Infarction artery occlusion: is the decision simple

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.

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

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.


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.


  • 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?


  • 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.