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.

Unrecognized SCAD

46-year-old female, active smoker, over the past two days experienced chest pain accompanied by cold sweats. At addmission TA 80/60mmHg. Cardiac and pulmonary findings appear to be within normal parameters.

ECG at admission:


ECHO shows akinesis of all apical segments.

Coronarography was performed:

On call interventional cardiologist failed to recognize SCAD

Loss of flow distally after stent placement; on-call doctor ends the procedure.

ECG after cath lab


Despite ongoing maximal drug therapy, the patient continues to experience symptoms with persistent ST elevation on the ECG.

Coronarography after 12h:

An intimal flap is observed at the distal edge of the stent, potential proximal propagation and the distal occlusion.


Confirmed SCAD type IIb/IV

Further continuation of drug therapy: ASA 100 mg, Clopidogrel 75 mg, Pantoprazol 40 mg, Atorvastatin 40 mg, Bisoprolol 2,5 mg

Follow up 3 months


The patient exhibits TIMI III flow with a residual intimal flap in the distal segment, yet remains asymptomatic without any new symptoms.


Based on what would you conclude that it is SCAD?

How would you perform the procedure if you have identified SCAD?

Recurrent SCAD

A 54-year-old female experienced short-term chest pains the day before admission. Two hours prior to admission, she reported severe chest pain radiating to her shoulders. She is hemodynamically stable with no significant arrhythmias.

Her vital signs include a blood pressure of 120/80 mmHg and a heart rate of 70 beats per minute.

Notable risk factors include hypertension, hypothyroidism, a history of smoking, menopause, and thyroid carcinoma surgery seven years ago. She has had no previous cardiovascular events. Additionally, it’s worth mentioning that her father passed away from pancreatic cancer.


ECG at admission:

TEE was preformed, EF 56%:

Lab values: Troponin 6.8, GFR 77 ml/min/1.74m2, K+  4.6, Gly 5.5, HOL 4.9, HDL 1.82, LDL 2.39, CRP 3.2

Initial therapy: ASA 300mg, Ticagrelor 180mg, Heparin 7000 i.v., Rosuvastatin 40mg

Coronary angiography:

Discharge therapy: ASA 75mg, Clopidogrel 75mg, Rosuvastatin 20mg, Bisoprolol 2.5mg , Ramipril 2.5mg, Euthyrox 100mcg

Control Coronary Angiography – 1 month after:


Initial and 1 month after

Six months following a previous episode of SCAD, the patient experienced severe chest pain radiating to both arms after strenuous activity. The patient remains hemodynamically stable with no significant arrhythmias observed.

Vital signs at the time of presentation show a blood pressure of 135/80 mmHg, a heart rate of 54 beats per minute, and a troponin level of 13.7.


TEE was preformed, EF 61%:

Coronary angiography:

Discharge therapy: ASA 75mg, Clopidogrel 75mg -discontinued after a month, Rosuvastatin 20mg, Bisoprolol 2.5mg , Ramipril 2.5mg, Euthyrox 100mcg

What do you think is the reason for SCAD and ACS?
How long would you keep DAPT after the first and second events?

SCAD in sisters; Different treatment approach

A 37-year-old female presented with a concerning episode of chest pain that radiated to her left arm, lasting approximately 10 minutes.

Notably, she has no known chronic diseases and does not possess any risk factors for cardiovascular disease.

Upon admission, her troponin level was measured at 2.27 ng/ml, prompting her admission to the Intensive Care Unit (ICU) for further evaluation and management.

ECG at admission:

An elective coronary angiography was done on the seventh day following her admission.

Coronary angiography:

RCA with 99% stenosis i medial segment and 80% in medio-distal segment.

PCI was preformed:

ECHO showed LV 4.72/3.28, EF:57%, hypokinesia of inferior wall.

One year later, a woman, 39 years old, presents with acute coronary syndrome (ACS), without risk factors for coronary heart disease (CHD), and without comorbidities.

She is the sister of a previous patient!

She is experiencing chest pain accompanied by nausea and vomiting. Symptoms started one day prior to admission. The pain is located behind the sternum and radiates to both arms down to the elbows.

Her troponin levels was measured at 0,00… 1,84… 12,55… 0,10 ng/ml

ECG at admission:

ECG during chest pain:

The patient was on medical therapy for 3 days, and subsequently, a coronary angiography was performed. In the meantime, there were multiple episodes of chest pain that responded to sublingual nitroglycerin (NTG) or NTG infusions.

