What is the Optimal Anticoagulation in <scp>HGNS</scp> Surgery in Patients with High‐risk Cardiac Comorbidities?

Hypoglossal nerve stimulation (HGNS) therapy has become a more frequently employed tool in the treatment of obstructive sleep apnea since its approval by the FDA in 2014. One of the benefits of HGNS therapy is the low morbidity associated with the procedure. With only two external incisions, minimal operative times, and no pharyngeal wounds or skeletal osteotomies, the procedure is being widely employed in patients of advanced age and complicated medical histories. Because of this, providers will inevitably encounter patients on anticoagulation. A 2020 review of the MAUD database noted 196 adverse events associated with HGNS surgery, of which 11.6% where labeled as “hematoma.”1 When medically feasible, cessation of anticoagulation, which includes antiplatelet therapy, direct oral anticoagulants (DOAC), and vitamin K antagonists (abbreviation); is preferred; however, some patients, particularly those with valvular heart disease or other high-risk cardiac disease, require some form of concurrent anticoagulation therapy during surgery. This article's goal is to clarify the best practice regarding the placement of the HGNS in patients needing anticoagulation during surgery. Cardiac implanted electronic devices (CIED) account for more than 200,000 procedures annually in the United States, and well over 1,000,000 procedures worldwide. Large, randomized trials have been completed to clarify how to manage patients with a high risk of thromboembolism (greater than 5% per year). The largest study, the BRUISE CONTROL-1 (BC-1) trial analyzed 661 patients undergoing either pacemaker or implanted cardiac defibrillator (ICD) placement.2 Heparin bridging was instituted in 326 patients and continuation of warfarin was performed in 335 patients. For those in the warfarin group, INR levels were less than 3.0 and less than 3.5 in the mechanical heart valve subgroup. The primary outcome, defined as a clinically significant device-pocket hematoma (CSH) requiring surgical intervention, prolonged hospitalization, or interruption of oral anticoagulation therapy, occurred in 3.5% (12 patients) versus 16% (54 patients) in the heparin-bridging group. Continuing warfarin therapy in this group reduced clinically relevant hematoma formation by 80% in comparison the to the heparin-bridging group. BRUISE CONTROL-2 (BC-2) trial expanded the analysis to patients taking DOAC and antiplatelet therapy.3 A total of 662 patients with nonrheumatic atrial fibrillation and those with a CHA2DS2-VASc score ≥2 who were taking a DOAC where enrolled in the study. BC-2 randomized patient to continued versus interrupted DOAC therapy. Primary endpoint of CSH was similar between the two studies. In comparison with warfarin continuation (BC-1 study), there was no significant difference in the rates of CSH in continued versus interrupted DOAC treated patients (2.1% in each group). Additional analysis in the BC-2 study focused on the concurrent use of antiplatelet therapy during CIED insertion. Of the 1343 patients included in the two studies, 404 patients were taking an antiplatelet medication (30.4%), of which 383/404 (93.9%) were on aspirin, 50/404 were on clopidogrel (12.3%), and 25/404 were on both (6.1%). Those patients on antiplatelet therapy developed CSH in 40/404 patients (9.8%) compared with only 40/935 of patients who were not taking antiplatelet medications (4.3%). Antiplatelet use was a predictive factor in development of CSH in patients on warfarin regardless of whether the warfarin was interrupted or continued (odds ratio [OR], 1.965; 95% CI, 1.202–3.213; p = 0.0071). In regard to DOAC therapy, a multivariate analysis adjusting for antiplatelet use demonstrated no difference in CSH in the interrupted vs continued DOAC group (OR, 0.858; 95% CI, 0.375–1.963; p = 0.7174). Confirmation of the BRUISE CONTROL-1 and 2 trials have come via two meta-analysis published in 2014 and 2015.4, 5 The 2014 study by Du et al. assessed 14 studies (including BC-1 and BC-2 with four additional prospective randomized trials) with a total of 3744 patients analyzed. There were significantly higher rates of CSH in the heparinized patients compared withthe patients continuing warfarin anticoagulation (hazard ratio 3.1, 95% CI 2.0–4.8). In addition, heparin usage was not associated with the reduction of thromboembolic events. To avoid clinically significant hematoma in HGNS surgery, and to reduce the risk of thromboembolism in high-risk populations requiring anticoagulation, a research guided practice should be used to optimize patient care when anticoagulation during surgery is required. Based on CIED research, continuation of warfarin should be considered instead of heparin-based therapies to reduce the risk of CSH. Antiplatelet therapies should be discontinued as able as concurrent anticoagulation and antiplatelet therapy has been shown to significantly increase the risk of CSH. Lastly, continuation of DOAC, although unlikely to increase the risk of CSH based on available data, has not been studied thoroughly enough to make definitives recommendations. The literature evaluated includes two prospective randomized cohort studies2, 3 (level 1), and two systematic review with meta-analysis4, 5 (level 2).