62 y.o. female presents with severe chest pain to her local health center. The pain started in the chest and extends to her left armpit and elbow.
Initial EKG showed STE D1-D3, V2-V6
Anterior STEMI diagnosis was confirmed
Loading dose of ASA (300mg) and Clopidogrel (300mg) was ordered as well as BB, Statin, ACEi, IPP
Due to the persistence of pain and changes on the ECG, fibrinolysis ordered in local health center. Two hour after therapy administration, the patient’s condition was not improving and there was no regression of EKG changes
Patient was transferred to a tertiary center for rescue PCI.
Admission:
Upon admission these were the vital parameters:
EKG: Sinus rhythm, HR: 75/min, STE in D1-D3, aVL, V1-V8; Q in V1-V6
TA: 145/100 mmHg
The Initial echocardiogram performed showed a dyskinetic, remodeled apex with a significantly reduced global contractile function and an EF of 35%
The patient reported that she has been taken medication for arterial hypertension as well as hormone substitution hormone therapy for hypothyreoidysm
She also reported that her father had “heart problems”
EKG upon admission
There was no significant dynamic in the EKG findings
After the initial non-invasive examination and LAB, the patient was sent to the cath lab for rescue PCI
Coronary angiogram:
The initial angiogram showed a normal slightly torturous RCA and LCx that were without significant disease
The proximal half of the LAD appears slightly tortuous without significant disease
A sudden occlusion is located at the mediodistal segment
The on call physician decided to proceed with PCI:
A workhorse wire is placed into the LAD
Several unsuccessful attempts are made to cross the lesion into the distal lumen, but the wire appears to go subintimal
Another several attempts are made to cross the lesion into the distal lumen using a second workhorse wire
All attempts to cross the lesion fail.
Due to the high dose of contrast and radiation used the on call operator decides to end the procedure
Aftermath
Patient was sent back to the coronary unit for further care
After the end of the procedure, the patient started complaining of worsening chest pain and her BP was 170/100 mmHg
Antihypertensive and analgetic medications were ordered
Unsurprisingly, there were no new EKG changes
Further therapy:
ASA, P2Y12 (Clopidogrel), LMWH 1mg per 10mg s.c., Bisoprolol 2,5mg, Irbesartan/hydrochlorothiazide 160/12,5mg, Pantoprazol 40mg, Lercanidipine 10mg, Atorvastatin 40mg, Levothyroxine 25mcg.
ECHO
The second ultrasound still showed dilated apex with akinesis to dyskinesia with good basal contractility. Apical wall thickness was measured at 6mm
The patient was stable during the morning visit with no new symptoms
But during the afternoon she began to experience shortness of breath and a drop in BP. Supportive medication was ordered, but the patient went into respiratory arrest
CPR was immediately started along with ambu mas ventilation. SpO2 was still dropping so the on call anesthesiologist intubated the patient and started mechanical ventilation.
Despite all efforts there was no improvement in the patients condition and she passed away.
1. What would you do if you were in the room with this patient?
2. Are there any elements to suspect SCAD underlying STEMI?
Based on what would you conclude that it is SCAD?
How would you perform the procedure if you have identified SCAD?
Part II
- The unexpected and tragic death of the patient following her admission to the hospital prompts a deep investigation into the underlying causes.
- Despite the efforts made by the medical team, including attempted rescue PCI and subsequent supportive care, the patient’s condition deteriorated rapidly, leading to respiratory arrest and ultimately her passing.
Autopsy:
- Endothelial and subendothelial infiltration by lymphocytes was noted
- Intima showed no signs of atherosclerotic changes!!
- A dissection of the media layer of the arterial wall, with a circumference greater than 79%, filled with hemorrhagic contents coupled with areas of hemorrhage in the adventitia!
Focal degenerative changes observed in the cardiomyocytes suggest ongoing damage to the heart muscle:
- Possibly worsened by fibrinolysis?
- Cardiac rupture?
