Endovascular aortic aneurysm repair by a multidisciplinary team: Lessons learned and six-year clinical update

Background: Endovascular aneurysm repair (EVAR) (using an Federal Drug Association-approved AneuRx® device) compared to conventional surgical repair of abdominal aortic aneurysm (AAA) previously rendered favourable outcomes regarding post-operative pain, avoidence of laparotomy, and rapid rehabilitation and hospital discharge in high-risk patients, including octagenarians. Objectives: To assess the safety, reduction in aneurysm-related deaths, and interim survival data up to 72 months after AAA exclusion by endoluminal endografts (EVAR). Design: We carried out an open, controlled, prospective, multidisciplinary EVAR study for the period 1998 to 2003 (six years). In the earlier part of the study, EVAR was compared with previously published results of conventional open aneurysmectomy surgery. Setting: Heart Unit, Panorama Medi-Clinic, Parow, South Africa. Participants: We recruited adult male and female patients presenting with AAA and fulfilling the inclusion criteria for endovascular repair, as recommended by the consensus 2003 meeting of the Vascular Association of South Africa (VASSA). All patients were offered open surgery as an alternative and were entered into the VASSA EVAR trial registry. Pre-operatively, AAA anatomy was assessed by spiral-computed tomography (CT), and selectively with conventional angiography and intravascular ultrasound (IVUS). Informed consent was obtained in accordance with the recommendations of the Senate of Surgery Paper 2, Ethical Guidelines, Great Britain and Ireland. Patients underwent EVAR by a multidisciplinary interventional team. Interventions: Two hundred and seven adult patient with AAA were assessed. Forty-four of the 207 (21.2%) were excluded from EVAR because of irreversible comorbid factors and complex aneurysm morphology. One hundred and sixty-three patients with a mean age of 70.7 years (range 60-91 years), underwent EVAR (1993-2003). Five patients were lost to follow-up (3%). Median AAA diameter was 56.9 mm and ASA ratings were I, 1.2%; II, 15.9%; III, 57%; IV, 22.6% and V, 2.4%. EVAR was performed in high- and low-risk categories of both sexes. Most patients were in ASA groups III and IV. Device deployed: EVAR was performed using a selection Of endografts over 72 months - AneuRx® (Medtronic) 47; Talent® (Medtronic) 49; Vanguard® three; Zenith® (Cook) one; Powerlink® (Endologix) 62; and other, one. Results: Thirty-day outcome: successful deployment 99%, primary stent patency 97%, surgical conversion 0.6%, procedural or intra-operative mortality 1.2%, 30-day mortality 4.3%, endoleaks 1.84%, and secondary intraprocedural endovascular interventions 24.5%. Peri-operative mortality was 3.1% (one aneurysm related). One patient had suspected endograft infection. Late mortality was 21.4% (35 patients due to co-morbidities, and one was aneurysm related). Follow-up was a median of 28.3 months (range 1-69 months). In 163 patients, two persisting endoleaks (1.2%) were detected. Endotension was detected in 3/163 (1.8% with average sac increase of 0.8 cm. Conversion to open surgery was needed in one patient (0.6%). Co-morbidities that contributed to late mortality included multi-organ failure, ischaemic heart disease (IHD), cardiomyopathy, renal failure, stroke and cancer. One procedural rupture was fatal (0.6%). Two late ruptures occurred; one was successfully endostented and the other patient died after a failed surgical intervention (0.6%). Endovascular repair of AAA is more expensive than conventional surgery. Introduction of the Endologix stent has reduced operative time from 120 to 60 minutes in uncomplicated patients. Newer-generation aortic stents allow better control of negative remodeling and stent migration. Conclusion: A multidisciplinary team can safely perform EVAR, with a low 30-day mortality rate in selected patients graded ASA II-IV and with favourable aortic aneurysm morphology. About 22% of patients with AAA are not suited for EVAR. Persisting late endoleaks occurred in 1.2% of the cohort study and were not device specific. Life-long follow-up post EVAR is a prerequisite to detect late device failure, endoleaks and aneurysm-sac enlargement, and to assure the durability of these mid-term results. Short-term aneurysm rupture prevention is a predictable outcome in high-risk groups.Revie

