A Case of Monomorphic Ventricular Tachycardia in an Immunocompetent Pediatric Patient With Histoplasmosis

To the Editors: Histoplasmosis is caused by the dimorphic fungus, Histoplasma capsulatum. Occupational and recreational activities, such as caving, construction and cleaning buildings, have been associated with causing infection.1 Most cases are asymptomatic or indistinguishable from other respiratory illnesses.2 A 17-year-old male with no significant medical history presented to his primary care provider with palpitations, chest tightness, dizziness and shortness of breath. There was no history of tobacco, drug, alcohol, excessive caffeine or energy drink intake. Initial findings and workup included an electrocardiogram, which showed nonspecific ST and T-wave abnormalities. Initial laboratory values were normal. Echocardiogram revealed mild pulmonary insufficiency with no right heart dilation and normal biventricular function. Holter monitor showed 1 episode of nonsustained ventricular tachycardia (VT) at 272 bpm lasting 7 beats. During the exercise stress test, the patient had an episode of polymorphic VT (Fig. 1) with a maximum rate of 300 bpm lasting less than a minute with symptoms of palpitations and lightheadedness. The patient was hospitalized in the pediatric intensive care unit, and cardiac magnetic resonance imaging showed normal biventricular systolic function and negative delayed hyperenhancement. Chest magnetic resonance imaging was significant for multiple calcified hilar and mediastinal lymph nodes, with a questionable ground-glass opacity in the left lung apex, suggesting granulomatous infection. The patient was started on metoprolol XL 25 mg.FIGURE 1.: Sinus rhythm with wide complex rhythm followed by ventricular tachycardia.Genetic evaluation ruled out long QT syndrome and showed a variant of unknown significance mutation in the MT-TL2 gene. The patient was switched to nadolol for possible catecholaminergic polymorphic VT, and LifeVest was used for interim protection. Computed tomography chest revealed multiple calcified hilar and mediastinal lymph nodes and questionable ground-glass opacity in the left lung apex, without calcified pulmonary granulomas or focal nodules. Infectious and oncologic workup were negative; however, the Histoplasma Yeast titer was 1:256, and he was started on itraconazole therapy. At 2- month follow-up visit, the patient was noted to have significant weight loss with poor appetite. A repeat computed tomography scan of the chest showed cavitary consolidation in the right upper lobe and tree-in-bud nodular opacities. Itraconazole treatment was extended to 6 months with significant weight gain. Repeat exercise stress test was normal after completion of antifungal therapy. He continued to be on nadolol and remained asymptomatic. While the exact etiology of VT remains unclear, effective management with nadolol and itraconazole led to significant clinical improvement. As per our review of the literature, there are no published reports that link histoplasmosis to VT. However, there is 1 publication that describes an association of mediastinal granuloma with monomorphic VT in the adult population.3 Our report describes a potential association of mediastinal Histoplasmosis with malignant ventricular arrhythmia, which can lead to substantial mortality. Successful management requires a combination of disease-specific therapy alongside antiarrhythmic drugs and potential intracardiac defibrillator placement.3