Rodolfo Pini

Fenestrated and Branched Endograft after Previous Aortic Repair

BACKGROUND Para-anastomotic aneurysms (P-AAA) and proximal aortic aneurysmal degeneration after previous aortic open repair (OR) or endovascular repair (EVAR) are challenging clinical scenarios. OR is technically demanding, and standard EVAR could be impossible due to the absence of proximal landing zone. The aim of the study is to report midterm results of fenestrated and branched endografts (FB-EVAR) to treat proximal aortic lesions after previous aortic repair. METHODS Since 2010, patients that underwent FB-EVAR after previous aortic repair were prospectively enrolled. Clinical or morphologic or intraoperative or postoperative data were collected and retrospectively analyzed. Primary end points were technical success and clinical success. Secondary end points were procedure-related events (endoleaks, target visceral vessels occlusion, mortality), midterm survival and freedom from FB-EVAR-related reinterventions. RESULTS Twenty patients (Male: 98%, age: 75 ± 6 years, American Society of Anesthesiologists [ASA] ≥ III: 100%) were enrolled. Fifteen patients (75%) underwent previous aortic OR and 5 (25%) standard EVAR. The mean time since the previous treatment was 12 ± 10 years. Present aortic lesions included thoracoabdominal aneurysms 12 (60%) and juxtarenal and pararenal aneurysms 8 (40%). The mean aortic aneurysm diameter was 67 ± 15 mm. All patients were at high risk for OR and had anatomies precluding standard EVAR. Seventy-two visceral vessels (renal arteries: 34, superior mesenteric artery: 20, celiac trunk: 18) were targeted: 49 fenestrations, 19 branches, and 4 scallops. An FB-EVAR tube and trimodular endograft was planned in 17 and 3 cases, respectively. Technical success was 95%; operative target vessel perfusion was 98.5%. Thirty-day mortality was 0%. Clinical success was 80% because there was a transient renal function worsening in 4 patients (>30% of baseline). One distal type I endoleak was detected and treated at 1-month. The mean follow-up was 15 ± 11 months. There were not proximal type I endoleaks, target visceral vessel occlusions, or aneurismal-related mortality. Survival at 1 year was 85 ± 5%. One late FEVAR-related reintervention occurred. CONCLUSIONS According to the reported data, FB-EVAR for treating P-AAA or proximal aneurysmal degeneration after previous aortic OR/EVAR in high-risk patients is a safe and/or effective solution.

Impact of postoperative transient ischemic attack on survival after carotid revascularization.

OBJECTIVE Major postoperative complications such as stroke and myocardial infarction are usually carefully evaluated in the analysis of carotid revascularization performance. Although transient ischemic attacks (TIAs) are often left unreported, they also may influence long-term outcome. The aim of our study was to evaluate the influence of postoperative TIA in the long-term survival of patients submitted to carotid revascularization. METHODS All consecutive patients submitted to either carotid artery stenting or carotid endarterectomy for symptomatic or asymptomatic carotid stenosis from 2005 to 2012 were retrospectively analyzed. Patients were stratified according to their postoperative (30-day) neurologic course (no symptoms, TIA, or stroke). Kaplan-Maier with log-rank analysis was performed to compare the 5-year survival of patients with postoperative TIA, stroke, or neither; factors affecting the 5-year mortality were evaluated by multivariable Cox proportional hazards models. RESULTS Over a total of 1390 carotid revascularizations (carotid endarterectomy, n = 868 [62.4%]; carotid artery stenting, n = 522 [37.6%]), neurological perioperative complications occurred in 67 (4.7%) cases (38, 2.7% TIA; 29, 2.0% stroke). At 5-year follow-up, overall survival was significantly lower in patients with postoperative TIA (78.4 ± 8.0% vs 97.4 ± 0.6%; P < .001) and postoperative stroke (68.2 ± 14.4% vs 97.4 ± 0.6%; P = .03) compared with patients without neurological complications. By means of multivariate Cox analysis, postoperative TIA and stroke were independent predictors of decreased survival (hazard ratio [HR], 3.10; 95% confidence interval [CI], 1.01-9.72; P = .04, and HR, 3.87; 95% CI, 1.13-13.19; P = .03, respectively), other than age >80 years, postoperative myocardial infarction, and chronic renal failure (HR, 2.07; 95% CI, 1.41-4.90; P = .01; HR, 4.33; 95% CI, 2.74-23.79; P = .04; HR, 2.54; 95% CI, 1.04-6.19; P = .04, respectively). CONCLUSIONS TIAs are significant events, possibly determined by a wider extent of atherosclerotic disease, with important effects on long-term mortality similar to that in strokes. Different from most trials evaluating the outcomes of revascularization techniques, the incidence of perioperative TIA should be accurately considered in the analysis.

