Partial Right Atrial Inflow Occlusion for Transient Systemic Hypotension During Deployment of Thoracic Stentgrafts.

PURPOSE: Temporary balloon occlusion of the inferior vena cava to lower cardiac output is a relatively infrequently used technique to induce controlled systemic hypotension. In this technical note, we describe the feasibility, reliability, and safety of partial occlusion of right atrial inflow and the effect on systemic blood pressure during the deployment of a thoracic stentgraft. MATERIALS AND METHODS: Twenty consecutive patients undergoing thoracic endovascular aortic repair, with proximal landing in zone 0-3 of the thoracic aorta, were prospectively included. Right atrial inflow occlusion was performed with a compliant occlusion balloon. RESULTS: Median time to reach a mean arterial pressure of 50 mmHg was 43 s. Median recovery time of blood pressure was 42 s. CONCLUSION: Partial right atrial inflow occlusion with an occlusion balloon is feasible with reliable results and without procedure-related complications.

Vascular access training for REBOA placement: a feasibility study in a live tissue-simulator hybrid porcine model.

BACKGROUND: The use of resuscitative endovascular balloon occlusion of the aorta (REBOA) in patients with severe haemorrhagic shock is increasing. Obtaining vascular access is a necessary prerequisite for REBOA placement in these situations. METHODS: During the EVTM workshop (September 2017, Örebro, Sweden), 21 individuals participated in this study, 16 participants and five instructors. A formalised curriculum was constructed including basic anatomy of the femoral region and basic training in access materials for REBOA placement in zone 1. Key skills: (1) preparation of endovascular toolkit, (2) achieving vascular access in the model and (3) bleeding control with REBOA. Scoring ranged from 0 to 5 for non-anatomical skills. Identification of anatomical structures was either sufficient (score=1) or insufficient (score=0). Five consultants performed a second identical procedure as a post test. RESULTS: Consultants had significantly better overall technical skills in comparison with residents (p=0.005), while understanding of surgical anatomy showed no difference. Procedure times differed significantly (p<0.01), with residents having a median procedure time of 3 min and 24 s, consultants 2:33 and instructors 1:09. CONCLUSION: This comprehensive training model using a live tissue-simulator hybrid porcine model can be used for femoral access and REBOA placement training in medical personnel with different prior training levels. Higher levels of training are associated with faster procedure times. Further research in open and percutaneous access training is necessary to simulate real-life situations. This training method can be used in a multistep training programme, in combination with realistic moulage and perfused cadaver models.

Outcomes after foot surgery in people with a diabetic foot ulcer and a 12-month follow-up.

OBJECTIVE: The aim of this study was to retrospectively measure the outcomes of foot-sparing surgery at one year follow-up for patients with diabetic foot ulcers (DFUs). We assessed wound healing and the need for further surgery in relation to the variables that influence healing. METHOD: Data were retrospectively collected by reviewing the electronic files of patients attending the Wound Expert Clinic (WEC). Outcomes of surgical debridement, toe, ray and transmetatarsal amputations were assessed. RESULTS: A total of 129 cases in 121 patients were identified for inclusion. The results demonstrated that complete wound healing was reached in 52% (61/117) of the patients within 12 months. The need for additional surgery or for major amputation was 56% (n=72/129) and 30% (n=39/129) respectively. The need for an additional procedure was particularly high after surgical debridement (75%, 33/44) and transmetatarsal amputation (64%, 7/11). Risk factors for non-healing or for a major amputation were: infection (p=0.01), ischaemia (p=0.01), a history of peripheral arterial occlusive disease (p<0.01) and smoking (p=0.01). Additional findings were that not all patients underwent vascular assessment and in half of the patients there was a delay in undergoing revascularisation. CONCLUSION: The results of the study reveal some areas for improvement including timely revascularisation and performance of multiple debridement procedures if needed in order to save a limb.

Thromboembolic complications after Zenith® Low Profile Endovascular Graft for infrarenal abdominal aneurysms.

