Thrombectomy of the Profunda Femoral Vein in Iliofemoral Deep Venous Thrombosis Using an Antegrade Popliteal Approach.

PURPOSE: Residual or undertreated inflow disease is a major cause of stent occlusion following endovascular thrombectomy for iliofemoral deep venous thrombosis (DVT). The profunda femoral vein (PFV) is an important inflow vessel alongside the femoral vein but is traditionally challenging to treat via an antegrade popliteal approach. This technical note describes a novel approach for PFV clearance in iliofemoral thrombectomy via the popliteal vein. MATERIALS AND METHODS: Eight patients underwent PFV clearance as part of iliofemoral DVT thrombectomy via an antegrade popliteal approach. In seven patients, a popliteal-profunda communicating vessel was identified permitting PFV access and thrombectomy. In one patient, a popliteal-profunda communicator was not identified and an 'up and over' approach via the femoral bifurcation from the same popliteal access was utilised. Thrombectomy was performed using the Inari ClotTriever device or Penumbra's Indigo system. RESULTS: Technical success in PFV thrombectomy was 100%. Six patients (75%) underwent stenting for an iliac stenotic lesion or May Thurner compression point. At the four-week ultrasound follow-up, the pelvic iliofemoral segment was patent in 7 patients (87.5%). The PFV was patent in 7 patients (87.5%) whereas the FV was only patent in 4 patients (50%). One patient underwent reintervention for iliofemoral stent occlusion. No PFV injury occurred and no post-procedure profunda reflux was identified. CONCLUSION: PFV clearance can be achieved via an antegrade popliteal approach in iliofemoral thrombectomy to optimise inflow, negating the need for alternative or additional venous access. PFV may maintain upstream iliofemoral vein patency even with an occluded femoral vein. LEVEL OF EVIDENCE: Level 4, Case Series.

Endovascular Treatment of an Extensive Iliocaval and Renal Vein Thrombosis Secondary to Inferior Vena Cava Stenosis and May-Thurner Type Iliac Vein Compression: A Case Report.

A 23-year-old presenting with an acute history of back pain, leg swelling, and claudication was diagnosed with an extensive iliocaval thrombosis, extending from the popliteal veins into the inferior vena cava (IVC) and left renal vein. He was treated with a combination of endovascular techniques, including EKOS and AngioJet. An underlying congenital IVC stenosis and May-Thurner type iliac vein compression were subsequently treated with venoplasty and stenting. To our knowledge, this is the first report of the use of EKOS for renal vein thrombosis and we highlight the complementary nature of different endovascular techniques for managing complex venous thrombotic disease.

Matrix metalloproteinase expression in the ascending aorta and aortic valve.

Extracellular matrix degradation and increased proteolytic enzyme (matrix metalloproteinase (MMP)) activity characterise abdominal aortic aneurysm formation. Post-stenotic dilatation of ascending aorta is associated with aortic stenosis and regurgitation, haemodynamically normal bicuspid aortic valve (BAV) and following AV replacement. We aimed to determine an association between ascending aortic pathology and abnormal AV, with particular reference to MMPs, and ascertain differences between BAV and tricuspid (TAV) AV. Subset of the study population (n=19) with a preoperative ascending aorta of >4 cm was analysed. Samples of ascending aorta and AV were obtained from 82 patients (TAV, n=54, BAV, n=28) undergoing surgery. Gene expression of MMP-1, -2, -9 and tissue inhibitor of metalloproteinase (TIMP)-1 and -2 was quantified by real-time RT-PCR. No significant difference was seen in gene expression level of MMPs, TIMPs and ratio of MMPs/TIMPs in ascending aorta and AV between patients with BAV and TAV. MMP-2/TIMP-1 in ascending aorta was greater in BAV, in the subset of patients with preoperative aortic dilatation (P<0.05). No difference exists in gene expression of MMPs in ascending aorta and AV between patients with BAV and TAV. However, patients with larger aortic diameters have increased MMP-2/TIMP-1. Modifying MMP expression may have a role in development of aneurysms.

Antithrombotic therapy following bioprosthetic aortic valve replacement.

The life expectancy of the general population is increasing. This has meant that more elderly patients are requiring aortic valve replacement (AVR). The choice of valve replacement and its durability are important. Bioprosthetic (tissue) heart valves were introduced into clinical use in the 1960s and were developed primarily to reduce the complications associated with thromboembolism (TE) and the need for lifelong oral anticoagulation, due to their low thrombogenicity compared to mechanical prostheses. This makes them suitable for use in elderly patients (aged>65 years) and in others where the risks of anticoagulation are higher or anticoagulation is contraindicated. There is thought to be a higher risk of TE for up to 90 days following bioprosthetic AVR. Guidelines for the management of patients with valvular heart disease published by the American College of Cardiology (ACC)/American Heart Association (AHA), the American College of Chest Physicians (ACCP) and the European Society of Cardiology (ESC) all recommend the use of an anticoagulation regimen for the first 3 months following bioprosthetic AVR. However, there is division of opinion and practice, despite these recommendations, and more recent studies have not supported the evidence for these guidelines. In this article, we review the literature on the use of anticoagulation in the first 90 days following bioprosthetic AVR.

Post-stenotic aortic dilatation.

Aortic stenosis is the most common valvular heart disease affecting up to 4% of the elderly population. It can be associated with dilatation of the ascending aorta and subsequent dissection. Post-stenotic dilatation is seen in patients with AS and/or aortic regurgitation, patients with a haemodynamically normal bicuspid aortic valve and following aortic valve replacement. Controversy exists as to whether to replace the aortic root and ascending aorta at the time of aortic valve replacement, an operation that potentially carries a higher morbidity and mortality. The aetiology of post-stenotic aortic dilatation remains controversial. It may be due to haemodynamic factors caused by a stenotic valve, involving high velocity and turbulent flow downstream of the stenosis, or due to intrinsic pathology of the aortic wall. This may involve an abnormality in the process of extracellular matrix remodelling in the aortic wall including inadequate synthesis, degradation and transport of extracellular matrix proteins. This article reviews the aetiology, pathology and management of patients with post-stenotic aortic dilatation.