 3.5 and post dilate to 4.0
The residual image could be more a flap at the stent entry, will not leave it like that. If not covered in the index procedure an angiographical control should be done in 48h
Good luck! Nice and challenging case
AS: Thank you Samer. Educational case and enthusiastic group !
SM: My pleasure !
NA: Thank you Samer. If you’re facing a case where you suspect SCAD and you don’t have IVUS/OCT, what would you change in your approach to the lesion comparing with the normal atherosclerotic plaque if you want to avoid any kind of complication?
AS: In order not to overwhelm Samer. He already said: Long stent with appropriate diameter
SM: Thank you Nagi. We usually keep a conservative management if flow is normal. If need to stent as Tony mention. Long stent with appropriate diameter. Before the proximal entry to distal if obvious on the angio
AS: Thks to Haytham Serhan who posted this interesting case
HS: The patient was sleeping and pain started at 5 in morning. Heavy smoker
SM: Interesting!! Not typical for SCAD (mainly man) more for plaque rupture. Did well by stenting proximal edge image. Deserve a control. Please let us know the control of you do it. Thanks for sharing
NA: Thanks to this omission, the discussion was animated between plaque rupture & SCAD…Instead of being the “everyday case”
HS: I asked the patient his brother 2 years ago has a cardiac arrest at age 39. And he died
SM: Should screen for familial hypercholesterolemia. Another element in favor of plaque rupture
HS: Yes they have
SM: Need aggressive lipid management for all primary and secondary prevention
HS: Ok thanks Dr. Samer. And to all too
Take home message
Spontaneous coronary artery dissection (SCAD) is an important but rare cause of ACS (0.1 to 0.4%), particularly in young women (82% in series) without traditional cardiovascular risk factors. The pathophysiology and treatment are different to ACS caused by plaque rupture or erosion.
SCAD classification: LINK to image
Contrast staining of the vessel wall (Type 1 SCAD) is the most recognized finding on coronary angiography (29% of cases). However, Type 2 SCAD due to intramural haematoma is the commonest presentation (67% of cases) and can be easily missed. Type 3 SCAD mimicking atherosclerosis is relatively uncommon, occurring in 4% of cases.
Particular case of pregnancy-associated SCAD: LINK to image
Intravascular imaging like intravascular ultrasound (IVUS) or optical coherence tomography (OCT) is required to confirm the diagnosis.
Most coronary dissections will heal spontaneously, and conservative treatment is recommended for uncomplicated cases. If no thrombus and intima is intact with only subintimal hematoma on imaging, stenting can be avoided and it will heal spontaneously.
Patients with left main stem involvement, complete vessel occlusion, ongoing chest pain, hemodynamic instability and sustained ventricular arrhythmias will require coronary revascularization.
PCI results are suboptimal in this challenging group of patients. PCI should be performed by experienced operators, with the use of IVUS/OCT and preferably with on-site surgical back-up due to the increased risk of complications. Stenting of the proximal segment seals the dissection entry if present and limits the risk of dissection/hematoma propagation.
Glycoprotein IIb/IIIa inhibitors have also been used but may delay healing of the intramural hematoma and lead to dissection extension. Dual antiplatelet therapy with aspirin and clopidogrel is generally accepted, without the need for ticagrelor or prasugrel. Beta-blockers are recommended in all patients, which may reduce arterial shear stress, facilitate healing and reduce long-term recurrence.
Although long-term prognosis is excellent, the risk of recurrent SCAD events is significant, with an average rate of 5% per year.