Coronary angiography:

In the medial segment of LAD, there is SCAD type II with TIMI flow I-II.

It has been decided to continue with medical therapy.
Th: ASA 100mg, Clopidogrel 75mg, Nebivolol 5mg, Atorvastatin 60mg, PPI, NTG prn.

ECHO showed LV:5.15/3.22, EF:55% hypokinesia of apex and distal half of lateral wall

Coronary angiography after 3 months shows complete recovery:

Author: Prim Dr sc med Vladimir Mitov, FACC, KC Zaječar

Did the first sister had SCAD?

Would you treat the first sister conservatively if you had this knowledge about SCAD?

SAP/Positive stres test/Stenosis LAD?

A 42 years old patient complains of chest pain on exertion for last 6 months. TEE shows normal LV with no wall motion abnormalities.
Fisk factors for CKD: obesity, positive family history for CKD.

After the positive stress test patient is referred for coronary angiography.


Beginning of stress test

End of stress test

Coronary angiography:

Due to suspected SCAD patient was hospitalized. Repeated coronary angiography at 2 weeks showed no changes.

IVUS: dissection and intramural haematoma in LAD.

IVUS-guided PCI was done:

DES 3.50×30 mm @ 12atm.

False lumen covered with stent.

Stent optimisation with NC baloon.


ECHO: normal LV with no wall motion abnormalities.

After PCI patient is stable, no chest pain.

Therapy on discharge: ASA, Clopidogrel, b-blocker, ACEi.

Authors: dr Vlada Zdravković, dr Dušan Vulović, dr Đorđe Stevanović, UKC Kragujevac

Would You do PCI without intravascular imaging?

Aortic dissection type B and SCAD

A 57 years-old female was admitted in regional hospital because of NSTEMI with OHCA due to the VF in October 2022.
Risk factors for cardiovascular diseases: hypertension, positive family history for CVD and smoker.

Three years ago Stanford B dissection was registered and conservatively treated.

After initial stabilisation patient was transferred to the tertiary center for coronary angiography and further diagnostic.
At the admission she was without any symptoms.
Status at the admission: alerted, oriented, hemodynamically and rhythmically stable, Killip I.

ECG on admission:


Coronary angiography:

Operators: Prof. Dr I. Ivanov, Doc. Dr M. Čanković, IKVBV Sremska Kamenica

Would you decide for PCI LAD?


  1. Great images of the case! Since patient was without chest pain, with a TIMI 2-3 flow in LAD, would opt for conservative treatment (no PCI, no DAPT or LMWH, control angio before dismission). Best regards for colleagues from IKVB Sremska Kamenica!

  2. It is a really great case. I am not an interventional cardiologist, however, it is very illustrative. And what did you do? Could you inform us about the FU of this patient, please?

  3. Thank you for these experience.
    I would also stay to a conservative approach.
    How do you explain the association of aortic dissection and SCAD?

  4. What do you think about contrast retension before LM? Calcium?

  5. Very interesting case. Of curse conservative approach is correct choice for this patients. Fibromuscular dysplasia can be pathophysiological mechanism who can explain aortic dissection and SCAD. Shadow (contrast retention) before LM is similar like calcium, but must think about aortic dissection especially in patients with history for aortic dissections and SCAD!


    Since the patient had NSTEMI complicated with VF and OHCA I wouldn’t be brave enough to proceed with conservative treatment without a further diagnostic.
    I would do intracoronary imaging to assess the distribution and MLA of the true lumen. If the true lumen is severely compromised I would proceed with PCI. I agree with Dr Mitov that FMD can be the cause.

             Part two


In the second act was planned PCI LAD with intravascular imaging ( OCT).

During the hospitalization, the patient had symptoms of COVID-19 infection and was transferred to COVID hospital Novi Sad.

Two weeks later OCT guided PCI LAD was performed.

OCT pullback before PCI


OCT pullback after stent implantation

Stent postdilatation

Final result:


Female 62y. old hospitalized in a regional hospital as NSTEMI.

Presented on September 23. with chest pain. ECG showed SVT with ST-segment depression. Baseline troponin level 1.8 (ref. value <0.04).

Risk factors for CVD: hypertension, obesity (BMI 36), positive family history of CVD

Referred for elective coronarography on December 1.





