Aorta, the Innocent Bystander of Bariatric Banding.

INTRODUCTION: Laparoscopic gastric banding (LAGB) is a common bariatric operation performed for obesity. Complications of LAGB commonly evolve around device malfunction and physiological changes secondary to the gastric banding. Complications of LAGB involving the aorta are rare. A case of gastric band misplacement around the aorta and subsequent successful retrieval of the misplaced device is reported. REPORT: A 45 year old obese woman presented as an emergency with food bolus obstruction secondary to gastric banding inserted 10 years previously. Investigations revealed that her gastric band was misplaced around both the oesophagus at the level of the gastro-oesophageal junction and the descending thoracic aorta at the level of T12. Successful and safe retrieval of the misplaced device is reported electively via a two staged approach: first covering the segment of supra-coeliac aorta at the level of the gastric band with a thoracic aortic stent graft (TAG), and, second, assessing for any oesophageal injury via endoscopy and finally extracting the misplaced device via laparoscopy. A Gore C-TAG device size 26 mm × 100 mm was successfully implanted percutaneously via unilateral femoral access during her first stage procedure. Her gastric band was safely retrieved during her second stage procedure with no complications. She recovered well post-operatively. DISCUSSION: Complications of LAGB involving the aorta are rare but potentially life threatening. Multidisciplinary pre-operative planning is necessary for safe removal of the gastric band.

Thoracic endovascular repair (TEVAR) versus open surgery for blunt traumatic thoracic aortic injury.

BACKGROUND: Blunt traumatic thoracic aortic injury (BTAI) is a life-threatening surgical emergency associated with mortality up to 8000 per year, most commonly caused by rapid acceleration/deceleration injury sustained through motor vehicle accident and/or blunt thoracic trauma. BTAI has high pre-hospital mortality following the primary injury, with only 10% to 15% of patients surviving long enough to reach the hospital. Open surgical repair had remained the standard treatment option for BTAI since successfully introduced in 1959. However, with technological advances, thoracic endovascular repair (TEVAR) offers an alternative treatment option for BTAI. TEVAR is a less invasive surgical approach for management of these already critical patients; many reports have described favourable early outcomes.Thoracic endovascular repair may appear to be superior to open repair for treatment of BTAI. However, its long-term results and efficacy remain unknown. No randomised controlled trials (RCTs) have provided evidence to support the superiority of the endovascular approach versus open repair in the treatment of BTAI. This review aims to address this matter. This is an update of a review first published in 2015. OBJECTIVES: To determine whether use of thoracic endovascular repair (TEVAR) for treatment of blunt traumatic thoracic aortic injury (BTAI) is associated with reduced mortality and morbidity when compared with conventional open surgery. SEARCH METHODS: The Cochrane Vascular Information Specialist searched the Cochrane Vascular Specialised Register, CENTRAL, MEDLINE, Embase, CINAHL and AMED databases and World Health Organization International Clinical Trials Registry Platform and ClinicalTrials.gov trials registers to 20 August 2018. SELECTION CRITERIA: We considered all published and unpublished randomised controlled trials (RCTs) comparing TEVAR and open surgery for BTAI. DATA COLLECTION AND ANALYSIS: Two review authors independently reviewed all RCTs identified by the Cochrane Vascular Information Specialist. MAIN RESULTS: We found no RCTs that met the inclusion criteria for this review. AUTHORS' CONCLUSIONS: We found no RCTs conducted to determine whether use of TEVAR for the treatment of BTAI is associated with reduced mortality and morbidity when compared to conventional open repair. Hence, we are unable to provide any evidence to guide the treatment option for this life-threatening condition. To perform a randomised controlled trial to clarify the optimal management of BTAI would be highly challenging due to the natural history of the condition. Despite the lack of RCT evidence, clinicians are moving forward with endovascular treatment of BTAI on the basis of meta-analyses of cohort studies and large clinical series.

Niacin promotes revascularization and recovery of limb function in diet-induced obese mice with peripheral ischemia.

Niacin can reduce vascular disease risk in individuals with metabolic syndrome, but in light of recent large randomized controlled trials outcomes, its biological actions and clinical utility remain controversial. Niacin can improve endothelial function, vascular inflammation, and vascular regeneration, independent of correcting dyslipidemia, in various lean rodent models of vascular injury. Here, we tested whether niacin could directly improve endothelial cell angiogenic function during combined exposure to excess fatty acids and hypoxia, and whether intervention with niacin during continued feeding of western diet could improve revascularization and functional recovery in obese, hyperlipidemic mice with peripheral ischemia. Treatment with niacin (10 µmol/L) increased human microvascular endothelial cell angiogenic function during exposure to high fatty acids and hypoxia (2% oxygen), as determined by tube formation on Matrigel. To assess revascularization in vivo, we used western diet-induced obese mice with unilateral hind limb femoral artery ligation and excision. Treatment for 14 days postinjury with once daily i.p. injections of a low dose of niacin (50 mg/kg) improved recovery of hind limb use, in association with enhanced revascularization and decreased inflammation of the tibialis anterior muscle. These effects were concomitant with decreased plasma triglycerides, but not increased plasma apoAI. Thus, niacin improves endothelial tube formation under lipotoxic and hypoxic conditions, and moreover, promotes revascularization and functional hind limb recovery following ischemic injury in diet-induced obese mice with hyperlipidemia. These data may have implications for niacin therapy in the treatment of peripheral ischemic vascular disease associated with metabolic syndrome.

