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.
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.
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?
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!
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?
Thank you for these experience.
I would also stay to a conservative approach.
How do you explain the association of aortic dissection and SCAD?
What do you think about contrast retension before LM? Calcium?
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.