EVAR: Critical applied aortic morphology relevant to type-II endoleaks following device enhancement in patients with abdominal aortic aneurysms

Endovascular repair (EVAR) of abdominal aortic aneurysms (AAA) is an established alternative option to conventional surgery for AAA, provided optimal anatomical morphology of the aneurysm sac, neck and outflow exists. In most documented series of EVAR, type-II endoleak occurrence is a universal procedural drawback. This is referred to as the Achilles heel of EVAR. This morphological study, addressing predominantly non-aneurysmal aortic anatomy, reveals the dyssynchronous origins of the renal ostia, ectopia of the superior mesenteric artery and median sacral artery, variations in the length of the infrarenal abdominal aorta, multiple mainstem renal arteries, and the presence of accessory renal arteries (in 13% of cadavers). Such potential vascular anomalies need careful consideration pre-operatively prior to EVAR. In a prospective, clinical study of EVAR in 163 patients over 60 months, using four different aortic stent devices, we demonstrated an intraprocedural type-II endoleak rate, before exclusion, of 3% (5/163). Most were related to patent lumbar arteries. An active policy of intraprocedural aneurysm pressure sac measurement and angiography was used to demonstrate type-I and type-II endoleaks, focusing on the applied anatomy of aortic side branches and variations. Selective intraprocedural coli embolisation and thrombin injection into the sac was utilised to thrombose persisting and large lumbar arteries that predisposed to retroleaks. We recorded a low incidence of persisting type-II endoleaks using this proactive treatment strategy by addressing variant aortic morphology and patent lumbar arteries during EVAR. One aneurysm-related death (0.6%) was observed due to late rupture after EVAR, and a single intraprocedural death was related to unpredictable aneurysm rupture. In conclusion, comprehensive anatomical knowledge of the abdominal aorta and its main collateral side branches, including variations, is a fundamental prerequisite if satisfactory and predictable results are to be achieved after EVAR, especially regarding prevention, diagnosis and treatment of type-II endoleaks. Intraprocedaral aneurysm sac pressure monitoring, coil embolisation and the use of injection of thrombin into the aneurysm sac of selected patients is useful in reducing the incidence of post-EVAR type-II persisting endoleaks.Conference Pape

The ASOS Surgical Risk Calculator: development and validation of a tool for identifying African surgical patients at risk of severe postoperative complications

Background: The African Surgical Outcomes Study (ASOS) showed that surgical patients in Africa have a mortality twice the global average. Existing risk assessment tools are not valid for use in this population because the pattern of risk for poor outcomes differs from high-income countries. The objective of this study was to derive and validate a simple, preoperative risk stratification tool to identify African surgical patients at risk for in-hospital postoperative mortality and severe complications. Methods: ASOS was a 7-day prospective cohort study of adult patients undergoing surgery in Africa. The ASOS Surgical Risk Calculator was constructed with a multivariable logistic regression model for the outcome of in-hospital mortality and severe postoperative complications. The following preoperative risk factors were entered into the model; age, sex, smoking status, ASA physical status, preoperative chronic comorbid conditions, indication for surgery, urgency, severity, and type of surgery. Results: The model was derived from 8799 patients from 168 African hospitals. The composite outcome of severe postoperative complications and death occurred in 423/8799 (4.8%) patients. The ASOS Surgical Risk Calculator includes the following risk factors: age, ASA physical status, indication for surgery, urgency, severity, and type of surgery. The model showed good discrimination with an area under the receiver operating characteristic curve of 0.805 and good calibration with c-statistic corrected for optimism of 0.784. Conclusions: This simple preoperative risk calculator could be used to identify high-risk surgical patients in African hospitals and facilitate increased postoperative surveillance. © 2018 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.Medical Research Council of South Africa gran

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)