Antiplatelet therapy after arch surgery for aortic dissection: it’s safe— is it also effective?

Thanks to the improvement of surgical techniques and perioperative management of acute type A aortic dissection (TAAD), the focus of attention has shifted from operative and in-hospital outcomes to mid- and long-term ones with growing interest in how the downstream aorta evolves. False lumen thrombosis has been proven to influence long-term results after both type A and type B acute aortic dissection, with residual patency of the false lumen linked to increased mortality at follow-up [1]. Some surgeons are wary of anticoagulants and antiplatelet drugs in patients with aortic dissection, as they fear they may negatively impact false lumen thrombosis. Studies showed how anticoagulants favour persistency of false lumen patency at follow-up, though no effect was shown on mortality or reoperation [2]. While anticoagulant therapy and its impact have been investigated, literature is lacking on antiplatelet drugs. The article by Zhang et al. [3] aims at describing the impact of antiplatelet therapy on the long-term evolution of descending thoracic aorta after TAAD. The group analysed a cohort of 1147 patients who underwent extensive aortic arch surgery for TAAD with either a total arch replacement or hybrid arch replacement (HAR) through debranching of the supra-aortic trunks and subsequent TEVAR. They then divided the patients into 2 groups: those who used antiplatelet therapy (AP) for indications such as coronary artery disease, atherosclerotic lesions of the aorta or previous cerebrovascular accidents(n = 393); and those who did not (NAP) (n = 754). Over a 5-year follow-up, there was no difference in false lumen thrombosis (AP 56.5%, NAP 47.1%), aortic re-dilation and incidence of reintervention or rupture (AP 4.0%, NAP 4.6%), thus proving that antiplatelet therapy is safe after arch surgery for TAAD [3]. The antiplatelet therapy group actually showed higher rates of false lumen thrombosis, though without statistical significance. The study is praiseworthy in dispelling any doubts on the negative impact of such a common therapy. It is also methodologically correct as they had follow-up CT scans re-evaluated by experienced surgeons who were blinded to which group the patients belonged to. While antithrombotic drugs had been proven not to negatively impact intrahospital mortality in type A acute aortic dissection [4], literature was lacking on their long-term effect. However, the study showed some inevitable biases. First of all, HAR was significantly more common in the antiplatelet group (21.9% vs 9.8%) since it was generally used in patients with more comorbidities. In most cases, HAR used longer stent grafts, which can positively influence aortic remodelling. Furthermore, Bentall or aortic valve replacement was performed in numerous patients, so many might need vitamin K antagonist for the presence of a mechanical aortic valve. No information was reported in the study on the concomitant use of anticoagulant therapy and its distribution in the 2 groups before and after surgery, so it could be a confounding factor. The main problem with the study is that its impact in daily clinical practice is limited. While knowing how anticoagulants impact outcomes after TAAD might influence the surgeon’s choice for the type of prosthetic valve used, the patients who use antiplatelet drugs mostly do so for other indications. Guidelines on the use of anticoagulant and antithrombotic drugs after aortic dissection are lacking, so their use is highly dependent on the clinical experience of the centre. At our institution, acetylsalicylic acid is routinely administered after open or endovascular aortic repair. Though there is no definite consensus on this, many patients who develop TAAD present underlying atherosclerosis and the role of complicated atherosclerosis and its inflammatory effects on the development of aortic dissection has been proven [5, 6]. Many centres suggested prophylactic antithrombotic therapy in patients with chronic atherosclerosis at risk of complications [7, 8]. As Hippocrates wrote, the physician must ‘do good, or do no harm’. Zhang’s group proved how antiplatelet therapy is safe after TAAD, but more evidence and subsequent guidelines and recommendations are needed to know if it can actually benefit patients with aortic disease. Conflict of interest: none declared.