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Intimal angiosarcoma is a most unexpected cause of aortic occlusion. We present the case of a 74-year-old woman with intimal angiosarcoma that manifested with the triad of congestive heart failure, acute renal failure, and abdominal angina. A review of the literature and discussion of postoperative outcomes follows.

OBJECTIVESThe purpose of this study was to examine the effect of atrial fibrillation (AF) on the immediate and long-term outcome of patients undergoing percutaneous mitral balloon valvulopl...

OBJECTIVES The purpose of this study was to assess the immediate and long-term outcome of repeat percutaneous mitral balloon valvuloplasty (PMV) for post-PMV mitral restenosis. BACKGROUND Symptomatic mitral restenosis develop in 7% to 21% of patients after PMV. Currently, most of these patients are referred for mitral valve replacement. However, it is unknown if these patients may benefit from repeat PMV. METHODS We report the immediate outcome and long-term clinical follow-up results of 36 patients (mean age 58 ± 13 years, 75% women) with symptomatic mitral restenosis after prior PMV, who were treated with a repeat PMV at 34.6 ± 28 months after the initial PMV. The mean follow-up period was 30 ± 33 months with a maximal follow-up of 10 years. RESULTS An immediate procedural success was obtained in 75% patients. The overall survival rate was 74%, 72% and 71% at one, two, and three years respectively. The event-free survival rate was 61%, 54% and 47% at one, two, and three years respectively. In the presence of comorbid diseases (cardiac and noncardiac) the two-year event-free survival was reduced to 29% as compared with 86% in patients without comorbid diseases. Cox regression analysis identified the echocardiographic score (p = 0.03), post-PMV mitral valve area (p = 0.003), post-PMV mitral regurgitation grade (p = 0.02) and post-PMV pulmonary artery pressure (p = 0.0001) as independent predictors of event-free survival after repeat PMV. CONCLUSIONS Repeat PMV for post-PMV mitral restenosis results in good immediate and long-term outcome in patients with low echocardiographic scores and absence of comorbid diseases. Although the results are less favorable in patients with suboptimal characteristics, repeat PMV has a palliative role if the patients are not surgical candidates.

Background Lower extremity bypass graft failure in patients with limb-threatening ischemia carries an amputation rate of greater than 50%. Redo bypass is often difficult due to the lack of conduit, adequate target, or increased surgical risk, and resultant limb salvage rates are reduced significantly compared with the index operation. We set forth to investigate whether endovascular treatment in this setting would result in an acceptable limb salvage rate. Methods A single-institution, retrospective review from June 2004 to December 2007 of patients with failed grafts who underwent endovascular treatment with percutaneous balloon angioplasty (PTA) of their native circulation was performed. Stents were selectively used in cases of post-PTA residual stenosis or flow-limiting dissection. Technical success was defined as a residual stenosis less than 30%. Percutaneous attempts at bypass graft salvage were excluded. Demographics, comorbidities, procedural data, and follow-up information were recorded. Descriptive, logistic regression and life-table analyses were performed. Results Twenty-four lower extremities were treated in 23 patients with failed bypass grafts. Average patency of the index graft before failure was 647 days (range 5-2758). Mean age was 68 years (range 51-85), 62% were male and 81% had diabetes mellitus (DM). 87.5% of limbs treated had TransAtlantic InterSociety Consensus (TASC) C and D lesions and 62% had multiple lesions. Technical success was achieved in 100%. Mean follow-up was 25.6 months. At follow-up, there were 17 PTA failures, which resulted in: amputation (4), redo-bypass (3), and redo-PTA (11). Freedom from surgical revision and PTA failure was 89% (+/− 0.07 SE) and 28% (+/− 0.09 SE) respectively. PTA secondary patency was 72% (+/− 0.09 SE) and limb-salvage was 81% (+/− 0.08 SE) at both 12 and 24 months. Overall survival was 83% (+/− 0.07 SE) and 77% (+/− 0.09 SE) at 12 and 24 months, respectively. Conclusions Endovascular treatment of patients with previously failed bypass grafts results in a high rate of limb salvage. This is a reasonable option in selected patients and the primary choice in those with poor targets, conduit, or excess surgical risk. Endovascular salvage should be considered before proceeding to primary amputation.

Objective— Survivin (SVV) is an inhibitor of apoptosis protein (IAP) that is upregulated in cancer and has recently been implicated in vascular injury. We sought to investigate the role of SVV in vein graft hyperplasia. Methods and Results— Adenoviral constructs expressing a dominant-negative (AdT34A) and wild-type (AdWT) SVV were used. Proliferation and apoptosis were assayed on endothelial cells (ECs) and smooth muscle cells (SMCs) from human saphenous vein. A rabbit carotid interposition vein graft model (N=31) was used, with adventitial gene transfer of SVV constructs. In vitro, overexpression of SVV was associated with protection from cytokine-induced apoptosis in ECs and SMCs; conversely, AdT34A directly induced apoptosis in these cells. SMC proliferation was increased by AdWT infection, whereas AdT34A reduced proliferation; both effects were serum-dependent. Expression of platelet-derived growth factor (PDGF) in SMCs was regulated by functional SVV expression in analogous fashion. In vivo, proliferation and apoptosis (7 days), as well as wall thickness (30 days), were modified by adenoviral-mediated SVV expression. Adventitial angiogenesis was regulated by the SVV-expressing constructs in a fashion parallel to wall thickness changes. Conclusions— SVV is a critical regulator of multiple processes, including proliferation, apoptosis, and angiogenesis, that determine the remodeling response of vein grafts following arterialization.

