Impact of Medicare denials on noninvasive vascular diagnostic testing

AbstractPurpose: The purpose of this study was to evaluate the impact of Medicare coverage limitations and claim denials on noninvasive vascular diagnostic testing. Methods: All Medicare claims for noninvasive vascular diagnostic studies from January 1, 1999, to December 31, 1999, were identified from the hospital billing database according to Current Procedural Terminology codes for carotid artery duplex ultrasound scan, venous duplex ultrasound scan, and lower-extremity arterial Doppler scan. Reasons for Medicare denial of payment for these tests were reviewed and a cost analysis was performed. Results: During the 1-year period, there were 1096 noninvasive vascular diagnostic studies performed on Medicare patients. Of these 1096 tests, 176 (16.1%) were denied by Medicare (19.6% of 408 carotid duplex ultrasound scans, 16.8% of 345 venous duplex ultrasound scans, and 11.1% of 343 lower-extremity arterial Doppler scans). Of the noninvasive vascular tests denied by Medicare, an abnormal result was present in 72.5% of carotid duplex ultrasound scans, 32.8% of venous duplex ultrasound scans, and 78.9% of lower-extremity arterial Doppler scans. Overall, 88.1% of all initially denied claims (N = 176) were ultimately reimbursed by Medicare after resubmission, including 77.1% of the 118 claims denied based on compliance rules for “medical necessity.” Conclusion: Because of coverage limitations, Medicare denials of noninvasive vascular diagnostic tests can lead to potential uncompensated physician and hospital technical fees if denied claims are unrecognized. Vascular laboratories performing these tests need to review compliance with Medicare guidelines. Improvements may need to be made at both the provider and Medicare carrier levels in obtaining reimbursement for appropriately ordered noninvasive vascular diagnostic studies. (J Vasc Surg 2001;34:846-53.

Outcome of the pivotal study of the Aptus endovascular abdominal aortic aneurysms repair system

ObjectiveEndovascular treatment of abdominal aortic aneurysm (AAA) is associated with benefits over open surgery, yet limitations remain with current endovascular devices. This study was performed to assess outcomes of AAA repair with the Aptus endograft and EndoAnchors (Aptus Endosystems, Sunnyvale, Calif).MethodsThis prospective, multicenter, single-arm investigational device exemption trial was conducted at 25 sites in the United States. A total of 155 patients were enrolled in the trial (mean age, 73 ± 8 years; male, 93.5%; mean AAA diameter, 53.6 ± 7.9 mm). The Aptus endograft is a two-component system: a multilumen, modular endograft with two docking limbs (Aptus Endograft System) and the Heli-FX Aortic Securement System comprising an electronically controlled applier (Heli-FX Applier) with helical EndoAnchors provided in a cassette and a deflectable sheath (Heli-FX Guide) designed for delivery of the applier to the target location for EndoAnchor implantation. The main eligibility criteria included proximal neck length of ≥12 mm, diameter of 19 to 29 mm, and infrarenal angulation of ≤60 degrees. The primary safety end point was freedom from major adverse events at 30 days, and the primary effectiveness end point was successful aneurysm treatment at 12 months. Thrombus-related events (TRE) were defined as limb occlusion or thromboembolism from the endograft. Subjects were observed for a median of 4.2 years, with imaging end points analyzed by a core laboratory and adverse events adjudicated by a clinical events committee.ResultsAmong 155 enrolled subjects, 153 (98.7%) underwent successful implantation of the Aptus endograft and a median of five EndoAnchors; two subjects were converted to open surgical repair during the initial procedure. Overall, the primary safety and effectiveness end points were met in 98.1% and 97.4% of the subjects, respectively. Aneurysm-related mortality was 0.6%, with one postdischarge cardiac death 18 days after implantation. There were no AAA ruptures. There were no fractures of stents or EndoAnchors. There was one type I endoleak and one type III endoleak. Stent graft migration was noted in five subjects, none associated with sac enlargement, type I endoleak, or EndoAnchor dislocation from the endograft. AAA sac shrinkage of ≥5 mm at 1, 2, and 3 years was observed in 60.3%, 72.9%, and 81.7%, respectively. Sixty-one subjects (39.4%) experienced 113 TRE, associated with 80 reinterventions (in 58 subjects) unassociated with limb loss or death. A root cause analysis of TRE identified small, out-of-specification docking limbs with graft infolding and high local shear, resulting in thrombus formation within the endograft with subsequent distal embolization in some cases.ConclusionsEarly results of the Aptus endograft trial met its safety and effectiveness end points; however, a high rate of TRE was observed because of manufacturing discrepancies. The findings confirm a low rate of type I and type III endoleaks, migration, and non-TRE reintervention with a high rate of aneurysm sac regression during midterm follow-up

Preventing β-amyloid fibrillization and deposition: β-sheet breakers and pathological chaperone inhibitors

Central to the pathogenesis of Alzheimer's disease (AD) is the conversion of normal, soluble β-amyloid (sAβ) to oligomeric, fibrillar Aβ. This process of conformational conversion can be influenced by interactions with other proteins that can stabilize the disease-associated state; these proteins have been termed 'pathological chaperones'. In a number of AD models, intervention that block soluble Aβ aggregation, including β-sheet breakers, and compounds that block interactions with pathological chaperones, have been shown to be highly effective. When combined with early pathology detection, these therapeutic strategies hold great promise as effective and relatively toxicity free methods of preventing AD related pathology

Intraneuronal pyroglutamate-Abeta 3–42 triggers neurodegeneration and lethal neurological deficits in a transgenic mouse model

It is well established that only a fraction of Aβ peptides in the brain of Alzheimer’s disease (AD) patients start with N-terminal aspartate (Aβ1D) which is generated by proteolytic processing of amyloid precursor protein (APP) by BACE. N-terminally truncated and pyroglutamate modified Aβ starting at position 3 and ending with amino acid 42 [Aβ3(pE)–42] have been previously shown to represent a major species in the brain of AD patients. When compared with Aβ1–42, this peptide has stronger aggregation propensity and increased toxicity in vitro. Although it is unknown which peptidases remove the first two N-terminal amino acids, the cyclization of Aβ at N-terminal glutamate can be catalyzed in vitro. Here, we show that Aβ3(pE)–42 induces neurodegeneration and concomitant neurological deficits in a novel mouse model (TBA2 transgenic mice). Although TBA2 transgenic mice exhibit a strong neuronal expression of Aβ3–42 predominantly in hippocampus and cerebellum, few plaques were found in the cortex, cerebellum, brain stem and thalamus. The levels of converted Aβ3(pE)-42 in TBA2 mice were comparable to the APP/PS1KI mouse model with robust neuron loss and associated behavioral deficits. Eight weeks after birth TBA2 mice developed massive neurological impairments together with abundant loss of Purkinje cells. Although the TBA2 model lacks important AD-typical neuropathological features like tangles and hippocampal degeneration, it clearly demonstrates that intraneuronal Aβ3(pE)–42 is neurotoxic in vivo

Endovenous stent-assisted coil embolization for a symptomatic femoral vein aneurysm

An 83-year old man presented with recurrent pulmonary embolism originating from a distal left superficial femoral vein aneurysm despite therapeutic anticoagulation. We treated the patient transluminally using the technique of stent-assisted coil embolization via percutaneous transpopliteal venous access. Follow-up by serial duplex ultrasonography and computer tomographic venography (CTV) demonstrated resolution of the aneurysm. Our case demonstrates that stent-assisted coil embolization may effectively exclude a saccular venous aneurysm and prevent recurrent pulmonary embolization