AAA aortic surgery Endoleak EVAR

Does AAA rupture after EVAR, and how ‘dramatic’ the presentation is?

01/04/2017

ref. JVS Jan 2017

Comparison of the outcomes between those occurring after endovascular repair (group 1) and those occurring without previous endovascular treatment (group 2) was made using the data collected and combining the results obtained by a previous study that analyzed the same findings between 1992 and 2003 from the same center to provide a total 22-year experience (1992-2014) at a single quaternary referral center.

Results

From May 1992 to September 2014, there were 1921 elective repairs of intact infrarenal AAAs, with 1288 endovascular and 633 open repairs. During 22 years, 40 of the 1288 patients (3.1%) who underwent endovascular repair for AAA had rupture. The proportion of patients with hypotension at presentation in group 1 (13/40) was significantly less than in group 2 (108/138; P < .01). The difference in perioperative 30-day mortality rate in group 1 (8/40 [20%]) compared with group 2 (68/138 [49%]) was significant (P < .01).

Conclusions

This study confirmed that endovascular AAA repair does not prevent rupture in all patients. The data suggest that rupture, when it does occur, may not be accompanied by such major hemodynamic changes and higher mortality rate as with rupture of an untreated AAA. Strict surveillance and follow-up are required, especially in patients with relatively large initial AAA diameter or presence of endoleak and graft migration, to reduce the rate of ruptures after endovascular repair. Complete prevention will remain challenging because rupture may occur without any predisposing abnormalities. With the advent of new-generation devices, continuous larger long-term studies are required to document reduction in rupture rates after endovascular aneurysm repair.

Aortic dissection

predicting the behaviour of dissection from level of CT enhancement!

01/04/2017

ref: JVS Jan 2017:

This relatively easy method of comparing the degree of enhancement of thrombus in the false lumen is easily obtainable and useful to a) understand the dynamics and b) predict outcome.

A total of 65 patients (42 men; mean age, 75 years) with type B IMH were evaluated retrospectively. On initial CT scans, attenuation of the false lumen (AFL) was determined before enhancement and in the early and delayed phases of contrast enhancement. Then enhancement of the false lumen (EFL) was calculated (AFL in the delayed image − AFL in the precontrast image). The Cox proportional hazards model was employed to estimate the risk of IMH-related events, including death or surgical repair.

Results

The mean AFL for precontrast CT, arterial phase enhanced CT, and delayed phase enhanced CT was 56.3 ± 10.5, 59.9 ± 10.8, and 63.7 ± 11.1 Hounsfield units, respectively, whereas the mean EFL was 7.4 ± 9.0 Hounsfield units. EFL was the only independent predictor of IMH-related events (n = 23; hazard ratio, 1.008; 95% confidence interval, 1.03-1.15; P = .0044) and IMH-related death/surgical repair (n = 10; hazard ratio, 1.111; 95% confidence interval, 1.017-1.213; P = .0197).

Conclusions

In patients with IMH, EFL is the most powerful predictor of IMH-related events, as well as IMH-related death or surgical repair.

carotid artery disease carotid disease Carotid stenting

Restenosis following Carotid endarterctomy: open redo or stenting??

01/04/2017

Source: JVS Jan 2017:

This is a challenging question for real life cases … here is the results from this very large cohort of patients:

We studied all patients in the Vascular Quality Initiative (VQI) database who underwent CEA or CAS after prior ipsilateral CEA between January 2003 and April 2015. Univariate methods (χ2 and t-test) were used to compare patients’ characteristics and outcomes ≤30 days and up to 1 year. Multivariate logistic and Cox regression analyses, adjusting for patients’ demographic and clinical characteristics, were used to compare the procedures with respect to ipsilateral stroke, death, myocardial infarction (MI), stroke/death, and stroke/death/MI.

Results

This cohort of patients with prior ipsilateral CEA underwent 2863 carotid interventions, 1047 (37%) CEA, and 1816 (63%) CAS. Characteristics were similar in both groups. The 30-day ipsilateral stroke rate comparing CEA vs CAS was 2.2% vs 1.3% (P = .09) for asymptomatic patients and 1.2% vs 1.6% (P = .604) for symptomatic patients. The 30-day mortality was 1.3% vs 0.6% (P = .04), and MI occurred in 1.4% of CEA vs 1.1% of CAS patients (P = .443). Cranial nerve injury occurred in 4.1% of the redo-CEA cases, and access site complications occurred in 5.3% of the CAS cases. CEA was associated with higher mortality at 30 days (adjusted odds ratio [aOR], 2.83; 95% confidence interval [CI], 1.13-7.14; P = .027) and at 1 year (adjusted hazard ratio, 2.17; 95% CI, 1.03-4.58; P = .042). However, there were no differences in postoperative stroke (aOR, 0.54; 95% CI, 0.20-1.45, P = .22), MI (aOR, 0.98; 95% CI, 0.31-3.10; P = .97), stroke/death (aOR, 1.38; 95% CI, 0.72-2.67; P = .22), and stroke/death/MI (aOR, 1.38; 95% CI, 0.80-2.37; P = .25) between CEA and CAS after adjusting for patient characteristics, and freedom from stroke at 1 year was also similar (CEA: 96.7% vs CAS: 96.4%; P = .78).

Conclusions

In this population-based study, we have shown higher mortality but similar stroke and MI associated with redo CEA compared with CAS after prior ipsilateral CEA. We recommend avoidance of redo CEA in very sick patients. Smoking cessation remains a potent target for improvement of outcomes of carotid revascularization in these patients.