Off-the-shelf multibranched endograft for urgent endovascular repair of thoracoabdominal aortic aneurysms

Objective: The aim of this paper was to report early and midterm results of endovascular repair of urgent thoracoabdominal aortic aneurysms (TAAAs) by the off‐the‐shelf multibranched Zenith t‐Branch endograft (Cook Medical, Bloomington, Ind). Methods: Between January 2014 and April 2016, all patients with urgent TAAAs (asymptomatic with diameter >8 cm, symptomatic, or ruptured TAAAs) and aortoiliac anatomic feasibility underwent endovascular repair by t‐Branch and were prospectively enrolled. Clinical, morphologic, intraoperative, and postoperative data were recorded. Follow‐up was performed by duplex ultrasound, contrast‐enhanced duplex ultrasound, and computed tomography angiography. Early end points were technical success (absence of type I or type III endoleak, loss of target visceral vessels [TVVs], conversion to open repair, or 24‐hour mortality), spinal cord ischemia, and 30‐day mortality. Follow‐up end points were survival, TVV patency, type I or type III endoleaks, and freedom from reintervention. Results: Seventeen patients (male, 71%; age, 73 ± 6 years; American Society of Anesthesiologists class 3/4, 60%/40%) affected by type II (47%), III (29%), and IV (24%) TAAAs were enrolled. The indications for t‐Branch were as follows: contained TAAA rupture, four (24%); symptomatic TAAA (pain or peripheral embolism), four (24%); and TAAA diameter ≥8 cm, nine (52%). The mean TAAA diameter was 80 ± 19 mm, with 63 TVVs. Fifteen patients (87%) needed adjunctive intraoperative procedures: 14 proximal thoracic endografts (thoracic endovascular aortic repair), 1 left carotid‐subclavian bypass, 2 endovascular hypogastric branches, and 2 surgical iliac conduits. In four cases (24%), a significant malorientation (≥60 degrees) of the main body occurred during t‐Branch deployment. Technical success was achieved in 14 cases (82%), with technical failures consisting of the loss of three renal arteries (TVV patency, 95%). Spinal cord ischemia occurred in one case (6%) with temporary paraparesis. The 30‐day mortality was 6% (one patient with ruptured type II TAAA died on postoperative day 7 of respiratory failure). Renal function worsening occurred in four patients (25%), with one case requiring permanent hemodialysis. The mean follow‐up was 11 ± 9 months. Survival at 1 month, 6 months, and 12 months was 94%, 82%, 82%, respectively. No TAAA‐related mortality and TVV occlusion occurred in the follow‐up. One type III endoleak was detected at 3 months and successfully treated. Freedom from reintervention at 1 month, 6 months, and 12 months was 88%, 82%, and 82%, respectively. Conclusions: The off‐the‐shelf multibranched endograft is a safe and effective therapeutic option for urgent total endovascular TAAA repair for which a custom‐made endograft is not obtainable in due time. However, the complex anatomy of these aneurysms needs a number of adjunctive and complex intraoperative procedures to achieve a durable repair.

