Case description
An 88-year-old Caucasian female presented to the emergency room complaining of shortness of breath with minimal exertion. This was associated with intermittent heart palpitations and fatigue. Her symptoms had gradually worsened over the prior month in response to family and emotional stress. She denied chest pain, cough, hemoptysis, nausea, vomiting, or diarrhea.
Her past medical history consisted of hypothyroidism, hypertension, and depression. Her only prior surgery was a hysterectomy. A recent echocardiogram revealed a normal ejection fraction with Grade 1 diastolic dysfunction. Family history was unremarkable. She did not use tobacco, alcohol, or illicit drugs. Her home medications included sertraline 25 mg daily, levothyroxine 25 mg daily, and lisinopril 20 mg daily.
A physical examination revealed the following vitals: a blood pressure of 147/52 mmHg, a temperature of 97.6°F, a respiratory rate of 20 breaths/minute, and a heart rate of 130 beats/minute. Cardiac auscultation demonstrated an irregular rhythm with a diastolic murmur heard best at the left upper sternal border, likely to be aortic in origin. An S3 gallop was present, and point of maximal impulse was laterally displaced. Auscultation of the lungs revealed bibasilar rales. Peripheral pulses were strong and equal bilaterally. There was moderate edema present in the lower extremities, and hepatojugular reflux was noted.
Laboratory testing identified the following values: white blood cell count of 8.8 × 103/μL, hemoglobin of 13.1 g/dL, platelet count of 277 × 103/μL, glucose level of 108 mg/dL, creatinine of 61.88 μmol/L, aspartate aminotransferase (AST) of 24 units/L, alanine aminotransferase (ALT) of 16 units/L, bilirubin total of 8.5 μmol/L, alkaline phosphatase of 98 units/L, and thyroid-stimulating hormone of 2.92 μIU/mL. All electrolytes were within normal limits. An initial electrocardiogram (ECG) revealed atrial fibrillation with a rapid ventricular response (Figure 1).
Intravenous diltiazem was initiated in order to control the ventricular rate. Shortly after, the patient’s rhythm converted to normal sinus rhythm spontaneously. She subsequently developed sinus pauses lasting up to 6 seconds; consequently, diltiazem was discontinued. Until a permanent pacemaker could be inserted, IV amiodarone was commenced in order to maintain sinus rhythm and prevent a rapid ventricular response. Following a loading dose of 150 mg, we administered 360 mg of amiodarone infused at a rate of 1 mg/min over 6 hours, after which a maintenance infusion rate of 0.5 mg/min was continued.
The next day, a routine laboratory evaluation illustrated an acute elevation to the following measurements: AST 1,881 units/L (normal high 35 units/L), ALT 1,048 units/L (normal high 35 units/L), alkaline phosphatase 143 units/L (normal high 129 units/L), total bilirubin 15.3 μmol/L (normal high 17 μmol/L), and creatinine 97.2 μmol/L (normal high 88 μmol/L) (Table 1). At that point, we reviewed all medications and obtained a hepatitis panel, which was normal. She had been on the same home medications for months without any change. A hepatic ultrasound identified venous congestion. We suspected amiodarone as a cause; thus, it was discontinued after administering a total dose of 960 mg over a 10-hour period. Signs of a hypersensitivity reaction such as itching, rash, or eosinophilia were not seen. Liver transaminases returned to baseline within 7 days. Further investigation with a cardiac echocardiogram demonstrated a left ventricular ejection fraction (LVEF) of 35%. Subsequently, a left heart catheterization revealed significant coronary artery disease with no clear revascularization targets, and a LVEF of 30%. She then received a permanent pacemaker, made an uneventful recovery, and was discharged on carvedilol, lisinopril, warfarin, and levothyroxine. Over the next 12 weeks, the patient suffered from progressive heart failure, which was managed both in the office and at home. Eventually, she died of advanced pump failure with progressive edema and respiratory failure.