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

Therapeutic Area

Other: Electrophysiology

Case Presentation

A 35-year-old African-American male with medical history of HIV-1 infection on 800 mg Darunavir, 150 mg Cobicistat, 200 mg Emtricitabine, and 10 mg Tenofovir Alafenamide presented with the complain of palpitations and sweating. He reported resting tachycardia, 120-140 beats per minute, from his smartwatch. Upon arrival, 12-lead electrocardiogram showed atrial flutter with variable A-V block. Patient's troponin I was <0.01 ng/ml. Subsequently, he underwent transesophageal echocardiogram and was successfully cardioverted to sinus rhythm with one dose of 200 joules of synchronized cardioversion. After multidisciplinary management, 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 with premature ventricular complexes. Currently, patient remains on rate control with anticoagulation treatment and frequent outpatient surveillance. Since the last incidence, no inpatient hospitalizations have been reported.

Background

Atrial fibrillation (AF) is the most common type of cardiac arrhythmia. It is due to abnormal electrical activity within the atria of the heart, causing them to fibrillate. This arrhythmia may be paroxysmal (less than seven days) or persistent (more than seven days) (1). 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 the mid- and long-term arrhythmia recurrence was observed to be mostly driven by those triggers (3). We present a patient who represents part of the growing study population of young HIV-1 positive male associated with arrhythmia recurrence.

Conclusions

The prothrombotic nature of HIV infection is well-documented (4). It is believed that HIV-1 infection elevates stroke risk via systemic mechanisms such as low-grade inflammation and heightened oxidative stress, or through direct cardiac toxicity potentially leading to AF (5). A key consideration in the treatment of atrial fibrillation in patients with HIV‐1 who are in combination antiretroviral therapy (ART), is the significant impact these drugs have on liver enzymes like CYP2C9 and CYP3A4 (6). These enzymes are crucial for metabolizing numerous medications, including various oral anticoagulants (6). Given this, there is a strong likelihood of interactions between vitamin K antagonists and ART, particularly with protease inhibitors (PIs) or non‐nucleoside reverse transcriptase inhibitors (NNRTIs) (7).

Additionally, ART regimens containing PIs with or without boosters like ritonavir or cobicistat, 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 protease inhibitors (5). Given these complex interactions, there may be 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.