Outcomes of peripheral artery disease and polyvascular disease in patients with end-stage kidney disease.

OBJECTIVE: Patients with peripheral artery disease (PAD) and end-stage kidney disease are a high-risk population, and concomitant atherosclerosis in coronary arteries (CAD) or cerebral arteries (CVD) is common. The aim of the study was to assess long-term outcomes of PAD and the impact of coexistent CAD and CVD on outcomes. METHODS: The United States Renal Data System was used to identify patients with PAD within 6 months of incident dialysis. Four groups were formed: PAD alone, PAD with CAD, PAD with CVD, and PAD with CAD and CVD. PAD-specific outcomes (chronic limb-threatening ischemia, major amputation, percutaneous/surgical revascularization, and their composite, defined as major adverse limb events [MALE]) as well as all-cause mortality, myocardial infarction, and stroke were studied. RESULTS: The study included 106,567 patients (mean age, 71.2 years; 40.8% female) with a median follow-up of 546 days (interquartile range, 214-1096 days). Most patients had PAD and CAD (49.8%), 25.8% had PAD alone, and 19.2% had all three territories involved. MALE rate in patients with PAD was 22.3% and 35.0% at 1 and 3 years, respectively. In comparison to PAD alone, the coexistence of both CAD and CVD (ie, polyvascular disease) was associated with a higher adjusted rates of all-cause mortality (hazard ratio [HR], 1.28; 95% confidence interval [CI], 1.24-1.31), myocardial infarction (HR, 1.78; 95% CI, 1.69-1.88), stroke (HR, 1.66; 95% CI, 1.52,1.80), and MALE (HR, 1.07; 95% CI, 1.04-1.11). CONCLUSIONS: Patients with end-stage kidney disease have a high burden of PAD with poor long-term outcomes, which worsen, in an incremental fashion, with the involvement of each additional diseased arterial bed.

Nationwide study of six-month readmissions in critical limb ischemia: Predictors and impact of revascularization strategies.

OBJECTIVE: There is a paucity of data regarding six-month readmissions in critical limb ischemia patients and the influence of management strategy during index-admission [endovascular, surgical, hybrid procedure, medical therapy, and amputation]. We aimed to investigate the incidence, predictors, and impact of management strategies on six-month readmission in patients with critical limb ischemia. METHODS: A secondary analysis of the Nationwide Readmissions Database (2016-2017) was conducted. Propensity score matching was performed for subgroup analysis. RESULTS: We identified 50,058 patients with primary diagnosis of critical limb ischemia. Six-month all-cause and critical limb ischemia-related readmission rate was 52.36% and 10.86%, respectively. The risk of all-cause readmission was lower with amputation but was similar among other subgroups. Patients receiving surgical [HR 0.62, CI(0.48-0.79), p < 0.001] and hybrid procedure [HR 0.65 (0.46-0.93), p = 0.02] had lower risk of unplanned critical limb ischemia-related readmission compared to endovascular, though the risk of unplanned revascularization/amputation during readmission was similar between the three strategies. The risk of non-critical limb ischemia-related readmission was higher with surgical [HR 1.13, CI(1.04-1.23), p = 0.003] and hybrid procedure [HR 1.17, CI(1.08-1.28), p < 0.001], driven by increased procedure-related/wound complications. Eventhough endovascular patients were older with more severe critical limb ischemia presentation, a lower proportion received home-health or placement upon discharge from index-admission. This could account for higher readmission without higher repeat revascularization in endovascular group. CONCLUSION: The risk of critical limb ischemia and non-critical limb ischemia-related readmission differ according to the management strategy. Significant differences in discharge disposition exist depending on revascularization strategy. Study findings identify opportunities for reducing readmissions by focusing on nonprocedural aspects like wound-care, discharge planning and placement.

Vascular complications associated with percutaneous left ventricular assist device placement: A 10-year US perspective.

