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Outcomes for symptomatic abdominal aortic aneurysms in the American College of Surgeons National Surgical Quality Improvement Program

Peter A Soden, Sara L Zettervall, Klaas H J Ultee, Jeremy D Darling, Dominique B Buck, Chantel N Hile, Allen D Hamdan, Marc L Schermerhorn
Journal of Vascular Surgery 2016, 64 (2): 297-305
27146791

BACKGROUND: Historically, symptomatic abdominal aortic aneurysms (AAAs) were found to have intermediate mortality compared with asymptomatic and ruptured AAAs; but with wider use of endovascular aneurysm repair (EVAR), a more recent study suggested that mortality of symptomatic aneurysms was similar to that of asymptomatic AAAs. These prior studies were limited by small numbers. The purpose of this study was to evaluate the mortality and morbidity associated with symptomatic AAA repair in a large contemporary population.

METHODS: All patients undergoing infrarenal AAA repair were identified in the 2011 to 2013 American College of Surgeons National Surgical Quality Improvement Program, vascular surgery targeted module. We excluded acute conversions to open repair and those for whom the surgical indication was embolization, dissection, thrombosis, or not documented. We compared 30-day mortality and major adverse events for asymptomatic, symptomatic, and ruptured AAA repair, stratified by EVAR and open repair, with univariate analysis and multivariable logistic regression.

RESULTS: There were 5502 infrarenal AAAs identified, 4495 asymptomatic aneurysms (830 open repair, 3665 [82%] EVAR), 455 symptomatic aneurysms (143 open repair, 312 [69%] EVAR), and 552 ruptured aneurysms (263 open repair, 289 [52%] EVAR). Aneurysm diameter was similar between asymptomatic and symptomatic AAAs when stratified by procedure type, but it was larger for ruptured aneurysms (EVAR: symptomatic 5.8 ± 1.6 cm vs ruptured 7.5 ± 2.0 cm [P < .001]; open repair: symptomatic 6.4 ± 1.9 cm vs ruptured 8.0 ± 1.9 cm [P < .001]). The proportion of women was similar in symptomatic and ruptured AAAs (27% vs 23%, respectively; P = .14) but lower in asymptomatic AAAs (20%; P < .001). Symptomatic AAAs had intermediate 30-day mortality compared with asymptomatic and ruptured aneurysms after both EVAR (1.4% asymptomatic vs 3.8% symptomatic [P = .001]; symptomatic vs 22% ruptured [P < .001]) and open repair (4.3% asymptomatic vs 7.7% symptomatic [P = .08]; symptomatic vs 34% ruptured [P < .001]). After adjustment for age, gender, repair type, dialysis dependence, and history of severe chronic obstructive pulmonary disease, patients undergoing repair of symptomatic AAAs were twice as likely to die within 30 days compared with those with asymptomatic aneurysms (odds ratio [OR], 2.1; 95% confidence interval [CI], 1.3-3.5). When stratified by repair type, the effect size and direction of the ORs were similar (EVAR: OR, 2.4 [95% CI, 1.2-4.7]; open repair: OR, 1.8 [95% CI, 0.86-3.9]) although not significant for open repair. Patients with ruptured aneurysms had a sevenfold increased risk of 30-day mortality compared with symptomatic patients (OR, 6.5; 95% CI, 4.1-10.6).

CONCLUSIONS: Patients with symptomatic AAAs had a twofold increased risk of perioperative mortality compared with patients with asymptomatic aneurysms undergoing repair. Furthermore, patients with ruptured aneurysms have a sevenfold increased risk of mortality compared with patients with symptomatic aneurysms.

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