Ascending and transverse aortic arch repair: the impact of glomerular filtration rate on mortality.

BACKGROUND: Recent studies have described the importance of renal glomerular filtration rate (GFR) as a determinant of perioperative mortality in patients with aneurysms that involve the thoracoabdominal and abdominal aorta. We studied the impact of GFR on mortality following repair of ascending and arch aneurysms. METHODS: Between February 1991 and August 2006, we performed 994 repairs of the ascending and transverse aortic arch. Nine hundred twenty patients had evaluable data for this study. Sixty-two percent were men (566/920); mean age was 65 years (range 17-89). We estimated the GFR using the Cockcroft-Gault equation. Mean preoperative serum creatinine was 1.2 +/- 0.9 mg/dl, mean GFR was 77 +/- 37 mL/min. Renal function data were arrayed in quartiles for univariate analysis and kept continuous for multivariable analyses. Multivariable analyses assessed demographics, extent of disease, acuity of presentation, and renal function measured by both creatinine and GFR. RESULTS: Overall 30-day mortality was 10.8% (99/920). In univariate analyses, GFR (P < 0.0001), serum creatinine (P < 0.0003), coronary artery disease (P > 0.03), acute dissection (P < 0.03), emergency presentation (P < 0.002), age (P < 0.009), pump time (P < 0.0001), cross-clamp time, (P < 0.03) and circulatory arrest time (P < 0.003) were associated with increased mortality. By multivariable analyses, only GFR (P < 0.0001), pump time (P < 0.0001), emergency status (P < 0.002) were significant independent risk factors for mortality. CONCLUSIONS: Preoperative renal function as defined by GFR was the most significant predictor of mortality during repairs of the ascending and transverse aortic arch. The use of GFR provides better preoperative risk stratification during these repairs than creatinine alone.

Recent advances in molecular mechanisms of abdominal aortic aneurysm formation.

Abdominal aortic aneurysm (AAA) is an increasingly common clinical condition with fatal implications. It is associated with advanced age, male gender, cigarette smoking, atherosclerosis, hypertension, and genetic predisposition. Although significant evidence has emerged in the last decade, the molecular mechanisms of AAA formation remain poorly understood. Currently, the treatment for AAA remains primarily surgical with the lone innovation of endovascular therapy. With advances in the human genome, understanding precisely which molecules and genes mediate AAA development and blocking their activity at the molecular level could lead to important new discoveries and therapies. This review summarizes recent updates in molecular mechanisms of AAA formation, including animal models, autoimmune components, infection, key molecules and cytokines, mechanical forces, genetics, and pharmacotherapy. This review will be helpful to those who want to recognize the newest endeavors within the field and identify possible lines of investigation in AAA.