Management of Direct Oral Anticoagulants in Acute Type A Aortic Dissection

TL;DR

This paper discusses how to manage patients on direct oral anticoagulants who develop a severe aortic dissection, focusing on the use of reversal agents and surgical outcomes.

Contribution

The study provides clinical insights into managing DOACs in ATAAD patients using reversal agents and surgical delay with factor repletion.

Findings

One patient treated with andexanet-alfa showed heparin insensitivity during surgery.

Four patients were successfully managed with surgical delay and factor repletion.

Andexanet-alfa use before surgery is discouraged due to risks of heparin insensitivity and pump thrombosis.

Abstract

Background
Direct oral anticoagulants (DOACs) are a commonly used class of anti-coagulants that may complicate surgical management of acute Type A aortic dissection (ATAAD).

Methods
 Surgical management and clinical courses were described for patients who presented to our institution with ATAAD while taking DOACs, after FDA approval of the two currently available reversal agents. A thorough literature review was completed for cases of administration of DOAC reversal agents in ATAAD.

Results
 The only patient treated with andexanet-alfa had heparin insensitivity while on cardiopulmonary bypass. Four other patients were successfully managed with a combination of surgical delay and factor repletion.

Conclusion
 This case series demonstrates that preoperative management of DOACs in patients with ATAAD may employ factor repletion with success. Literature review demonstrated a safety signal for heparin insensitivity or pump thrombosis when andexanet-alfa was administered before or while on cardiopulmonary bypass or extracorporeal membrane oxygenation. Our institutional clinical practice guidelines recommend against administration of andexanet-alfa within 4 to 6 hours before heparinization for surgery in ATAAD but recommend considering andexanet-alfa administration when there is life-threatening bleeding after heparin reversal that is thought to be due to Xa-inhibition with laboratory evidence of elevated anti-Xa activity.

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