Atrial fibrillation (AF) is a prevalent cardiac arrhythmia characterized by irregular atrial contractions that compromise ventricular function and cardiac output. In this study we investigated the impact of AF on myocardial oxygen utilization, hypothesizing that myocardial oxygen extraction is more pronounced in AF due to less efficient ventricular function and reduced myocardial blood flow.

We conducted a prospective, observational study involving 45 patients undergoing AF catheter ablation at the University of Washington Medical Center between 2022 and 2024, categorizing them based on their presenting rhythm, i.e., sinus rhythm (SR; N = 27) or atrial fibrillation (AF; N = 18). During AF procedures blood samples for oxygen analyses were collected from the pulmonary artery, coronary sinus (CS), and left atrium. Cardiac magnetic resonance imaging assessed CS blood flow and left ventricular mass.

Patients in AF exhibited significantly higher myocardial oxygen extraction than those in SR (10.8 ± 1.4 vs 8.9 ± 2.0 mL O2/dL blood, P = .001). Additionally, AF patients had lower cardiac power (0.74 ± 0.14 vs 1.07 ± 0.32 W, P = .004), reduced CS flow (56.2 ± 34.0 vs 65.0 ± 19.2 mL/s, P = .42), and increased heart rate (80.6 ± 17.4 vs 64.0 ± 10.7 bpm, P = .002). In the AF group, symptomatic patients had significantly higher myocardial oxygen extraction for dyspnea, exercise intolerance, and palpitations (P = .048, P = .018, and P = .028, respectively), with a trend observed for fatigue (P = .07). No significant differences were found between symptomatic and asymptomatic patients in the sinus rhythm (SR) group. Multivariable regression analyses demonstrated that AF and AF-related symptoms were strongly associated with increased myocardial oxygen extraction.

AF significantly affects myocardial oxygen utilization by reducing both myocardial blood flow and cardiac power, thereby requiring increased oxygen extraction. This 2-hit mechanism—reduced supply and increased demand—highlights the symptomatic challenges in managing AF and emphasizes the need for therapeutic strategies to optimize cardiac physiology in these patients.