TORSADES DE POINTES IN A PATIENT WITH HIV WHO ABANDONED TREATMENT: AN ATYPICAL PRESENTATION

Torsades de Pointes (TdP) is a rare but potentially fatal form of polymorphic ventricular tachycardia associated with QT interval prolongation, with an estimated annual incidence of 0.16% and mortality of up to 20%. Its causes include use of medications, electrolyte disturbances, and inflammatory and infectious conditions. People living with human immunodeficiency virus (HIV) are at increased risk of cardiovascular events, including arrhythmias, although TdP remains uncommon in this group.We report a case of HIV infection in a patient with long-term treatment abandonment who presented with recurrent TdP, likely arising from cardiomyopathy due to viral action. The patient is a 41-year-old woman with hypertension and HIV diagnosed in 2010, who had discontinued antiretroviral therapy (ART) 9 years earlier. She was referred to the emergency department due to refractory seizure episodes, intubated, sedated, and receiving intravenous phenytoin. Family members denied epilepsy and use of anticonvulsants and reported losartan and escitalopram as daily medications. She rapidly evolved with an episode of TdP and cardiorespiratory arrest, with return of spontaneous circulation after one cycle of resuscitation. Magnesium sulfate was administered, and she was transferred to the intensive care unit, where she experienced recurrent TdP episodes with spontaneous return to sinus rhythm. A transvenous pacemaker was placed, and an implantable cardioverter-defibrillator (ICD) was scheduled, as she had persistent QT prolongation even in the absence of high-risk drugs or electrolyte disturbances and after complete clearance of escitalopram. Echocardiography showed no major changes and an ejection fraction of 73%. A new viral load revealed 596,000 copies/mL and a CD4 count of 90 cells/mm³. After excluding opportunistic diseases, ART with tenofovir, lamivudine, and dolutegravir was initiated. During hospitalization, the patient had multiple appropriate ICD shocks, requiring an increased dose of beta-blocker and device adjustment. As viral load decreased with ART, the patient progressed in outpatient follow-up with beta-blocker tapering and no further ICD shocks. It is concluded that the seizure episodes likely resulted from low cardiac output secondary to arrhythmia and that the conduction disorder was due to cardiomyopathy associated with HIV. This suggests, in line with the literature, that uncontrolled chronic viral infection alone may predispose to malignant ventricular arrhythmias.