Incidence and risk factors for incisional hernia after open abdominal aortic aneurysm repair.

INTRODUCTION: Incisional hernia (IH) is common after open abdominal aortic aneurysm (AAA) repair. Recent studies reported incidence rates higher than previously stated. The aim of this study was to quantify the IH incidence after open AAA surgery. The secondary outcome was to identify the risk factors associated with the development of an IH. METHODS: Retrospective observational study of all consecutive patients who underwent an open repair of AAA, from January 2010 to June 2018, at our institution. Patients were free of abdominal wall hernias at the moment of inclusion in the study. Data were extracted from electronic records: baseline characteristics, surgical factors, and postoperative events. Computed tomography (CT) scans performed during follow-up were analyzed. RESULTS: A total of 157 patients were analysed. The IH incidence after open repair of AAA was 46.5% (73 patients). The median time for IH development was 24.43 months (IQR: 10.40-45.27), while the median follow-up time was 37.20 months (IQR: 20.53-64.12). The risk factors linked to IH were: active (HR: 4.535; 95% CI: 1.369-15.022) or previous smoking habit (HR: 4.652; 95% CI: 1.430-15.131), chronic kidney disease (HR: 2.007; 95% CI: 1.162-3.467) and previous abdominal surgery (HR: 1.653; 95% CI: 1.014-2.695). CONCLUSION: The incisional hernia after open abdominal aortic aneurysm repair affected a high proportion of the intervened patients. Previous abdominal surgery, chronic kidney disease, and smoking habit were independent factors for the development of an incisional hernia.

Incidence and risk factors for incisional hernia after open abdominal aortic aneurysm repair.

INTRODUCTION: Incisional hernia (IH) is common after open abdominal aortic aneurysm (AAA) repair. Recent studies reported incidence rates higher than previously stated. The aim of this study was to quantify the IH incidence after open AAA surgery. The secondary outcome was to identify the risk factors associated with the development of an IH. METHODS: Retrospective observational study of all consecutive patients who underwent an open repair of AAA, from January 2010 to June 2018, at our institution. Patients were free of abdominal wall hernias at the moment of inclusion in the study. Data were extracted from electronic records: baseline characteristics, surgical factors, and postoperative events. Computed tomography (CT) scans performed during follow-up were analyzed. RESULTS: A total of 157 patients were analysed. The IH incidence after open repair of AAA was 46.5% (73 patients). The median time for IH development was 24.43 months (IQR: 10.40-45.27), while the median follow-up time was 37.20 months (IQR: 20.53-64.12). The risk factors linked to IH were: active (HR: 4.535; 95% CI: 1.369-15.022) or previous smoking habit (HR: 4.652; 95% CI: 1.430-15.131), chronic kidney disease (HR: 2.007; 95% CI: 1.162-3.467) and previous abdominal surgery (HR: 1.653; 95% CI: 1.014-2.695). CONCLUSION: The incisional hernia after open abdominal aortic aneurysm repair affected a high proportion of the intervened patients. Previous abdominal surgery, chronic kidney disease, and smoking habit were independent factors for the development of an incisional hernia.

Long-Term Effects of Bosentan on Cardiovascular Events in Hispanic Patients with Intermittent Claudication: Four-Year Follow-up of the CLAU Trial : The CLAU Randomized Trial Long-Term Outcome.

INTRODUCTION: The Clinical and Endothelial Function Assessment after Endothelin Receptor Antagonist (CLAU) trial demonstrated the effect of bosentan on the endothelial function, inflammatory status and claudication distance in Hispanic patients with incipient peripheral arterial disease (PAD). Our aim was to assess the protective effect on cardiovascular events of bosentan versus conventional anti-atherosclerosis therapy. METHODS: CLAU included 56 patients with intermittent claudication, randomized 1:1 to receive bosentan for 12 weeks (n = 27) or placebo (n = 29), associating the best medical treatment. Log-rank and hazard ratio (HR) analyses were performed to estimate the relative efficacy of bosentan in preventing incidence of major adverse events (MAE) including target limb revascularization (TLR), amputation, myocardial infarction (MI), and all-cause death; major cardiovascular adverse events (MACE) including TLR, amputation, MI, stroke, and cardiovascular-cause death; and major adverse limb events (MALE), which combines TLR and amputation. RESULTS: During the follow-up period (34 ± 5 months), five MAE occurred in the control group only (17.2%), including two TLR, one amputation, one stroke, and an MI. The ratio of event-free survival for MAE to 3 years follow-up was higher in the group treated with bosentan (100% vs 66%, p = 0.01, HR = 76; 95% confidence interval 0.05-104,677, p = 0.24). A similar trend was observed in incidence of MACE (100% vs 66%, p = 0.01) and MALE (100% vs 80%, p = 0.15). CONCLUSION: Treatment with bosentan in the early low-to-mild stages of PAD may prevent cardiovascular events and the need for lower limb revascularization in the Hispanic population. Trial Registration ClinicalTrials.gov identifier NCT25102012.