Thoracic endovascular repair (TEVAR) versus open surgery for blunt traumatic thoracic aortic injury.

BACKGROUND: Blunt traumatic thoracic aortic injury (BTAI) is a life-threatening surgical emergency associated with mortality up to 8000 per year, most commonly caused by rapid acceleration/deceleration injury sustained through motor vehicle accident and/or blunt thoracic trauma. BTAI has high pre-hospital mortality following the primary injury, with only 10% to 15% of patients surviving long enough to reach the hospital. Open surgical repair had remained the standard treatment option for BTAI since successfully introduced in 1959. However, with technological advances, thoracic endovascular repair (TEVAR) offers an alternative treatment option for BTAI. TEVAR is a less invasive surgical approach for management of these already critical patients; many reports have described favourable early outcomes.Thoracic endovascular repair may appear to be superior to open repair for treatment of BTAI. However, its long-term results and efficacy remain unknown. No randomised controlled trials (RCTs) have provided evidence to support the superiority of the endovascular approach versus open repair in the treatment of BTAI. This review aims to address this matter. OBJECTIVES: To determine whether use of TEVAR for treatment of BTAI is associated with reduced mortality and morbidity when compared with conventional open surgery. SEARCH METHODS: The Cochrane Vascular Trials Search Co-ordinator searched the Cochrane Central Register of Controlled Trials (CENTRAL; 2015, Issue 7) and clinical trials databases for details of ongoing and unpublished studies. SELECTION CRITERIA: We considered all published and unpublished randomised controlled trials (RCTs) comparing TEVAR and open surgery for BTAI. DATA COLLECTION AND ANALYSIS: Two review authors independently reviewed all RCTs identified by the Trials Search Co-ordinator. MAIN RESULTS: We found no RCTs that met the inclusion criteria for this review. AUTHORS' CONCLUSIONS: We found no RCTs conducted to determine whether use of TEVAR for the treatment of BTAI is associated with reduced mortality and morbidity when compared to conventional open repair. Hence, we are unable to provide any evidence to guide the treatment option for this life-threatening condition. To perform a randomised controlled trial to clarify the optimal management of BTAI would be highly challenging due to the natural history of the condition. Despite the lack of RCT evidence, clinicians are moving forward with endovascular treatment of BTAI on the basis of meta-analyses and large clinical series.

Niacin receptor activation improves human microvascular endothelial cell angiogenic function during lipotoxicity.

OBJECTIVE: Niacin (nicotinic acid) as a monotherapy can reduce vascular disease risk, but its mechanism of action remains controversial, and may not be dependent on systemic lipid modifying effects. Niacin has recently been shown to improve endothelial function and vascular regeneration, independent of correcting dyslipidemia, in rodent models of vascular injury and metabolic disease. As a potential biosynthetic precursor for NAD(+), niacin could elicit these vascular benefits through NAD(+)-dependent, sirtuin (SIRT) mediated responses. Alternatively, niacin may act through its receptor, GPR109A, to promote endothelial function, though endothelial cells are not known to express this receptor. We hypothesized that niacin directly improves endothelial cell function during exposure to lipotoxic conditions and sought to determine the potential mechanism(s) involved. METHODS AND RESULTS: Angiogenic function in excess palmitate was assessed by tube formation following treatment of human microvascular endothelial cells (HMVEC) with either a relatively low concentration of niacin (10 µM), or nicotinamide mononucleotide (NMN) (1 µM), a direct NAD(+) precursor. Although both niacin and NMN improved HMVEC tube formation during palmitate overload, only NMN increased cellular NAD(+) and SIRT1 activity. We further observed that HMVEC express GRP109A. Activation of this receptor with either acifran or MK-1903 recapitulated niacin-induced improvements in HMVEC tube formation, while GPR109A siRNA diminished the effect of niacin. CONCLUSION: Niacin, at a low concentration, improves HMVEC angiogenic function under lipotoxic conditions, likely independent of NAD(+) biosynthesis and SIRT1 activation, but rather through niacin receptor activation.