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.

Žena 35 godina: kakva je vaša dijagnoza MINOCA/myocarditis/SCAD…???

Bolesnica 35 godina, 4.7.2020. primljena u ZC Zaječar iz bolnice u Negotinu zbog sumnje na AKS. Bol u grudima u toku noći koji je probudio iz sna i širi se u levu ruku.

Lična anamneza: leči se od steriliteta duži niz godina. Negira druge hronične bolesti.

U lab analizama: hs-Troponin T: 1487

Pulmo: normalan disajni šum. Cor: akcija ritmična, tonovi jasni, bez dodatnih tonova i šumova. TA:140/80 mmHg, Fr:80/min.

Pri prijemu bez bola u grudima.

EKG pri prijemu:

EHO srca: Ao: 2,8, LP: 3,8, LK: 5,6/3,5, EF: 63%, blago dilatirane šupljine sa EF:66%, bez segmentih ispada u kinetici, SPDK: 30mmHg. Perikard hiperehogen lako raslojen do 2,5mm ispred donjeg zida


U daljem toku hospitalizacije bolesnica bez bolova u grudima, hemodinamski stabilna.

U lab analizama se registruje peak hs-troponina T od 4000.

Elektrokardiografski evolucija anterolateralno:


Bolesnica je otpuštena na kućno lečenje sa terapijom: Cardiopirin 75mg, Vivace 5mg, Tensec 5mg, Rosuvas 20mg.

Otpusna dijagnoza Myocarditis acuta.


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

Da li vidite neku promenu na angiogramu?
Šta mislite o faktorima rizika pacijentkinje?
Koja bi bila Vaša dopunska dijagnostika?
Da li biste je otpustili sa ovom terapijom?


  • Hvala kolegama iz Zaječara na interesantnom prikazu. Ako uzmemo u obzir godine života, pol, kao i da se pacijentkinja leči od steriliteta, prva pomisao bi mogla biti SCAD. Takođe, gledajući nalaz koronarografije, možemo reći da postoje iregularnosti lumena distalne LAD, a pre svega snažne D1 (dual LAD) koje liče na SCAD tip 3 (naročito lezija na D1 ispod bifurkacije) koje opet idu u prilog SCAD. Sa druge strane, sličan nalaz bi mogao da se vidi i u vazospastičnoj angini, pa bi kod ovakvog nalaza koronarografije uvek trebalo dati i NTG da vidimo odgovor i bar isključimo vazospazam. Dalje, u periodu praćenja, nakon 3 dana imamo još ubedljivije EKG promene (pretpostavljam u odsustvu anginoznih tegoba), zbog čega bi bilo interesantno videti kontrolni ECHO, da li ima nekih ispada segmentne kinetike ili eventualno GLS ukoliko ima mogućnosti. Što se tiče dif. dijagnoze, SCAD tip 3 bi bila prva dijagnoza. Za vazospastičnu anginu morali bismo uraditi acetilholinski test koji nemamo, a za miokarditis obavezno MRI kako ne bismo “etiketirali” pacijentkinju sa dijagnozom prebolelog miokarditisa, a u pitanju je bila SCAD, iako nijedna od navedenih dijagnoza ne ide u prilog pacijentkinji koja planira trudnoću. Što se terapije tiče, opredelila bih se ASA, statin i BB.
    Još jednom hvala za interesantne slučajeve koji nas teraju na malo više razmišljanja i podstiču da unapredimo svoj rad.