Conclusion:
- The patient’s tragic demise was a result of a spontaneous coronary artery dissection (SCAD) followed by cardiac rupture (?)
- The challenges encountered during the attempted PCI procedure were likely exacerbated by the unique nature of SCAD, which can present difficulties in wire manipulation and stent placement due to the fragility and unpredictability of the dissected coronary artery.
- The utilization of fibrinolysis in this case, while initially deemed appropriate given the clinical presentation suggestive of STEMI, raises questions regarding its potential negative effects in cases of SCAD.
- Fibrinolysis, although beneficial in cases of thrombotic coronary artery occlusion, may exacerbate the risk of bleeding and increase the likelihood of adverse outcomes in patients with SCAD.
- In this scenario, fibrinolysis failed to improve the patient’s condition and may have contributed to the progression of the underlying pathology, ultimately leading to a fatal outcome.
No atherosclerotic leasions on other coronary arteries and impossibility to cross oclusion with a guidewire, might suggest a dissection as a possible cause. However, there are several issues: no data on what was a provocative factor (e.g. physical or emotional stress), why such a severe outcome with the occlusion of the distal LAD (SCAD propagation due to LMWH administration?). Very good case of why we need registries and continuous brainstorming on this topic. Again, very good case from UCC Nis.
A very complex case, on the basis of angiography a type 4 SCAD can be suspected and considering the clinical presentation, the decision to proceed to PCI seems inevitable. In all dissections with true lumen occlusion, placing the wire into the true lumen can be a challenge. The use of IVUS can help to find the true lumen, but even there you need experience and luck. In the end, it can be said from the first step to the unfortunate end, everything was done the way anyone would probably do it.
Very interesting case thanks to our colleagues from Nis. It looks like a SCAD case, but one cannot be sure about it without imaging, since the patient is not completely devoid of risk factors for atherosclerosis. There has been association of thyroid disorders and SCAD progression in a paper by Waterbury TM et al. Circ Cardiovasc Intv 2018 that might cause progression to SCAD type IV. It was a difficult task to wire distal LAD in this patient, knowing the anatomy that seems very tortuous. I would try with hydrophilic wire than confirm wire position using IVUS, since there is a high possibility that the wire would go subintimally. The workhorse wires would not be a good choice here.
Very challenging case.Findings of angiography without atherosclerosis in other arteries, extremely tortuous artery, preserved side branches, indicate SCAd. On the other hand, the patient’s age and comorbidities are not typical for scad. Anyway, I think there is no doubt that an attempt to recanalize the artery is indicated. After the failure of passing the workhorse wire, I would try with a Suoh 0.3 wire, composite core, dual coil , fat tip guidewire originally developed for tortuous collateral
channel tracking, atraumatic wire with excellent torque control.
Very difficult and challenging case. In first contact impression that is patient with standard STEMI (atherosclerotic), Women 62 y, STEMI anterior wall and fibrinolytic therapy. On coronary angiography single lesion in mid LAD with tortuosity vessel, impression that is SCAD type 4. Unfortunately with very challenging anatomy for wire crossing.
Thank you very much for the impressive case and pictures. If you have 62, years of females with STEMI, the decision for fibrinolytic therapy in non-PCI centres sounds good for physicians. I am afraid that we do not know in the patient room that it can be the SCAD.
That was very interesting and “tricky for decision” case. In the Centres without cath-labs thrombolisis will be administrated for sure, maybe with more demage? As we can see from this case, that was very challenging to deal interventional with distal part of LAD. According to my little experiences (the protocols don’t exist) there is not a tipical wire for this condition, because of tortuosity and very fragile part of the vessel.. In case that we success with the wire, the same reasons provide small possibilities to put OCT or IVUS there. As we can see, lot of “not knowing” still stand around us in SCAD and this platform is something that is very important for all of us. Thanks for sharing this case with us, I was in a similar situation a month ago and I know the feeling in that moment in the cath-lab. We are going to discuss very soon here about that.