BACKGROUND: Over the last decade, there has been a significant increase in the use of percutaneous left ventricular assist devices(p-LVADs). p-LVADs are being increasingly used during complex coronary interventions and for acute cardiogenic shock. These large bore percutaneous devices have a higher risk of vascular complications. We examined the vascular complication rates from the use of p-LVAD in a national database. METHODS: We conducted a secondary analysis of the National In-patient Sample (NIS) dataset from 2005 till 2015. We used the ICD-9-CM procedure codes 37.68 and 37.62 for p-LVAD placement regardless of indications. We investigated common vascular complications, defining them by the validated ICD 9 CM codes. χ2 test and t test were used for categorical and continuous variables, respectively for comparison. RESULTS: A total of 31,263 p-LVAD placements were identified during the period studied. A majority of patients were male (72.68%) and 64.44% were white. The overall incidence of vascular complications was 13.53%, out of which 56% required surgical treatment. Acute limb thromboembolism and bleeding requiring transfusion accounted for 27.6% and 21.8% of all vascular complications. Occurrence of a vascular complication was associated with significantly higher in-hospital mortality (37.77% vs. 29.95%, p < .001), length of stay (22.7 vs. 12.2 days, p < .001) and cost of hospitalization ($ 161,923 vs. $ 95,547, p < .001). CONCLUSIONS: There is a high incidence of vascular complications with p-LVAD placement including need for vascular surgery. These complications are associated with a higher in-hospital, LOS and hospitalization costs. These findings should be factored into the decision-making for p-LVAD placement.

Coxiella burnetii infection of the spine requiring neurosurgical intervention.

BACKGROUND: Infections from Coxiella burnetii, resulting in what is known as Q fever, are relatively rare and difficult to diagnose. Very few reports of spinal infection from C. burnetii have been reported rarely have these cases required surgical intervention. CASE DESCRIPTION: We report a patient with the previous vascular surgery and Q fever spinal osteomyelitis. Previously reported cases with spinal involvement have described initial infection of vascular grafts in proximity to the spine. Literature on spinal infection from C. burnetii reports only one case that required surgical intervention of the spine. We report a patient with L5-S1 diskitis who required surgical intervention and subsequent percutaneous drainage. CONCLUSION: Spinal infections from C. burnetii are rare; however, in the setting of a patient with osteodiscitis with negative cultures as well as a history of significant vascular disease with stents, the diagnosis of Q fever should be entertained. Operative and interventional procedures should also be considered in these patients to help alleviate pain and maintain neurologic function.

Guidewire fracture during orbital atherectomy for peripheral artery disease: Insights from the Manufacturer and User Facility Device Experience database.

BACKGROUND/OBJECTIVES: Orbital atherectomy (OA) is routinely being used for plaque modification to facilitate percutaneous revascularization in patients with peripheral arterial disease (PAD) and arterial calcification. Guidewire fracture (GWF) during OA, though anecdotally described, has not been studied in a systematic manner. We conducted a review of the Manufacturer and User Facility Device Experience (MAUDE) database to study the reports of wire fracture and its management and consequences. METHODS: We queried the MAUDE database for all events involving the current generation of the OA device: "Diamondback 360 Peripheral Orbital Atherectomy System", and "Stealth 360° Orbital PAD System". RESULTS: We identified 62 reports of GWF during OA for PAD. The superficial femoral artery was the most commonly involved atherectomy site. The wire fractured at the soft tip in a majority of cases (68%). Embolized wire fragments were left in the patient in 36 cases (58%), retrieved percutaneously in 10 cases (16%), and trapped by a stent against the arterial wall in eight cases (13%). Lastly, eight patients (13%) underwent surgery for removal of the wire fragment. CONCLUSIONS: This is the first published report to study the complication of GWF during peripheral OA. GWF is an uncommon but has significant procedural and clinical consequences. It results in a high rate of ancillary rescue procedures (including surgery) and is associated with a higher risk of arterial thrombosis and complications from wire retrieval attempts. The risk of wire fracture may be avoided with carefully adherence to the IFU.

Transient exposure to elastase induces mouse aortic wall smooth muscle cell production of MCP-1 and RANTES during development of experimental aortic aneurysm.