Influence of Statin Therapy on Type 2 Endoleak Evolution

BACKGROUND Endovascular repair (EVAR) for abdominal aortic aneurysm (AAA) is widely adopted; however, the procedure may be jeopardized by type 2 endoleak (T2E). Most T2Es regress over time, but their evolution is unpredictable. There is some evidence about the pleiotropic statin effect on AAA and thrombus stabilization, but there are no data on the influence of statins on T2E. The studys aim is therefore to evaluate a possible effect of statins on T2E evolution. METHODS A retrospective analysis of patients discharged from 2008 to 2013 with T2E after EVAR was performed. Patients were followed up with duplex ultrasound and computed tomography angiography and divided on statin and no statin users. The primary end point was to evaluate the T2E persistence at 6 months and during follow-up. The secondary end points were to compare the shrinkage (median and rate), the sac increasing rate, and reintervention at 6 months and during follow-up. RESULTS In the period examined, 756 EVARs were performed and 85 (11%) had T2E at discharge. Thirty-two (37%) patients with T2E were on statins. The median follow-up was 19 (interquartile range [IQR] 7) months. Statin and no statin patients had similar clinical and anatomical characteristics, endoprosthesis type, and medical therapy. At 6 months, patients on statins had lower T2E persistence ([26] 81% vs. [49] 93%, P = 0.16), reaching the significance at 36 months (11 ± 9% vs. 64 ± 7%, P = 0.001). By Cox analysis, statins are independently associated with T2E regression (hazard ratio 0.40, 95% confidence interval 0.020-0.81, P = 0.01), other characteristics are: >2 lumbar arteries or inferior mesenteric artery patency or oral anticoagulant therapy did not reduce T2E. At 6 months, statin patients had higher shrinkage rate and diameter reduction compared with no statin patients (18% vs. 3%, P = 0.03 and 11 mm (IQR 4) vs. 6 mm (IQR 4), P = 0.05, respectively). Freedom from growth diameter and reintervention rate were not significantly different (85 ± 9% vs. 81 ± 14%, P = 0.10 and 75 ± 17% vs. 37 ± 16%, P = 0.13, respectively). CONCLUSION Statin therapy seems to influence T2E regression and aortic sac stabilization after EVAR in the early medium follow-up; however, prospective studies need to confirm the present results.

Contralateral carotid occlusion in endovascular and surgical carotid revascularization: a single centre experience with literature review and meta-analysis.

OBJECTIVE/BACKGROUND The influence of contralateral carotid occlusion (CCO) on the outcome of carotid endarterectomy (CEA) and stenting (CAS) is debated. This study aims to evaluate CEA and CAS results in patients with CCO. METHODS All carotid revascularizations from 2005 to 2011 were analyzed, focusing on the role of CCO on 30-day cerebral events and death (CED). A meta-analysis was performed to evaluate the results of the literature by random effect. RESULTS Of the 1,218 carotid revascularizations performed in our institution, 706 (57.9%) were CEA and 512 (42.1%) were CAS. CED occurred in 3.6% of the CEAs and 8.2% of the CASs (p = .001). CCO was present in 37 (5.2%) CEAs and 38 (7.4%) CASs. In CEA, CCO patients had a higher CED compared with the non-CCO patients (16.2% vs. 2.9%, p = .001), as confirmed by multiple regression analysis (OR [odds ratio]: 5.1[1.7-14.5]). In CAS, CED was not significantly different in the CCO and non-CCO patients (2.6% vs. 8.7%, p = 0.23). The comparative analysis of the CCO patients showed a higher CED in CEA compared with that in CAS (16.2% vs. 2.6%, p = 0.04). Meta-analysis of 33 papers (27 on CEA and 6 on CAS) revealed that CCO was associated with a higher CED in CEA, but not in CAS (OR: 1.82 [1.57-2.11]; OR: 1.22 [0.60-2.49], respectively). CONCLUSION CCO can be considered as a risk factor for CED in CEA, but not in CAS. CAS appears to be associated with lower CED than CEA in CCO patients.

Nestin and WT1 expression in atheromathous plaque neovessels: association with vulnerability.