PURPOSE: The purpose of this study was to objectify and evaluate risk factors for thromboembolic complications after treatment with a Zenith(®) Low Profile Endovascular Graft (Zenith LP). Results were compared with those in the recent literature on endovascular aortic repair (EVAR) and with the thromboembolic complications in the patient group treated with a Zenith Flex Endovascular Graft in our institute in the period before the use of the Zenith LP. MATERIALS AND METHODS: All consecutive patients who were suitable for treatment with a Zenith LP endograft between October 2010 and December 2011 were included. The preprocedural computed tomography scan (CT), procedural angiographic images, and the postprocedural CT scans were evaluated for risk factors for and signs of thromboembolic complications. All patients treated between December 2007 and November 2012 with a Zenith Flex endograft were retrospectively evaluated for thromboembolic complications. RESULTS: In the study period 17 patients were treated with a LP Zenith endograft. Limb occlusion occurred in 35 % of the patients. Limb occlusions occurred in 24 % of the limbs at risk (one limb occluded twice). In one patient two risk factors for limb occlusion were identified. Between December 2007 and November 2012, a total of 43 patients were treated with a Zenith Flex endograft. No limb occlusion or distal embolization occurred. CONCLUSION: Despite that this was a small retrospective study, the Zenith LP endograft seems to be associated with more frequent thromboembolic complications compared with the known limb occlusion rates in the literature and those of the patients treated with a Zenith Flex endograft in our institute.

Differences in mortality, risk factors, and complications after open and endovascular repair of ruptured abdominal aortic aneurysms.

OBJECTIVE/BACKGROUND: Endovascular aneurysm repair (EVAR) for ruptured abdominal aortic aneurysm (rAAA) has faced resistance owing to the marginal evidence of benefit over open surgical repair (OSR). This study aims to determine the impact of treatment modality on early mortality after rAAA, and to assess differences in postoperative complications and long-term survival. METHODS: Patients treated between January 2000 and June 2013 were identified. The primary endpoint was early mortality. Secondary endpoints were postoperative complications and long-term survival. Independent risk factors for early mortality were calculated using multivariate logistic regression. Survival estimates were obtained by means of Kaplan-Meier curves. RESULTS: Two hundred and twenty-one patients were treated (age 72 ± 8 years, 90% male), 83 (38%) by EVAR and 138 (62%) by OSR. There were no differences between groups at the time of admission. Early mortality was significantly lower for EVAR compared with OSR (odds ratio [OR]: 0.45, 95% confidence interval [CI]: 0.21-0.97). Similarly, EVAR was associated with a threefold risk reduction in major complications (OR: 0.33, 95%CI: 0.15-0.71). Hemoglobin level <11 mg/dL was predictive of early death for patients in both groups. Age greater than 75 years and the presence of shock were significant risk factors for early death after OSR, but not after EVAR. The early survival benefit of EVAR over OSR persisted for up to 3 years. CONCLUSION: This study shows an early mortality benefit after EVAR, which persists over the mid-term. It also suggests different prognostic significance for preoperative variables according to the type of repair. Age and the presence of shock were risk factors for early death after OSR, while hemoglobin level on admission was a risk factor for both groups. This information may contribute to repair-specific risk prediction and improved patient selection.

Ruptured AAA: state of the art management.

Since its introduction more than two decades ago, endovascular aneurysm repair (EVAR) has become the primary choice for elective treatment of abdominal aortic aneurysms (AAA) in many medical centers. The (dis)advantages, including 30-day mortality and long-term survival, of both open and endovascular elective AAA repair have been studied extensively, including four randomized trials. On the contrary, the survival benefit of EVAR for ruptured AAAs is not as well established as in elective situations. In the absence of randomized trials, the best treatment modality for ruptured AAA has not been revealed. In this manuscript, we describe the design and (preliminary) results of recently completed and ongoing randomized trials. Furthermore, the trends in management and the results of the treatment of ruptured AAA in our tertiary center over a 20-year period are presented. In the last decade, a progressive increase in the proportion of patients managed by EVAR was observed. This increase was associated with an overall increase in the number of treated patients and, simultaneously, a decrease in the overall 30-day mortality (53% versus 39%) was seen when comparing the two last decades. The 30-day mortality rates were significantly lower in the patients treated with EVAR (24%) compared to open repair (52%). The survival advantage for EVAR after ruptured AAA persisted during the first 5 years after repair, but was lost after that period. The estimated 5-year survival was 44% and 39% for EVAR and open repair, respectively. These data support that endovascular repair is an effective and safe strategy as a primary treatment modality for ruptured AAA.

Natural killer cells and CD4+ T-cells modulate collateral artery development.