    Srdačan pozdrav

  • Drage kolege,
    Zahvalio bih Prof Apostolović što nam je omogućila prikaz slučaja, sa vašom diskusijom, na sada već establiširanom mestu, upravo za ovakve situacije i slučajeve! Nakon prve hospitalizacije i koronarografije zbog godina starosti i pola bili smo skoro sigurni da se radi o SCAD-u ali na angiografiji nismo videli promene koje bi to potvrdile, osim preomena na LAD koje je Mila već opisala, a nama tada nisu delovale tako značajne. S obzirom da smo imali značajni skok trponina, bez ehokardiografsken potvrde i KB i miokarditisa, izabrali smo dijagnozu miokarditisa kao kompromis koji bi potvrdio ukazao na leziju miokarda koja je svakako laboratorijski verifikovana, a nismo imali jasne kriterijume nizašta. Upravo pitanje koje je Prof Apostolović postavila MINOCA/MIOKARDITIS/SCAD je bila naša dilema? Naravno, prikaz i cela priča ima nastavak.

  • Poštovani,
    Hvala kolegama iz Zaječara što su publikovali ovako interesantan slučaj. Pre svega bih voleo više da znam o prethodnim faktorima rizika za aterosklerozu i to numerički nivoi lipida, glikemije, HbA1C kao i terapiji koju je dobijala za lečenje steriliteta.
    Iako lezije na sistemu leve koronarne arterije podsećaju na SCAD bez intravaskularnog imaging-a je teško isključiti spazam i aterosklerozu. Promene zahvataju veliku D granu (slažem se sa Milom za double LAD anatomiju) što odgovara i elektrokardiografskim promenama na inicijalnom EKG zapisu. Kontrolni EKG odgovara evolutivnim promenama infarkta. ali to ne može opredeliti u pravcu SCAD vs MINOCA .
    Što se tiče terapije obzirom da nemamo pouzdanu Dg SCAD-a i da sumnjamo na tip 3 SCAD mišljenja sam da nema prepreke za DAPT (tip II je povezan sa povišenom incidencijom MACE uz DAPT Cerrato E DISCO registry Eur Heart J 2021). Ovome u prilog i ne baš normalan izgled LAD.
    Hvala na prilici da komentarišem ovaj slučaj!

  • Poštovani,
    Hvala na komentaru ovog interesantnog slučaja.
    U laboratorijskim analizama na prijemu: Holesterol 5.7 mmol/l, Trigliceridi 1.8mmol/l. Kontrolna laboratorija (3 dana kasnije): Holesterol 4.0 mmol/l, Trigliceridi 1.1 mmol/l, HDL 0.7 mmol/l, LDL 2.8 mmol/l, HgA1c 5.6%.

  • Poštovane kolege,
    pacijentkinja nije imala klasične faktore rizika.
    Naravno da se izdvaja kao ,,upozorenje,, to što je lečila sterilitet i primala hormonsku terapiju.
    Većina interventnih kardiologa bi napisala kao zaključak, da nema značajnih sušenja na epikardnim arterijama i da je potreban nastavak medikamentne terapije.
    Drago mi je da smo izoštrili čula kada je u pitanju SCAD, te da o njemu razmišljamo.
    Promene na Dg grani i kratkom segmentu LAD, koje imaju glatke ivice i imaju karakter ,,tubularnog,, suženja, mogu da odgovaraju i SCADu ali možda i spazmu.
    Odgovor može da nam da jedino IV imaging, posebno kada je terapijski pristup u pitanju.
    Smatrama da prikazana pacijentkinja ima MINOCA Dg, da nema elemenata za miokarditis. Ali, pošto nemamo ehokardiografski potvrđene regionalne ispade kontraktiliteta, u postavljanju dijagnoze (pored IV imaginga)
    pomogla bi magnetna rezonanca srca. MR bi dala odgovor da li se radi o nekrozi miokarda (MINOCA) ili Dif dg edemu miokarda (Myocarditis).
    Zahvaljujem neizmerno ekipi iz Zaječara što je podelila ovaj slučaj sa nama. Uskoro sledi drugi deo slučaja.

