West Nile Virus (WNV) myocarditis is nearly fatal, according to the current medical literature. We report a previously healthy 37-year-old Caucasian male who presented to our facility with two days of progressive lower extremity weakness, fever, edema, and shortness of breath found to have left ventricular global hypokinesis with an ejection fraction of less than 25%, consistent with acute viral myocarditis. He also has concomitant WNV meningoencephalitis due to his altered mentation. He was found to have a positive serum WNV IgM suggestive of a diagnosis of WNV myocarditis. He was intubated and was placed on vasoactive pressors for supportive care due to evidence of mixed cardiogenic and septic shock. After two weeks of hemodynamic support, we discovered a near-complete cardiac recovery, as shown on a repeat transthoracic echocardiography (TTE) and a normalized mean arterial blood pressure. This is a unique case report because near fatality is often associated with WNV myocarditis secondary to tachyarrhythmia, and there are currently no documented cases that are suggestive of cardiac recovery from the current literature.
Hypothyroidism is known to cause bradycardia, but there are no direct comparisons of the level of thyroid-stimulating hormone (TSH) to heart rate (HR) to assist in therapeutic hormonal management. This case presents a patient who developed symptomatic junctional bradycardia and underwent serial TSH testing to attempt to improve her HR while minimizing systemic toxicity from levothyroxine. The patient had a history of paroxysmal atrial fibrillation on beta-blocker therapy and hypothyroidism and developed symptomatic junctional bradycardia following a lapse in her thyroid supplementation. Upon initiation of hormonal replacement therapy, serial TSH levels were assessed as she continued to have episodic bradycardia with severe hypertension. Given the lack of evidence correlating TSH levels to HR, this case report calls for further studies to be conducted to create reliable guidelines in therapeutic management to prevent bradycardia events while minimizing systemic levothyroxine toxicity.
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