Assessment of renal function by means of cystatin C following standard and fenestrated endovascular aneurysm repair.

BACKGROUND: Cystatin C (Cyst C) is more sensitive marker for early renal injury. However, serum creatinine (sCr) and estimated glomerular filtration rate (eGFR) are still used as the standard renal markers after endovascular aortic aneurysm repair (EVAR). The goal of this study was to compare the efficacy of Cyst C, sCr, and eGFR as markers of renal function after EVAR. PATIENTS AND METHODS: This study examined 29 patients (27 men) with a mean age of 76.9 years (range, 55-89 years) undergoing standard (n = 19) and fenestrated (n = 10) EVAR for abdominal aortic aneurysm (AAA) of mean diameter 6.9 cm (range, 5.5-10 cm). Cyst C and sCr were measured and eGFR calculated before and 1 day and 1, 6, and 12 months after EVAR. RESULTS: At 24 hours after procedure, a significant increase in Cyst C (P < 0.005) and sCr (P = 0.028) and significant decrease in eGFR (P = 0.04) were seen. Cyst C continued to increase and was significantly higher at 1 (P < 0.002), 6 (P < 0.005), and 12 (P < 0.005) months compared with baseline. By contrast, sCr and eGFR did not show any significant change at 1, 6, and 12 months from the baseline level. Cyst C increased significantly postoperatively regardless of the baseline renal function. None of the patients required renal replacement therapy. CONCLUSIONS: EVAR is associated with a significant increase in Cyst C starting 24 hours after the procedure and is maintained for 12 months. sCr and eGFR only show significant change at 24 hours and therefore may underestimate long-term renal damage after EVAR.

Effect of endovascular and open abdominal aortic aneurysm repair on thrombin generation and fibrinolysis.

BACKGROUND: Abdominal aortic aneurysm (AAA) is associated with a prothrombotic diathesis that may increase the risk of cardiovascular events. This diathesis is exacerbated in the short term by open aneurysm repair (OAR) and endovascular aneurysm repair (EVAR). However, the effect of EVAR and OAR on coagulation and fibrinolysis in the medium and long term is poorly understood. The purpose of this study was to investigate the medium-term effects of EVAR and OAR on thrombin generation, neutralization, and fibrinolysis. METHODS: Prothrombin fragment (PF)1+2, thrombin antithrombin (TAT) complex, plasminogen activator inhibitor (PAI) activity, and tissue-plasminogen activator (t-PA) antigen were measured in eight age-matched controls (AMCs), 29 patients with AAA immediately before (preoperatively) and 12 months after EVAR (post-EVAR), and in 11 patients at a mean of 16 months after OAR (post-OAR). RESULTS: Preoperatively, PF1+2 levels were significantly higher in patients with AAAs than in AMC. PF1+2 levels post-EVAR and post-OAR were significantly lower than preoperative values and similar to AMC. There was no significant difference in TAT, PAI, or t-PA between AMC, AAA preoperatively, and post-EVAR. Post-OAR, PAI activity was significantly higher than in preoperative patients. CONCLUSIONS: AAA is associated with increased thrombin generation without upregulation of fibrinolysis. The prothrombotic, hypofibrinolytic diathesis observed in patients with AAA returns toward normal in the medium term after EVAR and OAR, although there is a trend toward decreased fibrinolysis post-OAR.

Changes in thrombin generation, fibrinolysis, platelet and endothelial cell activity, and inflammation following endovascular abdominal aortic aneurysm repair.

BACKGROUND: Abdominal aortic aneurysm (AAA) is a chronic inflammatory condition associated with a prothrombotic, hypofibrinolytic diathesis that may increase the risk of cardiovascular events. The effect of endovascular aneurysm repair (EVAR) on this prothrombotic diathesis is not fully understood, especially over the medium and long term. A better understanding of these postintervention changes may improve the risk of cardiovascular complications in the long term. The purpose of this study was to examine thrombin generation, fibrinolysis, platelet and endothelial activation, and the inflammatory response during the 12 months following EVAR. METHODS: Twenty-nine patients (mean age, 76.9 years) undergoing EVAR for AAA (mean diameter 6.9 cm) had prothrombin fragment (PF) 1 + 2, thrombin-antithrombin complex (TAT), plasminogen activator inhibitor (PAI) activity, tissue plasminogen activator (t-PA) activity and antigen, soluble P- and E-selectin, and highly sensitive C-reactive protein (hsCRP) measured before and at 24 hours, and 1, 6, and 12 months after surgery. RESULTS: PF1 + 2 were markedly elevated prior to EVAR and remained so at 24 hours and 1 month, but had decreased significantly at 6 and 12 months. TAT was also elevated prior to EVAR and increased still further by 24 hours, but fell to below baseline levels thereafter. PAI activity and t-PA antigen were normal prior to EVAR, increased significantly at 24 hours, and then fell to baseline levels. t-PA activity was only detectable at 1 and 6 months; there was a significant rise in soluble P- and E-selectin after EVAR, which was sustained for 12 months. hsCRP increased transiently in response to EVAR but returned to preoperative levels by 1 month. CONCLUSIONS: The prothrombotic, hypofibrinolytic diathesis associated with AAA is normalized 12 months after EVAR. This beneficial systemic effect of EVAR for AAA disease may help protect patients against future thromboembolic cardiovascular events.

Carotid artery pseudoaneurysm after carotid endarterectomy: case series and a review of the literature.

BACKGROUND: Pseudoaneurysm (PA) after carotid endarterectomy (CEA) is a rare complication with incidence less than 1%. There is a potential for rupture, embolization, thrombosis or compression of cranial nerves. OBJECTIVE: We reviewed our experience and compare it to the literature to raise awareness of this rare though serious condition. It is crucial to treat these patients early to avoid the hazardous consequences. METHODS: A review of the case records of patients who had CEA at University Hospital Birmingham (UHB) NHS Foundation Trust from 1990-2007, was undertaken. Information of patients including their aetiology, presenting features, treatment and results was collected. The English-language literature was searched using PubMed database for post CEA pseudoaneurysm. RESULTS: Five patients developed post CEA PA. This represents 0.4% of the 1200 CEA performed at our hospital in the last 18 years. The timing of their presentation varied from three days to eight months after the original operation. All had patch reconstruction after CEA. Patches were intact at exploration of the PAs. There was one death and one stroke. The literature revealed 154 carotid PAs after CEA and two cases following carotid stenting 52 of these cases had infected PA. Patients with synthetic patches have the least incidence of infection. More than 80% had open surgery and 9% had endovascular repair. CONCLUSION: Post CEA surveillance is necessary to detect patients with PA early. Factors that favour infection must be avoided. Endovascular repair of carotid PA should be encouraged in specialised centres.