INTRODUCTION Neoangiogenesis is crucial for the progression and vulnerability of atheromasic lesions. Since adult vasa vasorum, which represent the neoangiogenetic burden of healthy arteries, constitutively express Nestin and Wilms Tumor (WT1), the aims of the present study are: i) to describe and quantify Nestin and WT1 in plaque neovessels; ii) to investigate the relationship between neovessel phenotype and plaque instability. METHODS We prospectively evaluated 49 consecutive carotid endarterectomy specimens. Histopathological characteristics were separately collected, particularly the intraplaque histological complications. Immunohistochemistry was carried out for CD34, Nestin and WT1; the density of positivity was evaluated for each marker. RT-PCR was performed to assess Nestin and WT1 mRNA levels on the first 10 plaques and on 10 control arteries. RESULTS Six (12.2%) plaques showed no neoangiogenesis. In the others, the mean immunohistochemical densities of CD34, Nestin, and WT1-positive structures were 41.88, 28.84 and 17.68/mm2. Among the CD34+ neovessels, 68% and 42% expressed Nestin and WT1 respectively, i.e., nearly 36% of the neovessels resulted to be Nestin+/WT1-. Furthermore, complicated plaques (n=30) showed significantly more CD34 and Nestin-positive vessels than uncomplicated plaques (n=13; P=0.045 and P=0.009), while WT1 was not increased (P=0.139). RT-PCR confirmed that WT1 gene expression was 3-fold lower than Nestin gene in plaques (p=0.001). CONCLUSIONS Plaque neoangiogenesis shows both a Nestin+/WT1- and a Nestin+/WT1+ phenotype. The Nestin+/WT1- neovessels are significantly more abundant in complicated (vulnerable) plaques. The identification of new transcription factors in plaque neoangiogenesis, and their possible regulation, can open new perspectives in the therapy of vulnerable plaques.

Inflammatory Mediators and Cerebral Embolism in Carotid Stenting: New Markers of Risk

Purpose To investigate serological predictors of risk for cerebral embolism after carotid artery stenting (CAS). Methods Twenty consecutive symptomatic and asymptomatic patients (13 men; mean age 74 years) with carotid artery stenosis undergoing standardized filter-protected CAS (Wallstent) were preoperatively evaluated to identify unstable plaque (duplex ultrasound), complicated aortic plaque (transesophageal echocardiography), and inflammatory status [high-sensitivity C-reactive protein (hs-CRP) and serum amyloid-A protein (SAA) serum levels]. Aortic arch type, carotid tortuosity, and complexity of the procedure were considered. Cerebral embolism was evaluated by comparing the number, volume, and side (ipsilateral and non-ipsilateral) of preoperative and postoperative cerebral lesions detected on diffusion-weighted resonance magnetic imaging (DW-MRI) and through light and scanning electron microscopy analysis of cerebral protection filters obtained from CAS. Results All CAS procedures were completed with no complications. All patients had a negative preoperative DW-MRI, but at least 1 asymptomatic cerebral lesion appeared on DW-MRI after the procedure in 18 (90%) patients. Female gender was associated with a higher number of cerebral lesions (18.2±10.9 vs. 8.3±8.8 for men, p=0.03). Carotid plaque morphology, supra-aortic vessel anatomy, and procedure complexity did not correlate with number or volume of new cerebral lesions. Complicated aortic plaque was associated with a higher volume of non-ipsilateral cerebral lesions than uncomplicated plaque (235.0±259.3 vs. 63.6±63.2 mm3, respectively; p=0.02). Hs-CRP ≥5 mg/L and SAA ≥10 mg/L were significantly associated with a higher number of new cerebral lesions [16.2±10.7 vs. 4.3±3.4 for hs-CRP <5 mg/L (p=0.02) and 14.8±10.3 vs. 2.8±3.4 for SAA <10 mg/L (p=0.006), respectively]. Hs-CRP ≥5 mg/L and SAA ≥10 mg/L also correlated with greater surface involvement by embolic materials in the protection filters at microscopic analysis [37.0% (5.1%) vs. 26.9% (2.5%) for hs-CRP <5 mg/L, p=0.004; 35.9% (13.5%) vs. 22.2% (6.9%) for SAA <10 mg/L, p=0.02]. Conclusion In addition to female gender and the presence of complicated aortic plaque, inflammatory status can be a predictor of cerebral embolism in CAS.