Differential mRNA expression of inflammasome genes NLRP1 and NLRP3 in abdominal aneurysmal and occlusive aortic disease.

NLRP1 and NLRP3 inflammasomes might differentially mediate the chronic inflammatory response in abdominal aortic aneurysm (AAA) and aortic occlusive disease (AOD). We measure differential relative gene expression of NLRP1 and NLRP3 inflammasomes in aortic tissues from 30 patients undergoing AAA open repair compared to aortic biopsies from 30 patients undergoing surgery to treat AOD. Aortic wall samples from autopsy without aortic disease were used as controls. NLRP3 was overexpressed in patients with AAA and AOD (RQ 1.185 ± 0.15, and 1.098 ± 0.05, respectively) compared to donors (RQ 1.001 ± 0.08) (OR 2.8, 95% CI 1.2-4.3, p < 0.05 for AAA and OR 2.1, 95% CI 1.1-3.8, p < 0.05 for AOD). NLRP1 gene expression was significantly upregulated in patients with AOD (RQ 1.197 ± 0.09). Meanwhile, NLRP1 was normal expressed in AAA (RQ 1.003 ± 0.07) as well as in autopsy aortic specimens (RQ 1.005 ± 0.11). Enhanced NLRP1 expression in AOD was even significant when compared to AAA (OR 2.3, 95% CI 1.2-3.3, p < 0.05) or controls (OR 2.2, 95% CI 1.1-3.1, p < 0.05). According to our findings, NLRP3 could be involved in the common etiology of AAA and AOD, whereas NLRP1 appears to have a specific role in AOD development.

Differential mRNA expression of inflammasome genes NLRP1 and NLRP3 in abdominal aneurysmal and occlusive aortic disease.

NLRP1 and NLRP3 inflammasomes might differentially mediate the chronic inflammatory response in abdominal aortic aneurysm (AAA) and aortic occlusive disease (AOD). We measure differential relative gene expression of NLRP1 and NLRP3 inflammasomes in aortic tissues from 30 patients undergoing AAA open repair compared to aortic biopsies from 30 patients undergoing surgery to treat AOD. Aortic wall samples from autopsy without aortic disease were used as controls. NLRP3 was overexpressed in patients with AAA and AOD (RQ 1.185 ± 0.15, and 1.098 ± 0.05, respectively) compared to donors (RQ 1.001 ± 0.08) (OR 2.8, 95% CI 1.2-4.3, p < 0.05 for AAA and OR 2.1, 95% CI 1.1-3.8, p < 0.05 for AOD). NLRP1 gene expression was significantly upregulated in patients with AOD (RQ 1.197 ± 0.09). Meanwhile, NLRP1 was normal expressed in AAA (RQ 1.003 ± 0.07) as well as in autopsy aortic specimens (RQ 1.005 ± 0.11). Enhanced NLRP1 expression in AOD was even significant when compared to AAA (OR 2.3, 95% CI 1.2-3.3, p < 0.05) or controls (OR 2.2, 95% CI 1.1-3.1, p < 0.05). According to our findings, NLRP3 could be involved in the common etiology of AAA and AOD, whereas NLRP1 appears to have a specific role in AOD development.

Anteromedial thigh perforator flap to cover the inguinal region in a crossover femorofemoral bypass.

We report the case of a 48-year-old male with an exposition of a femorofemoral crossover bypass in the inguinal region and superficial femoral occlusion. This was successfully treated using an anteromedial thigh (AMT) pedicled flap based on the perforator vessel of the descending branch of the lateral circumflex femoral artery. Our report focuses on: i) considering the AMT flap as a safe and easy option to cover the inguinal region in cases of bypass exposure; ii) describing the attachment of this flap to the deep femoral artery in a patient with superficial femoral occlusion, in spite of some literature controversy.