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Relevant clinical history and physical exam
The 34-year-old white healthy woman, with no risk factors, no family history of cardiovascular disease, previous ECG was normal (done 1 year ago for an ordinary medical check-up), and with no preceding emotionally or physically stressful trigger event. She admitted to the emergency department complaining of exertional chest pain (3 hours before, no physical exercise or stress), sweating and weakness. Unremarkable physical examination: PA=100/60 mmHg (left and right), HR=85 bpm.
Relevant test results prior to catheterization
• Chest radiography was normal. Electrocardiographic examination showed: sinus rhythm, ST elevation in anterior leads V2, V4 and lateral lead V5, Poor R wave progression V1, V3.
• High peak troponin: 60.69 pg/ml (normal<14 pg/ml), Blood account: Hb=13.6 g/dl, WG=8700 /mm3, PQ=260000 /mm3, CRP: 44 mg/l, Kidney and lever functions: normal.
• Echocardiography revealed: Hypokinetic inter-ventricular septum and adjacent anterior wall at mid and basal cavity level, ejection fraction was 43%, no valvular abnormalities, normal RV, normal PASP.
Relevant catheterization findings
Normal coronary arteries (TIMI 3) Cardiac Magnetic Resonance Imaging: Non-dilated LV with low ejection fraction 48%.
RV: Normal Late gadolinium enhancement subendocardial pattern typical of an ischemic injury in the anterior interventricular artery (LAD).
Territory CCTA: Revealed no evidence of atheromatous changes within any of the coronary arteries.
The chest pain associated with a raised troponin, dynamic ECG changes echocardiography findings, inpatient coronary angiography arranged within 32 hours (she had Clopidogrel therapy 300 mg oral dose of prehospital care). The primary percutaneous coronary intervention show a normal flow with complete filling of the distal territory (TIMI 3)
The patient had no more chest pain a few minutes later, and the ECG showed:
* No persistent ST elevation
* Deep Q waves in V1 to V4
* T-wave inversion in V1 to V6
CAG after 30 days: same as the first one (TIMI 3)
* In previously reported literature, the incidence of chest pain coincided with ST-segment elevation with normal coronary artery is variable (range: 1.4-13%).
* The proposed mechanisms for Myocardial infarction with ‘normal’ coronary arteries (MINCA) include coronary vasospasm, coronary thrombosis in situ or embolization from a distal source with spontaneous lysis, cocaine abuse, viral myocarditis, aortic dissection, hypercoagulable states, autoimmune vasculitis and carbon monoxide poisoning.
* But without intravascular ultrasound, it is not possible to say that coronary artery disease is absent.
* Our case: Mechanism? Treatment? Follow-up?