Impact of kidney ischemic lesions on renal function after fenestrated endovascular repair

OBJECTIVE Fenestrated endovascular aortic repair (fEVAR) is being used increasingly in the treatment of complex aortic aneurysms; however, this procedure can be associated with visceral and renal complications. Because the causes of possible renal function (RF) impairment have not been fully examined yet, we conducted a study to investigate whether there are risk factors associate with renal ischemic lesions (RILs) and if they influence RF in patients treated for complex aortic aneurysm with fEVAR. METHODS We evaluated the clinical, anatomic, and technical characteristics of consecutive patients treated with fEVAR from 2008 to 2014. RIL were identified by postoperative computed tomography angiography and the volume of renal parenchyma involved quantified. A decrease in RF (>30% glomerular filtration rate reduction) was evaluated at discharge, and at the 6- and 12-month follow-ups. RESULTS Among 53 patients, we analyzed 38 (72%) juxta/pararenal and 15 (28%) thoracoabdominal aortic aneurysms (33 [64%] with ≥3 fenestrations) and 102 renal arteries. Fifteen patients (30%) showed RIL, which was caused by accessory renal artery (ARA) coverage in 6 cases (38%), distal embolism in 6 (38%), renal artery thrombosis in 2 (18%), and iatrogenic embolization for intraoperative bleeding during fEVAR in 1 (6%). The volume of renal parenchyma involved was less than 25% in 10 (67%) and 25% to 50% in 5 (33%) cases. In no cases was more than 50% renal volume affected. On multivariate analysis, RIL predictors were the presence of ARA (odds ratio [OR], 8.00; 95% confidence interval [CI], 1.16-54.89; P = .03) and extensive thrombosis of the pararenal aorta (OR, 39.93; 95% CI, 3.36-474.23; P = .003). At discharge, chronic renal failure (CRF; OR, 4.80; 95% CI, 1.27-18.09; P = .01), diabetes (OR, 8.44; 95% CI, 1.33-53.51; P = .01), and extensive thrombosis of the pararenal aorta (OR, 5.50; 95% CI, 1.32-29.92; P = .01) were significantly associated with worsening RF. RIL, independent from volume, did not influence the postoperative RF. At 6 months and 1-year, preoperative CRF and perioperative declines in RF were identified as the only risk factors for worsening RF. CONCLUSIONS RIL is a common fEVAR complication and is primarily owing to ARA coverage and aortic thrombus embolization. However, RIL does not influence RF, which is predicted by preoperative CRF, diabetes, and extensive aortic thrombus.

Endovascular treatment of late coronary-subclavian steal syndrome

OBJECTIVE Coronary-subclavian steal syndrome (CSSS) is a rare cause of myocardial ischemia subsequent to stenosis or occlusion of the subclavian artery (SA) proximal to internal thoracic artery (ITA) coronary bypass. Only single cases have been reported in published studies to date. We report a significant series of patients with late CSSS treated through an endovascular approach. METHODS We reviewed a series of consecutive patients treated for CSSS. The clinical, anatomic, and technical characteristics of the procedures were considered. Follow-up was performed through clinical and laboratory (electrocardiography, echocardiography, duplex ultrasonography) evaluations. RESULTS From January 2005 to March 2013, 10 patients with CSSS were treated; 7 had stable and 3 unstable angina. Of the 10 patients, 8 had left SA stenosis (6 ostial to the origin and 2 in the middle segment), 1 had proximal occlusion of the left SA, and 1 had stenosis in the innominate artery (proximally to a right internal thoracic artery). Arterial access was at the brachial artery through surgical exposure (n=6), or radial artery percutaneously (n=3). In 1 case of proximal occlusion of the left SA, simultaneous femoral and percutaneous radial access was necessary. Predilatation of the stenotic lesion was performed in 6. Balloon expandable stents were used in 7 patients with proximal ostial stenosis or occlusion and self-expandable stents in 2 with nonostial lesions. In 1 other patient with proximal heavy calcified stenosis, cutting-balloon predilatation was performed, resulting in dissection of the SA and occlusion of the ITA graft; blood flow was restored in the left upper arm and myocardium by adjunctive dilatation of the SA and endovascular coronary revascularization. No patients developed angina during the follow-up period (15±7 months). CONCLUSIONS A tailored endovascular approach can be used to treat CSSS. However, the occurrence of potentially lethal complications is possible and needs prompt correction.

