Our patient is a 75-year-old African-American woman with a history of diabetes mellitus, hypertension, hyperlipidemia, and four prior cerebrovascular accidents with mild right sided residual weakness and ventral hernia status after surgical repair. She has no prior history of smoking, alcohol use, illicit drug use, or family history of premature coronary artery disease. She initially presented with shortness of breath, rhinorrhea, and cough productive of yellowish sputum and tested positive for influenza A for which she was started on oseltamivir. On her second day of hospitalization she reported mild retrosternal chest pain accompanied with a Troponin I elevation up to 0.3 ng/mL with an unchanged EKG showing right bundle branch block (RBBB) (Figure 1(a)). She received Aspirin, Clopidogrel, and Heparin drip in addition to Diltiazem and Atorvastatin as treatment for a NSTEMI.
On the following day, she underwent a coronary angiogram revealing only minor luminal irregularities and no significant CAD (Figure 2(a)). Two days later, she underwent nasopharyngolaryngoscopy for progressive dysphonia that showed inflammatory changes of true and false vocal folds, mild granulation changes of the subglottis, and pachydermia. This was deemed secondary to her upper respiratory tract infection and the resulting acute tracheobronchitis. Subsequently, she was started on intramuscular dexamethasone 10 mg Q8 hours.
One day later, she complained of severe retrosternal chest pain with a blood pressure of 90/65 mmHg, heart rate of 95 bpm, and oxygen saturation of 95% on room air. Cardiovascular exam was unremarkable revealing regular heart rate and normal S1 and S2 with no appreciated murmurs, rubs, or gallop. She had no JVD and clear lungs on auscultation. Distal pulses were well felt without appreciated lower extremity edema. The EKG however showed ST elevation in the anterior leads, V2 to V5 (Figure 1(b)). Bedside echocardiogram revealed a left ventricular ejection fraction (EF) of 30-35% and regional wall motion in the form of apical dyskinesis and severe hypokinesis in the mid to apical anteroseptal, anterior, apical inferior, inferoseptal, and lateral segments. Of note, the pre-MI echocardiogram showed a normal EF with no appreciated regional wall motion abnormalities. The Troponin I level was 0.1 ng/mL (cutoff value of 0.2 ng/mL). She was immediately transferred to the catheterization lab where the angiogram surprisingly revealed a filling defect, likely a thrombus, occluding the midsegment of the LAD (Figure 2(b)). Subsequently, a 2.5 x 18 mm drug eluting stent was deployed with pre- and postballoon dilation resulting in TIMI III flow (Figure 2(c)). Eptifibatide was started in addition to Ticagrelor, Aspirin, Deltiazem, and Atorvastatin. The chest pain resolved shortly after the intervention and the EKG returned to baseline (Figure 1(c)).
Blood work revealed a platelet count of 461 k/cumm, hemoglobin of 10.5 mg/dL, and white blood cell count of 9 k/cumm. Homocysteine level was mildly elevated (15.5 micromoles/L, normal range 3.2-10.7). High sensitivity CRP was elevated at 40.9 mg/L. Factor VIII activity (325%, normal range: 63-150), factor XI activity (211%, normal range: 71-124), and thrombin antithrombin complex (13.7 ng/mL, normal range: 0.7-3.2) were all increased while factor VII activity was normal. Fibrinogen level and protein C and S activity were normal. Cardiolipin antibody, JAK2 V617F mutation, and Factor V Leiden were all negative.