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Inotropic support was gradually withdrawn as BP improved after restoration of coronary blood flow.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.