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Inflammation Tied to Endovascular AAA Repair Failure

— Association with endoleaks and residual sac expansion, but which comes first?

Last Updated October 26, 2015
MedpageToday

This article is a collaboration between ľֱ and:

In endovascular repair for abdominal aortic aneurysm (AAA), systemic inflammatory disease is associated with both endoleaks and residual sac expansion, which in turn increase the risk of aneurysm rupture, a small single-center study showed.

Patients with inflammatory conditions -- such as allergic rhinitis, osteoarthritis, or gout -- had a 51.0% rate of endoleak coupled with late sac expansion compared with 21.4% for those without systemic inflammation during a mean follow-up of 5.2 years (P=0.01), , of VA Connecticut Healthcare Systems in West Haven, and colleagues reported.

Action Points

  • Patients with systemic inflammatory disease are at high risk for postoperative complications, endoleak (persistent blood flow within the aneurysm sac), sac expansion, and additional interventions after endovascular aortic aneurysm repair (EVAR).
  • These data suggest systemic inflammatory disease (SID) is a risk factor for EVAR failure and that patients with SID require increased surveillance and perhaps adjunctive pharmacological therapy.

Such inflammatory conditions were associated with a 5.18-fold higher odds of endoleak and sac expansion by the end of long-term follow-up (OR 5.18, 95% confidence interval 1.56-17.16, P=0.007).

"It is possible that these patients might benefit from alternative strategies to prevent aneurysm rupture," they wrote online in .

The researchers suggested that patients with the condition require increased surveillance and may need pharmacological therapy. Of particular interest is the antibiotic doxycycline, which study co-author , also of VA Connecticut Healthcare Systems in West Haven, noted might inhibit the growth of AAAs and is currently undergoing investigation for that use in the randomized, double-blind trial.

In an published with the study, , and , both of VA Puget Sound Health Care System and University of Washington in Seattle, called the situation a "chicken or the egg" problem.

"Their observations support the intuitive idea that excessive systemic inflammation leads to a failure of aortic wall fibrosis and contraction, resulting in retarded sac shrinkage," they wrote. "Why should this cause more endoleaks, primarily an anatomic problem? Instead of the conventional wisdom that endoleaks cause a failure of sac shrinkage, perhaps the reverse is true: does failure of sac shrinkage foster endoleaks?"

"Some directions for further study may be found in disorders in transforming growth factor–β signaling and the SMAD genes, both of which share clinical associations with aneurysmal diseases and osteoarthritis," they concluded.

But Sobel and Tang offered an important caveat to Shalaby's study, noting that the "classification of systemic inflammatory disease was based on a diagnosis proffered by others and lacked independent confirmation or, even better, some objective measurements of inflammation."

The novel hypothesis requires more evidence before it can be translated into practice, agreed , director of the Center for Aortic Diseases at the University of Chicago.

Specifically, "I would be interested in knowing the values of the actual inflammatory markers to see if treatment of the inflammation prior to EVAR improved outcomes," he told ľֱ in an email. "This paper does not change my practice yet."

The investigators analyzed records from 79 patients who had undergone endovascular aneurysm repair (EVAR) at VA Connecticut Healthcare Systems between 2002 and 2011. Specialist-confirmed systemic inflammatory disease was identified in 64.6% of the patients, and this cohort was more likely to have hypertension and had higher mean body mass index at the time of the intervention.

At 30 days post-repair, the systemic inflammation group had more major complications (23.5% versus 3.6%, P=0.02). At 1 year, inflammation group patients had a higher incidence of endoleaks (45.1% versus 17.9%, P=0.02), specifically type II endoleaks (33.3% versus 7.1%, P=0.01). The group still had more endoleaks than their non-inflammatory counterparts at the end of follow-up (68.7% versus 28.6%, P<0.001).

"Patients who have a Type II endoleak...are the patients at risk of rupture," Dardik told ľֱ. "In other words, their endovascular aneurysm repair isn't working."

Because of their endoleak disadvantage, the inflammation group had higher incidence of additional interventions (21.6% versus 3.6%, P=0.03) throughout follow-up.

"A good percentage of patients in practice do have inflammation," Dirdik emphasized. "Because they're at a new risk of long-term failure, we have to treat them better."

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    Nicole Lou is a reporter for ľֱ, where she covers cardiology news and other developments in medicine.

Disclosures

The study was funded by the VA Connecticut Healthcare System, West Haven.

The study authors and editorialists disclosed no relevant conflicts of interest.

Milner reported consulting for Gore, Cook, Medtronic, Trivascular, and Maquet.

Primary Source

JAMA Surgery

Shalaby SY, et al "Systemic inflammatory disease and its association with type II endoleak and late interventions after endovascular aneurysm repair" JAMA Surgery 2015; DOI: 10.1001/jamasurg.2015.3219.

Secondary Source

JAMA Surgery

Sobel M, Tang GL "Inflammation, endoleaks, and aortic remodeling -- the chicken or the egg" JAMA Surgery 2015; DOI: 10.1001/jamasurg.2015.3246.