The failure of vein bypass grafting in the coronary or lower extremity circulation is a common clinical occurrence that incurs significant morbidity, mortality, and cost. Vein grafts are uniquely amenable to intraoperative genetic modification because of the ability to manipulate the tissue ex vivo with controlled conditions. Although the pathophysiology of vein graft failure is incompletely understood, numerous relevant molecular targets have been elucidated. Interventions designed to influence cell proliferation, thrombosis, inflammation, and matrix remodeling at the genetic level have been described, and many have been tested in animal models. Both gene delivery and gene blockade strategies have been investigated, with the latter now reaching the stage of advanced clinical trials. This review describes the basic and translational science of genetic interventions for vein graft disease and the current state of application in the clinic.

ObjectivePercutaneous transluminal angioplasty (PTA) has had an expanding role as primary therapy for vein graft stenosis with variable results. The aim of this study is to identify patient and graft characteristics predictive of failure after PTA of infrainguinal vein grafts.MethodsRetrospective review from Jan 2004 to Mar 2007 of patients undergoing angioplasty for failing grafts. Demographics, comorbidities, procedural data, and follow-up information were recorded. PTA failure was defined as first significant event including restenosis by duplex scan (>3.5 × velocity ratio), occlusion, redo-PTA, surgical revision, or amputation. Descriptive, logistic regression and life-table analyses were performed.ResultsEighty-seven grafts in 79 patients underwent PTA. Mean age was 70 years (median 70; range, 39-89 years), 71% were male and 52% were symptomatic (40% with limb-threat). Mean follow-up was 17 months (median 17.4; range, 0.03-39.8 months). Freedom from PTA failure was 58% (standard error [SE] 0.0574) at 12 months. Predictors of PTA failure by multivariate analysis were: time from bypass 2 cm (HR 2.7; 95% CI 1.33-5.83; P = .007) and multiple stenoses (HR 2.5; 95% CI 1.29-5.1; P = .007). PTA patency for grafts with favorable lesions (single, less than 2 cm lesions in grafts older than 3 months) was 71% vs 35% for unfavorable lesions at 12 months. Limb-salvage was 95% and 90% and overall survival was 92% and 81% at 12 and 24 months, respectively.ConclusionPTA of failing infrainguinal vein grafts is a reasonable primary therapy for favorable lesions. Early graft stenosis, long, and multiple stenoses are markers for procedural failure and are better served with surgical revision.

OBJECTIVES The purposes of this study were to analyze coronary specimens from patients with diabetes mellitus (DM) and to compare them with specimens from patients without DM. BACKGROUND Diabetes mellitus is associated with an increased incidence of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Increased hypercellular smooth muscle cell proliferation with exaggerated intimal hyperplasia formation may be responsible for this predisposition. METHODS Eighteen coronary atherectomy specimens with restenosis after PTCA from patients with DM were compared with 18 coronary atherectomy specimens with restenosis after PTCA from patients without DM. Total and segmental areas were quantified on trichrome-stained tissue of hypercellular tissue, collagen-rich sclerotic tissue, atheroma and thrombus. Demographic and angiographic data were similar in both groups. RESULTS The percentage of total plaque area composed of hypercellular tissue was lower in restenotic specimens from patients with DM than in restenotic specimens from patients without DM (19 ± 6% vs. 44 ± 5%; p = 0.003). The percentage of collagen-rich sclerotic tissue area was larger in restenotic specimens from patients with DM than in restenotic specimens from patients without DM (77 ± 9% vs. 53 ± 4%; p = 0.004). The percentages of atheroma and thrombus were similar in both groups. CONCLUSIONS Intimal hypercellular tissue content is reduced in restenotic tissue from patients with DM. Collagen-rich sclerotic content is increased in restenotic lesions from patients with DM. These results suggest an accelerated fibrotic rather than a proliferative response in diabetic lesions from patients with restenosis after PTCA.

Objectives The healing response to vascular injury is characterized by neointimal thickening. Proliferation and phenotypic transformation of vascular smooth muscle cells (SMCs) have been implicated in this process. We sought to investigate the role of survivin, a dual regulator of cell proliferation and apoptosis, in lesion formation after diverse forms of vascular injury. Methods Rabbits underwent either carotid interposition vein grafting (n = 17) or bilateral femoral balloon injury (BI; n=29); some in the BI group were placed on a high-cholesterol diet. A subset of BI arteries were treated with local adenoviral gene delivery of a survivin dominant negative-mutant (AdT34A) versus vector or saline controls. Survivin expression in vessels was analyzed by quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and by immunohistochemistry (IHC), which also included markers of SMC differentiation. Specimens of human tissue including failed lower extremity bypass grafts and carotid plaque were also examined. Results RT-PCR and IHC demonstrated increased survivin expression in all experimental models, colocalizing at early times with proliferating and α-actin-expressing cells but was largely absent in mature, contractile SMCs. Delivery of AdT34A after BI attenuated neointimal hyperplasia. Conclusion These studies provide strong evidence supporting a role for survivin in the cellular response to vascular injury. Clinical relevance The regulation of cell proliferation, death, and phenotype after vascular interventions remains incompletely understood. We investigated the role of the inhibitor of apoptosis protein survivin in diverse models of vascular injury. The results suggest that survivin is an important modulator of the generalized vascular injury response and may represent a relevant target for therapies targeting intimal hyperplasia.