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.
ECG:
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?
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.