Antiplatelet Therapy for Extensive Repaired Type A Aortic Dissection

Antiplatelet therapy may be administered as indicated for extensive repaired TAAD as it does not affect long-term outcomes.

Extensive repaired type A aortic dissection (TAAD) can be treated efficaciously and safely as needed with antiplatelet therapy, according to findings published in the European Journal of Cardio-Thoracic Surgery.

Long-term descending thoracic aorta (DTA) prognosis is associated with DTA remodeling. Investigators aimed to assess the effect of antiplatelet therapy on long-term DTA prognosis following extensive arch repair for subacute or acute TAAD. Primary outcomes were DTA remodeling (aortic redilation and false lumen [FL] thrombosis) and overall survival. Secondary outcomes were major bleeding events (MBEs) and DTA reintervention or rupture.

The retrospective cohort study included 1147 patients with TAAD admitted to Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. Patients were stratified into an antiplatelet cohort (n=393) and a non-antiplatelet cohort (n=754), based on antiplatelet use at discharge and during follow-up, from January 2010 to December 2019. Follow-up (outpatient visits and telephone consultations; median follow-up period, 64.0 months; IQR, 41.9-94.0 months) ended when the antiplatelet therapy regimen was changed or with patient death. Regarding patient death, there were 22 (9 aortic-related) in the antiplatelet cohort and 52 (21 aortic-related) in the non-antiplatelet cohort.

Patients in the antiplatelet cohort vs non-antiplatelet cohort were more likely to have coronary artery disease (17.3% vs 0.0%), hyperlipidemia (49.1% vs 26.3%), hypertension (87.0% vs 77.9%), higher body mass index (median 26.7 vs 25.9), and were older (mean age 50.7±10.8 years vs 47.0±10.2 years; all P <.001).

Antiplatelet therapy can be administered as indicated on extensive repaired TAAD.

Patients who received concomitant coronary artery bypass graft with absence of hemorrhage risk for those with other antiplatelet indications, had antiplatelet therapy initiated soon after surgery. First-line regimen was single antiplatelet therapy (aspirin 100 mg/d). There were 4 patients who used short-term dual antiplatelet therapy (aspirin 100 mg/d and clopidogrel 75 mg/d), 6 patients who switched to clopidogrel during follow-up due to aspirin intolerance, and in the non-antiplatelet cohort there were 36 patients who initiated antiplatelet therapy (cardiovascular disease prevention).

Aortic redilation was not independently predicted by antiplatelet therapy at the celiac artery (β±standard error [SE] = 0.049±0.136, P =.72), diaphragm (β±SE = 0.143±0.152, P =.35), or pulmonary artery bifurcation (β±SE = -0.128±0.203, P =.53) levels in a multivariate linear mixed model. The 5-year FL complete thrombosis rates in the stent uncovering segment were 56.5% in the antiplatelet cohort and 47.1% in the non-antiplatelet cohort (P =.12). The 1-year FL complete thrombosis rates in the stent covering segment were 92.4% in the antiplatelet cohort and 92.1% in the non-antiplatelet cohort (P =.27).

Survival rates at 5 years were 94.3% in the antiplatelet cohort and 95.6% in the non-antiplatelet cohort. At 10 years they were 85.3% in the antiplatelet cohort and 86.4% in the non-antiplatelet cohort, and overall were similar between groups (hazard ratio [HR], 1.18; 95% CI, 0.71-1.95; P =.53). The 5-year cumulative aortic-related death incidences were 2.1% in the antiplatelet cohort and 1.6% in the non-antiplatelet cohort, with non-aortic related death as the competing risk (sub-distribution hazard ratio [sHR], 0.84; 95% CI, 0.54-2.60; P =.65).

The 5-year cumulative major bleed event (MBE) incidences were 2.3% in the antiplatelet cohort and 2.1% in the non-antiplatelet cohort (sHR, 0.82; 95% CI, 0.56-2.67; P =.62). Throughout follow-up, overall MBEs occurred in 10 patients in the antiplatelet cohort and 20 patients in the non-antiplatelet cohort, with intracranial as the most common hemorrhage site. The 5-year cumulative DTA reintervention or rupture incidences were 4.0% in the antiplatelet cohort and 4.6% in the non-antiplatelet cohort, with death as the competing risk (sHR, 0.85; 95% CI, 0.49-1.19; P =.58). Throughout follow-up, overall DTA reintervention or rupture occurred in 17 patients in the antiplatelet cohort and 51 in the non-antiplatelet cohort.

Study limitations include the between-group baseline characteristics not being completely comparable and bias due to there being a large number of patients without follow-up data.

Antiplatelet therapy did not impact long-term DTA FL thrombosis, redilation, reintervention or rupture, MBEs or overall survival on extensive repaired TAAD,” the investigators wrote. “Antiplatelet therapy can be administered as indicated on extensive repaired TAAD.”


Zhang B, Dun Y, Liu Y, et al. The impact of antiplatelet therapy on the descending thoracic aorta fate and long-term prognosis of extensive repaired type A aortic dissection. Eur J Cardiothorac Surg. Published online May 11, 2023. doi:10.1093/ejcts/ezad186