PERSISTENT ATRIAL FIBRILLATION AFTER CATHETER ABLATION IN HUMAN IMMUNODEFICIENCY VIRUS TYPE‐1 POSITIVE PATIENTS

Abstract

Therapeutic Area: Other: Electrophysiology Case Presentation: A 35-year-old with HIV-1 on 800 mg Darunavir, 150 mg Cobicistat, 200 mg Emtricitabine, and 10 mg Tenofovir Alafenamide presented with palpitations. Initial vitals significant for 120-140 beats per minute. 12-lead electrocardiogram showed atrial flutter with variable A-V block. Patient's troponin I was <0.01 ng/ml. He underwent transesophageal echocardiogram and was successfully cardioverted to sinus rhythm. Patient was discharged on Sotalol 80 mg twice a day and Dabigatran 150 mg twice a day. 45 days after initial presentation, patient underwent successful outpatient atrial flutter ablation. 65 days status post ablation, he again presented and was admitted due to atrial fibrillation. Currently, patient remains on rate control with Sotalol. Background: Atrial fibrillation (AF) is the most common type of cardiac arrhythmia. Researcher studies have found that Human Immunodeficiency Virus (HIV)-positive patients had an incidence of 18.2 AF diagnoses per thousand person-years, compared to 8.9 in patients without HIV (2). Non-pulmonary vein triggers are highly prevalent in HIV-positive AF patients and are associated with mid- and long-term arrhythmia recurrence (3).The prothrombotic nature of HIV infection and its association with stroke is believed to be secondary to systemic mechanisms such as low-grade inflammation and heightened oxidative stress, or through direct cardiac toxicity potentially leading to AF (4,5).A key consideration in the treatment of AF in patients with HIV‐1 who are in combination antiretroviral therapy (ART) particularly with protease inhibitors (PIs) or non‐nucleoside reverse transcriptase inhibitors (NNRTIs), is the significant impact these drugs have on liver enzymes which are crucial for metabolizing various oral anticoagulants (6,7).Additionally, ART regimens containing PIs can notably increase the serum concentration of antiarrhythmic drugs (5). Notably, ritonavir has been shown to significantly raise serum digoxin concentration (5). There are also reports of increased beta blocker and verapamil levels when combined with PIs (5). Conclusions: Given these complex interactions, there is a need for tailored guidelines for adjusting dosages of drugs, such as Eliquis and antiarrhythmic medications in HIV patients with atrial fibrillation. The role of HIV‐1 infection as an additional stroke risk factor, potentially extending beyond the CHA2DS2‐VASc score, must be further investigated.