  • Hvala kolegama iz Zaječara na zanimljivom prikazu.
    Gledano angiografski postoji lezija Dg ali lezija LAD nakon koje je i protok usporen. Ekg evolucija takodje ide u tom pravcu (LAD) . Imidzing sigurno daje odgovor na pitanje, ali takodje nosi i rizik za propagaciju disekcije, tako da sigurno nije jednostavna odluka sta raditi…

             Drugi deo


Bolesnica je 24.06.2021. godine ponovno primjena iz bolnice u Negotinu u ZC Zaječar zbog sumnje na STEMI prednjeg zida. Bol u grudima koji traje poslednja 2h i širi se u levu ruku.
U Negotinu Troponin:12525 pg/ml
Pulmo: normalan disajni šum.
Cor: akcija ritmična, tonovi jasni, bez dodatnih tonova i šumova. TA:120/80 mmHg, Fr:80/min.


EHO srca: Aorta 2,9, LP: 3,7, LK: 5,5/4,3, EF: 50%, hipokinezija vrha i apikalnog segmenta septuma, SPDK: 22mmHg. Perikard bez raslojavanja.



U daljem toku hospitalizacije bolesnica je bolova u grudima. Hemodinamski stabilna.

EKG na otpustu:

Terapija na otpustu: ASA 100mg, Clopidogrel 75mg, Bisoprolol 7,5mg, Amlodipin 5mg, Rosuvastatin 40mg

Dijagnoza na otpustu: MINOCA u čijoj osnovi je SCAD

Da li mislite da je ovo SCAD?
Da li biste ušli u proceduru sa cutting balonom?
Da li bi konzervativno lečenje podrazumevalo samo jedan antitrombocitni lek?

Dana 26.08.2021 urađena je rekoronarografija.



    1. Drage kolege,
      vreme je najbolji učitelj. Kolege iz Zaječara su nam poslale i novi akutni koronarni događaj kod pacijentkinje, gde vidimo ,,dinamiku promena,, na LAD i Dg grani. Sada je jasnije da se radi o SCADu.
      Mislim da ovaj slučaj treba lečiti konzervativno, s obzirom na anatomiju LAD i kliničku prezentaciju AKS/SCAD.
      Sada već više znamo o DATT i trebalo bi ostaviti jedan antitrombocitni lek, kao i isključiti antikoagulantnu terapiju kada postavimo Dg SCAD.
      Zamoliću Darija da postavi i kontrolnu koronarografiju, nakon 3 meseca!

    1. Da, sada je definitivno jasno da je u pitanju bila SCAD, odnosno da je ovo rekurentna SCAD. Nastaviti sa OMT, DAPT i obavezno BB koji jedino dokazano smanjuje rizik od rekurentne SCAD. Odličan prikaz! Videćemo i nalaz kontrolne koronarografije. Hvala kolegama iz Zaječara!
      Srdačan pozdrav,

    1. Možete pogledati i kontrolnu koronarografiju i uporediti snimke, IZNAD KOMENTARA.
      Hvala i Dariju koji maestralno obavlja, za sada tehnički posao!

    1. Nakon svega, jasno je da u pitanju SCAD sa progresijom u odnosu na prvu koronarografiju. Licno bih se takodje odlucio za konzervativni pristup.

    1. Drage kolege,
      Veliki pozdrav i odličan prikaz za sve nas. Ako sala nema mogućnosti za IVUS ili OCT (ili se na SCAD i ne misli 🥴) onda vreme naravno da odgovor. Mene sada interesuje koje je objašnjenje rekurentnog SCAD-a kod ove mlade žene koja se leči od steriliteta? Da li je urađena neka dopunska dijagnostika u tom pravcu?

  1. Draga Aleksandra,
    nije rađena dopunska dijagnostika.
    Da li ti predlažeš nešto????

             Treći deo


Kontrolni EHO srca i ERGO test urađeni nakon dve godine.

EHO: Globalna i regionalna kontraktilna funkcija leve komore su očuvene

ERGO test:
U miru:

Tokom testa:



Da li je bezbedno pacijentu sa istorijom SCAD raditi ERGO test?