Aortoesophageal fistula after thoracic aortic stent-graft placement: a rare but catastrophic complication of a novel emerging technique.

OBJECTIVES: Our goal was to report characteristics and outcomes of 6 patients with aortoesophageal fistula (AEF) after thoracic endovascular aortic repair (TEVAR). BACKGROUND: Neurologic events are severe complications of TEVAR. With growing experience of TEVAR, other yet unexpected devastating complications have emerged. METHODS: Between July 1999 and August 2008, 268 patients underwent TEVAR for various thoracic aortic diseases at our institution. RESULTS: Six of 268 patients (age 49 to 77 years, 50% female patients) developed AEF (incidence 1.9%) within 1 to 16 months after the procedure. Indications for TEVAR were acute aortic dissection (n = 3), chronic aortic dissection (n = 1), and thoracic aortic aneurysm (n = 2). Four patients presented with sudden massive hematemesis whereas 2 patients were readmitted for new-onset fever and elevated markers of inflammation that preceded hematemesis. Esophago-gastro-duodenoscopy identified deep esophageal ulcerations at the level of the implanted aortic stent-graft in 4 patients, but only mild erosive lesions within the proximal esophagus without signs of active bleeding in the remaining 2 patients. Surgical repair was performed in only 1 patient and declined in the remaining because of comorbidities and multiorgan system failure. Despite this, all patients died due to fatal rebleeding (n = 4) or mediastinitis (n = 2). CONCLUSIONS: AEF is a rare and unusual complication of TEVAR that occurs relatively early after the procedure and is almost invariably fatal. New-onset fever with elevated inflammatory markers or hematemesis should heighten clinical suspicion of AEF in TEVAR patients and prompt computed tomography or esophago-gastro-duodenoscopy in the hope of detecting, triaging, and treating this early to improve the otherwise dismal outcomes of these patients.

Aortic remodeling in type B aortic dissection: effects of endovascular stent-graft repair and medical treatment on true and false lumen volumes.

PURPOSE: To analyze aortic remodeling processes in terms of true (TL) and false lumen (FL) volumes in patients with type B aortic dissection undergoing thoracic endovascular aortic repair (TEVAR) versus patients treated medically. METHODS: Serial contrast-enhanced computed tomography (CT) scans of 27 type B dissection patients (24 men; mean age 60+/-13 years) who underwent TEVAR (n = 17) or medical therapy only (n = 10) were analyzed. TL and FL volumes over the entire descending aorta at baseline and at follow-up were quantified by 3-dimensional reconstruction. RESULTS: Follow-up in the 27 patients was a mean 14+/-6 months. TEVAR resulted in a continued gain in total TL volume (132+/-56 mL at baseline, 164+/-51 mL early after TEVAR, and 220+/-68 mL at follow-up, p<0.001), whereas TL volume was almost unchanged in the medical therapy group (113+/-34 to 120+/-41 mL, p = 0.195). Total FL volume decreased significantly in TEVAR patients during follow-up (257+/-147 mL at baseline to 178+/-140 mL, p<0.001), whereas there was no significant change in FL volume in the medical therapy patients. The increase of TL and the decrease of FL volume in the TEVAR group were mainly observed in the descending thoracic aorta. CONCLUSION: TEVAR for type B aortic dissection results in a significant increase in TL and a decrease in FL volumes, not only acutely but also over time due to continued remodeling processes primarily in the thoracic aorta, with little impact on abdominal aortic volumes. Our data provide insight into the mechanism of a potential therapeutic benefit of TEVAR over medical therapy in type B dissection, which remains to be confirmed in a randomized clinical trial.

Clinical implications of systemic inflammatory response syndrome following thoracic aortic stent-graft placement.

PURPOSE: To quantify inflammatory markers in a large cohort of patients undergoing thoracic endovascular aortic repair (TEVAR) and investigate if profound biomarker elevations may be predictors of postprocedural death. METHODS: We analyzed data from 103 patients (70 men; mean age 64.5+/-11.2 years, range 22-83) undergoing TEVAR between July 1999 and December 2006. Baseline as well as at least 3 serial measurements of C-reactive protein (CRP), fibrinogen, white blood cell (WBC) count, and D-dimers were performed within the first 20 days after TEVAR. RESULTS: Compared with baseline, all inflammatory biomarker levels rose significantly. WBC peaked 2 days after the procedure, whereas CRP, fibrinogen, and D-dimers showed a sustained elevation up to 20 days after TEVAR. Inflammatory responses were more pronounced in patients with acute aortic pathology compared with chronic aortic diseases. There was evidence of greater increase in biomarkers with an increasing number of stent-grafts implanted. Kaplan-Meier analysis suggested that increasing maximum D-dimer values postoperatively were associated with decreased survival after TEVAR (p=0.036) in a subset of patients; however, multivariate analysis failed to identify postinterventional biomarker elevation as independent predictor of in-hospital death. CONCLUSION: Postprocedural inflammatory responses characterized by elevations of CRP, fibrinogen, D-dimers, and WBC are observed in all patients undergoing TEVAR. Our data indicate that this response is more pronounced in patients with acute aortic pathology and those receiving >1 stent-graft.

Effect of atorvastatin (10 mg/day) on glucose metabolism in patients with the metabolic syndrome.

Large interventional studies have shown that statins may reduce the incidence of type 2 diabetes mellitus. However, it is uncertain whether short-term statin therapy can affect insulin sensitivity in patients with the metabolic syndrome. We evaluated the effect of atorvastatin (10 mg/day) in 10 insulin-resistant subjects (age 40 +/- 12 years, body mass index 33.6 +/- 5.2 kg/m(2), triglycerides 2.84 +/- 1.99 mmol/L [249 +/- 175 mg/dl], glucose 6.06 +/- 0.67 mmol/L [109 +/- 12 mg/dl)] using the homeostasis model assessment (HOMA) index (parameter of insulin resistance derived from fasting glucose and fasting insulin concentrations; 5.7 +/- 2.6) in a randomized placebo-controlled, double-blind, crossover study. Subjects were randomized to receive placebo or atorvastatin, each given for 6 weeks separated by a 6-week wash-out period. At the beginning and end of each treatment phase, the patients underwent an oral glucose tolerance test, a 72-hour continuous glucose measurement, and a detailed lipid determination, including a standardized fat tolerance test. Compared with placebo, atorvastatin resulted in a significant (p = 0.05) reduction in the HOMA index (-21%), fasting C-peptides (-18%), glucose (area under the curve during the oral glucose tolerance test, -7%), and a borderline (p = 0.08) reduction of insulin (-18%). The parameters derived from the continuous 72-hour glucose monitoring did not change. A significant reduction also occurred in the total and low-density lipoprotein cholesterol concentrations, although the fasting and postprandial triglyceride concentrations did not change significantly. However, we found a significant correlation between atorvastatin-induced changes in the HOMA and baseline HOMA and between the atorvastatin-induced changes in triglycerides and insulin concentrations. The free-fatty acid, interleukin-6, and high sensitivity C-reactive protein concentrations did not change. Our data indicated that in insulin-resistant, nondiabetic subjects, 6 weeks of atorvastatin (10 mg/day) resulted in significant improvement in insulin sensitivity.