PURPOSE: Abdominal aortic aneurysm (AAA) is associated with chronic transmural inflammation and destruction of the elastic media. The purpose of this study was to elucidate molecular mechanisms that might orchestrate leukocyte recruitment into the outer aortic wall by determining whether CC chemokines contribute to development of aneurysm degeneration in an elastase-induced mouse model of AAA. METHODS: Adult male C57BL/6J mice underwent transient elastase perfusion of the abdominal aorta to induce development of AAA. At various intervals after elastase perfusion (0, 4, 7, 14 days), real-time reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assays were used to measure aortic wall expression of the CC (beta) chemokines, monocyte chemoattractant protein-1 (MCP-1) and regulated on activation, normal T-cell expressed and secreted (RANTES). Expression of these chemokines by cultured mouse aortic smooth muscle cells (AoSMC) was similarly assessed after transient (5 minutes) exposure to elastase solutions in vitro. RESULTS: Mouse aortic diameter (mean +/- SEM) increased to aneurysmal proportions by 14 days after elastase perfusion (from 0.51 +/- 0.03 mm to 1.34 +/- 0.32 mm; 163% increase; P <.05), with macrophage infiltration of the outer aortic wall beginning within 7 to 10 days. Increased aortic wall messenger RNA expression for MCP-1 (28-fold) and RANTES (11-fold) was observed on day 4, with maximal production of chemokine protein on day 7 (MCP-1, from 7.07 +/- 0.06 ng/mL to 19.60 +/- 0.19 ng/mL; P <.001; RANTES, from 0.23 +/- 0.006 ng/mL to 2.03 +/- 0.057 ng/mL; P <.001). Neither MCP-1 nor RANTES was detected in normal mouse aorta with immunohistochemistry, but both chemokines were abundant in AAA. Within 48 hours of transient exposure to elastase, cultured mouse AoSMC exhibited pronounced induction (>90-fold) of MCP-1 and RANTES, despite concomitant decrease in cell numbers. CONCLUSIONS: Increased mouse aortic wall expression of MCP-1 and RANTES occurs early in development of elastase-induced AAA and before onset of the chronic inflammatory response. Moreover, elastase directly stimulates AoSMC chemokine production in vitro. Elastase-induced medial SMC production of CC chemokines may therefore provide an important link between enzymatic injury, leukocyte recruitment, and aneurysmal degeneration of the aortic wall.

Secondary aortoesophageal fistula after endoluminal exclusion because of thoracic aortic transection.

Secondary aortoesophageal fistula (AEF) is a rare but catastrophic complication that occurs after thoracic aortic reconstruction. Recently endoluminal stent grafts have been used in selected patients with a thoracic aortic aneurysm, dissection, or traumatic aortic transection. A 24-year-old woman had massive upper gastrointestinal tract bleeding 15 months after endoluminal stent graft placement because of traumatic descending thoracic aortic transection. Evaluation demonstrated an AEF from the mid-esophagus to the endoluminal stent graft. The endoluminal graft was explanted, with primary repair of the thoracic aortic defect and simultaneous primary repair of the esophageal injury. The patient is well 15 months after open repair of the AEF.

Monocyte chemotactic activity in human abdominal aortic aneurysms: role of elastin degradation peptides and the 67-kD cell surface elastin receptor.

BACKGROUND: Chronic inflammation is a characteristic feature of abdominal aortic aneurysms (AAAs), but the molecular signals responsible for recruiting monocytes into the outer aortic wall are unresolved. The purpose of this study was to examine whether AAA tissues elaborate chemotactic activity for mononuclear phagocytes and to determine whether this activity is attributable to interactions between elastin degradation peptides (EDPs) and their cell surface receptor, the 67-kD elastin binding protein (EBP). MATERIAL AND METHODS: Soluble proteins were extracted from human AAA tissues, and chemotactic activity for differentiated U937 mononuclear phagocytes was measured by use of a modified Boyden chamber. Chemotactic activity induced by N -formyl-Met-Leu-Phe was used as a positive control and checkerboard analysis was used to distinguish chemotaxis from chemokinesis. Inhibition of chemotaxis was tested by peptide competition, blocking antibodies and galactosugar-mediated dissociation of the 67-kD EBP. RESULTS: AAA extracts stimulated a concentration-dependent increase in monocyte migration that reached up to 24% of the maximal effect induced by N -formyl-Met-Leu-Phe. Checkerboard analysis demonstrated that AAA extracts stimulated chemotaxis without a chemokinetic effect. AAA-derived chemotactic activity was eliminated by competition with Val-Gly-Val-Arg-Pro-Gly (VGVAPG), a repetitive peptide found in human elastin that binds to cellular elastin receptors, and decreased nearly 40% in the presence of BA-4, an antielastin monoclonal antibody that can block EDP-mediated chemotactic activity. Monocyte chemotaxis in response to both VGVAPG and AAA extracts was abolished in the presence of lactose, a galactosugar that specifically dissociates the 67-kD EBP, but it was unaffected by either glucose, fructose, or mannose. CONCLUSIONS: These findings indicate that soluble EDPs released within human AAA tissue can subsequently attract mononuclear phagocytes through ligand-receptor interactions with the 67-kD EBP, thereby providing a plausible molecular mechanism to explain the inflammatory response that accompanies aneurysmal degeneration. Better understanding of factors regulating inflammatory cell recruitment may lead to novel forms of therapy for early stages of aneurysmal degeneration.