OBJECTIVE: The immune system is thought to play a crucial role in regulating collateral circulation (arteriogenesis), a vital compensatory mechanism in patients with arterial obstructive disease. Here, we studied the role of lymphocytes in a murine model of hindlimb ischemia. METHODS AND RESULTS: Lymphocytes, detected with markers for NK1.1, CD3, and CD4, invaded the collateral vessel wall. Arteriogenesis was impaired in C57BL/6 mice depleted for Natural Killer (NK)-cells by anti-NK1.1 antibodies and in NK-cell-deficient transgenic mice. Arteriogenesis was, however, unaffected in J alpha281-knockout mice that lack NK1.1+ Natural Killer T (NKT)-cells, indicating that NK-cells, rather than NKT-cells, are involved in arteriogenesis. Furthermore, arteriogenesis was impaired in C57BL/6 mice depleted for CD4+ T-lymphocytes by anti-CD4 antibodies, and in major histocompatibility complex (MHC)-class-II-deficient mice that more selectively lack mature peripheral CD4+ T-lymphocytes. This impairment was even more profound in anti-NK1.1-treated MHC-class-II-deficient mice that lack both NK- and CD4+ T-lymphocytes. Finally, collateral growth was severely reduced in BALB/c as compared with C57BL/6 mice, 2 strains with different bias in immune responsiveness. CONCLUSIONS: These data show that both NK-cells and CD4+ T-cells modulate arteriogenesis. Promoting lymphocyte activation may represent a promising method to treat ischemic disease.

Interleukin 10: a new risk marker for the development of restenosis after percutaneous coronary intervention.

Genetic factors appear to be important in the process of restenosis after percutaneous coronary intervention (PCI), as well as in inflammation, a pivotal factor in restenosis. An important mediator in the inflammatory response is interleukin (IL)-10. Our aim was to study whether genetic variants in IL-10 predispose to the risk of restenosis. The GENetic DEterminants of Restenosis (GENDER) study included 3104 patients treated with successful PCI. Target vessel revascularization (TVR) was chosen as primary end point. Genotyping of the -2849G/A, -1082G/A, -592C/A and +4259A/G polymorphisms of the IL-10 gene was performed by MassArray platform. After adjusting for clinical variables, three polymorphisms significantly increased the risk of restenosis (-2849AA: relative risk (RR), 1.7, 95% confidence interval (CI), 1.2-2.5; -1082AA: RR, 1.4, 95% CI, 1.1-1.8 and +4259GG: RR, 2.0, 95% CI, 1.4-2.8). To further exclude possible involvement of neighboring genes due to LD in the IL-10 locus, additional polymorphisms were genotyped. The results reveal that association of the IL-10 gene with restenosis is independent of flanking genes. Our findings demonstrate that IL-10 is associated with restenosis and therefore support the hypothesis that anti-inflammatory genes also may be involved in developing restenosis. Furthermore, they may provide a new targeting gene for drug-eluting stents.

Murine models of myocardial and limb ischemia: diagnostic end-points and relevance to clinical problems.

Ischemic disease represents the new epidemic worldwide. Animal models of ischemic disease are useful because they can help us to understand the underlying pathogenetic mechanisms and develop new therapies. The present review article summarizes the results of a consensus conference on the status and future development of experimentation in the field of cardiovascular medicine using murine models of peripheral and myocardial ischemia. The starting point was to recognize the limits of the approach, which mainly derive from species- and disease-related differences in cardiovascular physiology. For instance, the mouse heart beats at a rate 10 times faster than the human heart. Furthermore, healing processes are more rapid in animals, as they rely on mechanisms that may have lost relevance in man. The main objective of the authors was to propose general guidelines, diagnostic end points and relevance to clinical problems.

Anti-MCP-1 gene therapy inhibits vascular smooth muscle cells proliferation and attenuates vein graft thickening both in vitro and in vivo.

OBJECTIVE: Because late vein graft failure is caused by intimal hyperplasia (IH) and accelerated atherosclerosis, and these processes are thought to be inflammation driven, influx of monocytes is one of the first phenomena seen in IH, we would like to provide direct evidence for a role of the MCP-1 pathway in the development of vein graft disease. METHODS AND RESULTS: MCP-1 expression is demonstrated in various stages of vein graft disease in a murine model in which venous interpositions are placed in the carotid arteries of hypercholesterolemic ApoE3Leiden mice and in cultured human saphenous vein (HSV) segments in which IH occurs. The functional involvement of MCP-1 in vein graft remodeling is demonstrated by blocking the MCP-1 receptor CCR-2 using 7ND-MCP-1. 7ND-MCP1 gene transfer resulted in 51% reduction in IH in the mouse model, when compared with controls. In HSV cultures neointima formation was inhibited by 53%. In addition, we demonstrate a direct inhibitory effect of 7ND-MCP-1 on the proliferation of smooth muscle cell (SMC) in HSV cultures and in SMC cell cultures. CONCLUSIONS: These data, for the first time, prove that MCP-1 has a pivotal role in vein graft thickening due to intimal hyperplasia and accelerated atherosclerosis.