Brugada syndrome unmasked by a mosquito

Two weeks after returning from missionary work in Haiti, a 53-year-old woman with no significant past medical history presented with 5 days of worsening fevers, chills, diaphoresis, myalgias, and severe nausea. Notably, she did not take malaria prophylaxis while in Haiti. Her temperature was 40.1 C, her blood pressure was 100/ 58 mmHg, and her heart rate was 102 beats per minute. Physical examination was remarkable only for her ill appearance. Initial lab work revealed anemia (hemoglobin, 10.4 g/dL; hematocrit, 29.4%), thrombocytopenia (23,000/mm), and evidence of acute renal failure (blood urea nitrogen, 58 mg/dL; creatinine, 4.2 mg/dL). Other labs were within normal limits. Malaria was considered high on the differential diagnosis. A parasite smear was therefore obtained, and the findings were consistent with Plasmodium falciparum infection (5.5% parasitemia). She was admitted to the intensive care unit for hydration and initiation of antimalarial therapy. Her severe nausea prevented administration of oral medications; therefore, the infectious disease consultant recommended treatment with intravenous quinidine. Prior to initiation of quinidine, an electrocardiogram (ECG) was obtained (Figure 1). No prior ECGs were available for comparison. Prominent ST segment elevation was noted, prompting reassessment of the patient. She denied chest pain. Cardiac enzymes were normal, and an urgent echocardiogram demonstrated normal ventricular function with mild mitral regurgitation. Given that suspicion for acute coronary syndrome was low, the ECG findings were managed conservatively. Overnight, she defervesced and appeared to improve clinically. Cardiac enzymes remained negative. A repeat ECG obtained several hours after admission revealed complete resolution of the ST elevation (Figure 2). Repeat ECGs remained normal through the time of discharge, and no ventricular arrhythmias were noted on telemetry. On the basis of the characteristic ECG appearance, a presumptive diagnosis of Brugada syndrome was made. The patient did not have a history of presyncope, syncope, or agonal night-time breathing or a family history of sudden death. Two weeks following discharge, she was seen in the outpatient electrophysiology clinic to discuss further risk stratification. A procainamide challenge, followed by programmed ventricular stimulation (electrophysiology study), was recommended. The procainamide challenge revealed ST segment changes consistent with Brugada syndrome. She was not inducible for ventricular arrhythmias during the electrophysiology study. On the basis of these findings as well as her lack of symptoms, there was no indication for an implantable cardioverter defibrillator.