Impact of iliac artery anatomy on the outcome of fenestrated and branched endovascular aortic repair

Objective: Fenestrated and branched endovascular aneurysm repair (FB‐EVAR) is a valid option to treat juxtarenal and pararenal abdominal aortic aneurysms and thoracoabdominal aortic aneurysms. Because successful deployment depends on complex maneuvers, hostile iliac artery anatomy (HIA) can prejudice the FB‐EVAR outcome. The aim of the study was to evaluate the impact of HIA on FB‐EVAR outcome. Methods: Between 2010 and 2015, all patients undergoing FB‐EVAR were prospectively categorized according to iliac anatomy (friendly iliac artery anatomy [FIA] or HIA). HIA was defined as the presence of one of the following: severe (>90‐degree) iliac angle, extensive (>50%) iliac circumferential calcification, hemodynamic iliac stenosis or obstruction, external iliac artery diameter <7 mm, or previous aortoiliac/femoral graft. Early end points were technical success (absence of type I or type III endoleak, target visceral vessel [TVV] loss, conversion to open repair), intraoperative adjunctive maneuvers (IAMs; iliac percutaneous transluminal angioplasty/stenting, surgical iliac conduit, intra‐aortic graft rotations, several attempts of TVV cannulation), intraoperative technical problems (iliac rupture, significant endograft twisting, difficult TVV cannulations, TVV injuries, TVV loss), and 30‐day mortality. Follow‐up end points were survival, TVV patency, and freedom from reintervention. Results: Ninety‐four patients (male, 87%; age, 73 ± 6 years) with 59 (63%) juxtarenal and pararenal abdominal aortic aneurysms and 35 (37%) thoracoabdominal aortic aneurysms underwent FB‐EVAR, for a total of 324 TVVs; 60 (64%) patients had HIA and 34 (36%) had FIA. Patients with HIA and FIA had similar preoperative clinical characteristics, except for coronary artery disease, peripheral artery occlusive disease, and American Society of Anesthesiologists class 4 (47% vs 24% [P = .03], 12% vs 0% [P = .04], and 28% vs 9% [P = .03], respectively). Technical success was 96% (HIA, 97%; FIA, 95%; P = .6). In HIA, adjunctive iliac procedures were performed in 32 cases (surgical conduit, 14 [15%]; percutaneous transluminal angioplasty/stenting, 27 [29%]). Endograft twisting and difficult TVV cannulation occurred in 13 (14%) and 33 (35%) cases, respectively (HIA 18% vs FIA 15% [P = .09]; HIA 28% vs FIA 21% [P = .03]). TVV cannulation failed in nine cases and injury occurred in five (TVV patency rate, 97.8%; HIA 94.7% vs FIA 98.3%; P = .3). One (1%) iliac rupture occurred in HIA, needing surgical repair. Overall, 44 (47%; HIA 55% vs FIA 25%; P = .03) IAMs were necessary. Perioperative mortality was 4% (HIA 3% vs FIA 5%; P = .9). At multivariate analysis, predictors of IAMs were external iliac diameter <7 mm (odds ratio [OR], 12.5; 95% confidence interval [CI], 2.2–71.4; P = .004) and extensive iliac calcifications (OR, 8.3; 95% CI, 1.4–50.0; P = .02). The mean follow‐up was 24 ± 17 months, with an overall survival of 87% and 71% at 1 year and 3 years, respectively, significantly lower in HIA compared with FIA (at 3 years, HIA 60% vs FIA 92%; P = .02). On multivariate analysis, HIA was a significant predictor of late mortality (OR, 3.6; 95% CI, 1.1–13.2; P = .04). Freedom from reintervention (87%) and 3‐year TVV patency (92%) were similar in the two groups. Conclusions: HIA does not significantly affect the early outcome of FB‐EVAR. However, in patients with HIA, procedures are technically more demanding and late mortality is increased. Iliac characteristics should be taken into account to correctly stratify the surgical risk in FB‐EVAR.