Dexmedetomidine Associated With Decreased New-Onset AF in Critical Illness

Patients with critical illness treated with dexmedetomidine therapy may have decreased risk for new-onset atrial fibrillation (NOAF), according to findings published in the Journal of the American Medical Association Network Open.

Investigators sought to determine whether the incidence of NOAF among patients with critical illness could be affected by treatment with dexmedetomidine. Occurrence of NOAF within 7 days of intensive care unit (ICU) admission was the primary outcome. Hospital length of stay, ICU length of stay, and in-hospital mortality were secondary outcomes.

Using medical records from the Medical Information Mart for Intensive Care-IV database of patients admitted to the Beth Israel Deaconess Medical Center in Boston from 2008 through 2019, the investigators conducted a retrospective propensity score-matched cohort study. They included 8015 critically ill patients (age, 61.0 [SD, 17.1] years; 65.4% men) who were then propensity score-matched 1:3, with 2106 patients in the dexmedetomidine group treated with dexmedetomidine within 48 hours of ICU admission and 5909 patients in the no dexmedetomidine group who were never treated with dexmedetomidine. Included patients were hospitalized in the ICU and at least 18 years of age. The investigators used multivariate imputation for imputing missing data prior to propensity score matching.

Among all eligible patients before propensity score matching (N=22,237), the dexmedetomidine group vs no dexmedetomidine group had higher mean sequential organ failure assessment scores, greater frequency of sepsis, lower Charlson Comorbidity Index scores (mean 4.86 [SD, 2.83] vs 5.80 [SD, 2.95]), and they were younger (60.61 [SD,16.02] years vs 66.44 [SD,16.66] years). The groups were comparable for age, sex, race/ethnicity, sepsis, and mean sequential organ failure assessment scores.

There was a decreased risk for NOAF associated with dexmedetomidine treatment (17.6% of patients in the dexmedetomidine group vs 22.4% of patients in the no dexmedetomidine group; hazard ratio [HR], 0.80; 95% CI, 0.71-0.90). This association was sustained through sensitivity analyses. Patients in the dexmedetomidine group vs no dexmedetomidine group had a significantly longer time from ICU admission to AF onset (median 2.1 days [IQR, 1.5-2.9] vs median 1.3 days [IQR, 0.2-2.2]; P <.001). There were no significant differences in medication use for electrical cardioversion, rhythm control, or rate control concerning treatment for AF.

There was a longer hospital length of stay among patients in the dexmedetomidine group vs the no dexmedetomidine group (median 10 days [IQR, 6.6-16.3] vs 8.8 days [IQR, 5.9-14.0]; P <.001). There was a longer ICU length of stay among patients in the dexmedetomidine group vs the no dexmedetomidine group (median 4.0 days [IQR, 2.7-6.9] vs 3.5 days [IRQ, 2.5-5.9]; P <.001).

The investigators found an association between treatment with dexmedetomidine and decreased risk of in-hospital mortality (6.3% deaths in the dexmedetomidine group vs 12.8% deaths in the no dexmedetomidine group; HR, 0.43; 95% CI, 0.36-0.52). These associations were sustained through sensitivity analyses.

Study limitations include the retrospective design and the unmeasured confounders that may have influenced results.

“This cohort study found that dexmedetomidine was associated with decreased risk of NOAF in 2 different propensity score-matched ICU cohorts, supporting generalizability of the results,” the investigators wrote.  “These findings suggest that use of dexmedetomidine may be associated with a protective outcome against NOAF in patients with critical illness.”