A 28-year-old gravida 1 para 1 presented to her local emergency department (ED) on postpartum day 5 for chest heaviness and a "slow heartbeat." The patient had no significant past medical history, and there was no known family history of cardiac disease or genetic syndromes. There were no complications during pregnancy. The patient delivered a healthy female infant via vacuum-assisted vaginal delivery at 39 2/7 weeks and was discharged home on postpartum day 2. There was no record of intrapartum or postpartum bradycardia during that hospital admission. Initial assessment in the ED revealed a heart rate of 30-40 beats per minute (bpm) and blood pressure (BP) 158/77 mmHg. Atropine 0.5 mg IV was given, causing the patient's heart rate to increase to 80 bpm and systolic blood pressure to rise to 170-180 mmHg. Due to concern for postpartum preeclampsia, labetalol 20 mg IV was administered and a magnesium sulfate infusion was initiated. Computed tomography (CT) of the head showed no acute intracranial event. CT angiography of the chest was negative for pulmonary embolism. Due to concerns regarding the patient's cardiac status, the patient was transferred to our medical center.
Upon arrival to our center, the patient was alert and oriented. Oxygen saturation was normal. Mean arterial pressure remained below 50 mmHg and heart rate ranged between 40 and 60 bpm. A dopamine infusion was initiated and the patient's blood pressure improved. She complained of a worsening headache but no lightheadedness, shortness of breath, or chest pain. Physical exam, including cardiac exam, was unremarkable. Routine laboratory tests were normal. Preeclampsia work-up was negative. Troponin T was 0.01 ng/mL (normal < 0.01 ng/mL) and NT-proBNP was 324 pg/mL (normal < 124 pg/mL). Electrocardiogram showed sinus bradycardia but was otherwise unremarkable. Transthoracic echocardiogram (TTE) revealed a left ventricular ejection fraction (LVEF) of 35%, numerous wall motion abnormalities and an estimated right ventricular systolic pressure (RVSP) of 46 mmHg. These findings suggested possible ischemia or infarction due to multivessel spontaneous coronary artery dissection (SCAD) or PPCM. Repeat troponin T was elevated at 0.03 ng/mL. Aspirin 325 mg was administered. Coronary angiogram showed a 20% lesion in the mid left anterior descending artery but no SCAD. Optical coherence tomography was also negative for SCAD. Right heart catheterization confirmed the RVSP of 48 mmHg.
Dopamine infusion was successfully weaned the following day. The patient's only complaint was dyspnea on exertion. Enalapril was initiated. Cardiac MRI performed on hospital day 3 confirmed left ventricular systolic dysfunction with LVEF of 50% and mild basal hypokinesis but no myocardial delayed enhancement to suggest edema, fibrosis or infarction. The patient was discharged home on hospital day four. Given the constellation of symptoms and diagnostic test results, the final diagnosis was PPCM.
One month after discharge, TTE showed completely normal cardiac structure and function with an LVEF of 63%. The patient reported persistent intermittent bradycardia to 40 bpm mostly during periods of anxiety and in the evenings, without associated dyspnea or chest pain. On 24-hour Holter monitor, her heart rhythm was sinus with occasional sinus arrhythmia and heart rate ranging between 41 and 130 bpm (average, 61 bpm). During a treadmill exercise stress test, the patient achieved 13.0 METS and 113% of predicted functional capacity. ECG showed no signs of ischemia. Heart rate was 89 bpm at baseline, increasing to 173 bpm at peak exercise. Blood pressure was 102/78 mmHg at baseline, increasing to 160/72 mmHg at peak exercise. Enalapril was continued to complete a minimum of 6 months of treatment.