Why the study?
Guidelines recommend beta-blockers as first-line therapy for type B aortic dissections but do not differentiate an ideal agent.
Does high dose continuous intravenous labetalol compared to esmolol combination therapy improve hemodynamic safety in patients with type B aortic dissections?
Does high dose continuous intravenous labetalol compared to esmolol combination therapy improve hemodynamic safety in patients with type B aortic dissections?
In patients with type B aortic dissection, high-dose continuous intravenous labetalol was associated with a non-statistically significant higher incidence of hemodynamic instability compared to an esmolol combination regimen.
Labetalol infusion may confer higher hemodynamic instability risk than esmolol combinations in TBAD; leaves open optimal β-blocker selection pending prospective trials.
Background: Medical management for type B aortic dissections (TBADs) require aggressive blood pressure and heart rate control to minimize further dissection extension and to restore perfusion to vital organs. Current guidelines recommend β-blockers (BB) as first-line therapy, however do not differentiate an ideal agent for use. Objective: This study evaluated the hemodynamic safety of continuous infusion labetalol compared to esmolol combination (EC) therapies for TBADs. Methods: This single-center, retrospective analysis identified patients with a TBAD who received high dose continuous intravenous labetalol (HD-CIVL) or EC therapies. Patients who received HD-CIVL or EC therapies for a minimum of 2 hours, during which a minimum of 4 blood-pressure readings were recorded, were included. The primary end point was the incidence of hemodynamic instability with the use of HD-CIVL versus EC therapies. Results: A total of 20 patients receiving HD-CIVL and 22 patients receiving EC therapy were included in the analysis. Ten (50%) of patients receiving HD-CIVL and 7 (32%) of patients receiving EC therapies met the clinical definition of hemodynamic instability ( P = .23). Patients experiencing hemodynamic instability were all due to hypotension, with one also being due to bradycardia. Over half the patients in both groups had discontinued therapy ( P = .06) and were administered bolus fluids ( P = .27). Only one patient receiving HD-CIVL required vasopressor administration while none in the EC group ( P = .48). Conclusion: Our study suggests that HD-CIVL is associated with a nonstatistical significant higher incidence of hemodynamic instability compared to an EC regimen in TBADs. Further studies are warranted in this patient population.
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Myers et al. (2020) studied this question.
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