Coronarography was presented to 8 interventional cardiologists for interpretation.



Bridge: 1

SCAD+Bridge: 2


Due to the lack of an OCT catheter the patient was referred to CTA.


CTA: calcified plaque in proximal LAD with 25% stenosis 20mm from ostium.  Medial LAD is very thin with loss of opacification at 50mm from ostium.


Control coronarography was done on December 23, with a plan to do OCT.

After NTG administration.

Initially planned OCT was not done.


Do you agree with the myocardial bridge as a diagnosis?

Would you do an OCT after the administration of NTG?

What are possible adverse events in OCT imaging of the coronary artery with a myocardial bride?

Coexistence of Spontaneous Coronary Artery Dissection, Takotsubo Cardiomyopathy, and Myocardial Bridge:

STEMI/MINOCA/unrecognized SCAD

Female 41. years old presents to regional hospital Leskovac with chest pain that started 30 minutes ago with unprovoked, severe chest pain that propagated to the left arm a lower jaw and was accompanied by headache.

STEMI diagnosis was confirmed, and she was loaded with Aspirin and Clopidogrel and transported to the PCI center (KBC Niš). The patient complained of elevated blood pressure during her menstrual cycle which was accompanied by headaches.

Risk factors for CVD: arterial hypertension, obesity (BMI >40)

ECG on admission:

LAB: TnI 2.180; K 3.1; Hol 4.47; LDL 2.49; HDL 1.24; TRIG 1.6

In CICU she received LMWH (Clexane 100mg c.s) and was sent to the cath lab.

Angiography showed moderate lumen narrowing in mid-LAD with TIMI3 flow.

Angiogram SCAD; classified  as normal (without significant lesions)

After returning from a cath lab, the patient is asymptomatic.

During her stay in CICU she was on DAPT an LMWH (Clexane 100mg BID).

ECG after cath lab:

ECHO day one:

After a hearth team discussion and angiography review, SCAD was suspected.

On the fourth-day control angiography an OCT were performed confirming SCAT type 2 with intramural hematoma and no flap i mid-LAD.

LMWH was discontinued.

Patient discharged with 1 month DAPT and the Clopidogrel 75mg permanently.

ECG on discharge:

Coronary angiograpy after one month:

ECHO after one month:


1. Do you think that first angiographic results are misinterpreted often?
2. Would you do an OCT in the acute phase on a patient like this?
3. Since the patient didn’t undergo a PCI would you give DAPT up to one month?
4. Should a patient like this be sent to cardiac rehabilitation?

SCAD LAD, left LV function evolution

A 47-year-old female, 10 minutes before admission to the hospital, felt pain between her shoulder blades, then a sharp stabbing recurrent chest pain that lasted 2-3 minutes in each episode. The pain was accompanied by shortness of breath and nausea.
She is an administrative worker in a hospital, under lots of stress lately.
CVD risk factors: smoker (3 pack-years), positive family history of CVD.

During the exam she suddenly lost conscience; ECG showed VF, and she was defibrillated.


ECG after DC shock: ST elevation in inferior and lateral leads.

Premedication (Brilique 180mg, tbl. Aspirin 300mg, LMWH 0.6 s.c) and Cath lab was activated.

Angiography showed SCAD type 2 on mid-distal LAD with a lumen reduction of 99%.


After returning from a cath lab, the patient is asymptomatic, and ECG changes are in regression.


50 minutes after angiography she complains of chest pain again. ECG shows ST elevation in inferior and lateral leads.


Cath lab was activated a second time. Angiography showed SCAD type 4.

After multiple balloon pre-dilatations with Artimes 1.25x15mm stents, Resolute Onyx 2.5×18 at 12 atm, Resolute Onyx 2.75×18 at 14 atm, Resolute Onyx 2.75×15 at 18 atm were implanted in LAD. TIMI3 flow was restored.

After the PCI patient was asymptomatic with ECG changes resolution.

She received DAPT and Bisoprolol 5mg; LMWH was discontinued after 2 days.


Day one:

Day four:

Day 26:

Author: prof. dr Svetlana Apostolović, Klinika za KVB, UKC Niš

Operator: prof. dr Zoran Perišić, Klinika za KVB, UKC Niš

1. Do you think the fast progression of scad is due to intensive DAPT?
2. What do you think about the PCI technique used?
3. Would you continue LMHW after stent implantation?

Epilogue;  60 days later.