Case Report
A 19-year-old non-obese (BMI=20.2kg/m2) girl presented
with chest pain associated with nausea and vomiting of 1 hour duration.
She was pale and sweaty with a tachycardia of 110 beats/min. Her
systolic blood pressure was 60 mm Hg, which responded to intravenous
fluid therapy and inotropic support. There was no history of smoking,
drug or analgesic abuse, previous episodes of arterial or venous
thrombosis. There is no significant medical or surgical history and she
was not on any medicine (including herbal). There was no peripheral
edema and all peripheral pulses were present. Her heart sounds were
normal and there were no signs of heart failure. She had never
previously experienced chest pain at rest or on exertion.
Electrocardiography (ECG) showed sinus rhythm with ST elevation in I,
avL, V4-V6 with reciprocal changes in inferior leads (Figure 1).
Transthoracic echocardiography showed anterior wall to be hypokinetic
with left ventricular ejection fraction (LVEF) 40% (Figure 2). Urgent
coronary angiography (CAG) was done which revealed ostial 99% lesion in
left main coronary artery (LMCA) with distal TIMI I flow (figure 3a).
Intracoronary bolus of nitroglycerine 50µg did not improve coronary
blood flow. Immediate angioplasty (door-to-balloon time = 25 minutes)
and stenting to LMCA was done and TIMI III flow achieved (figure 3b).
Post angioplasty, imaging showed plaque in left anterior descending
(LAD) artery, normal circumflex (Lcx) and right coronary artery (RCA).
There was no collateral blood flow to the left circulations from RCA.
Optical coherence tomography (OCT) was done which confirmed well
expanded stent and presence of atherosclerotic plaque in mid LAD. We
were able to finish the procedure without any IABP support.
Inotropic support was gradually withdrawn as BP improved after
restoration of coronary blood flow. During hospital stay she was
evaluated for possible etiology of AMI. All laboratory parameters were
within normal limits. Hemoglobin 9.8 gm/dl (n=12-16), serum creatinine
0.84 mg/dl (n=0.5-1.2 mg/dl), Homocysteine 7.53 umol/L (n= 4.4-13.5),
phospholipid antibody 0.71GPL u/l (<10), Total Cholesterol
(TC) 107mg/dl (0-200), Triglyceride(TG) 66mg/dl (0-150), Low Density
Lipoprotein (LDL) 62 mg/dl (0-100), serum cortisol 34.23, Thyroid
Stimulating Hormone (TSH) 2.34 μIU/ml(0.4-4.2).She was evaluated for the
cause of anemia by hematologist. The blood picture was suggestive of
Nutritional Iron Deficiency Anemia. She was discharged on oral Iron
therapy.
There was no coronary artery anomaly. CT aortogram did not reveal any
disease in the aorta or its major branches. Her father had AMI at the
age of 39 years and medical records revealed coronary atherosclerosis to
be the cause of AMI. The patient was discharged on 4th day on dual
antiplatelet therapy, beta blocker, statin. Levels of protein C, protein
S and antithrombin III were performed after 8 weeks of AMI and were
found to be normal. All other laboratory parameters Anti Phospholipid
Antibody (APLA) panel (Lupus anticoagulant, anticardiolipin Antibody,
Anti beta 2 glycoprotein), Antinuclear Antibody (ANA) were normal. The
indicators pointing towards atherosclerosis as the possible etiology
were a) plaque in mid LAD, b) very strong family history of coronary
artery disease (CAD) and c) absence of any biochemical or imaging
abnormality that suggested an alternative etiology.