Objective To conduct a test of noninferiority for CardioCel (Admedus, Brisbane, Australia), a chemically engineered bovine pericardium over autologous pericardium treated intraoperatively with ...glutaraldehyde in a chronic juvenile sheep model of pulmonary valve (PV) and mitral valve (MV) reconstruction. Methods We replaced the posterior leaflet of the MV and of 1 PV cusp with patches in ewes aged 10 months. There were 2 groups: CardioCel (n = 6) and control (n = 4). All valves were competent. Echocardiography was performed before euthanasia. The collected data were function, macroscopy, histology, and calcium contents. The primary end points were thickening and calcium content. Results All animals survived until sacrifice after 7 months. The valves had normal echo. The macroscopic aspect of the valves was excellent. Examination of the slides for both groups revealed a continuous endothelium on both sides of the patch and a layer of new collagen developed on both sides between patch and endothelium and interstitial cells and smooth muscle cell in these layers. The patch had not thickened but the 2 layers of new collagen for the PV showed a median thickening of 37% in the CardioCel group and 111% in the control group ( P = .01), and for the MV a thickening of 108% and 251%, respectively, was seen ( P = .01). The median calcium content in the PV was 0.24 μg/mg (range, 0.19-0.30) in the CardioCel group versus 0.34 μg/mg (range, 0.24-0.62) in controls ( P = .20). In the MV it was 0.46 μg/mg (range, 0.30-1.0) in the CardioCel group and 0.47 μg/mg (range, 0.29-1.9) in controls ( P = 1.0). Conclusions In this growing lamb model the CardioCel patch allowed accurate valve repair at both systemic and pulmonary pressure. The mechanical properties of CardioCel after 7 months were preserved with a more controlled healing than the treated autologous pericardium and without calcification.
CONTEXT Dilated cardiomyopathy (DCM), a genetically heterogeneous disorder,
causes heart failure and rhythm disturbances. The majority of identified DCM
genes encode structural proteins of the ...contractile apparatus and cytoskeleton.
Recently, genetic defects in calcium and potassium regulation have been discovered
in patients with DCM, implicating an alternative disease mechanism. The full
spectrum of genetic defects in DCM, however, has not been established. OBJECTIVES To identify a novel gene for DCM at a previously mapped locus, define
the spectrum of mutations in this gene within a DCM cohort, and determine
the frequency of DCM among relatives inheriting a mutation in this gene. DESIGN, SETTING, AND PARTICIPANTS Refined mapping of a DCM locus on chromosome 3p in a multigenerational
family and mutation scanning in 156 unrelated probands with DCM, prospectively
identified at the Mayo Clinic between 1987 and 2004. Relatives underwent screening
echocardiography and electrocardiography and DNA sample procurement. MAIN OUTCOME MEASURE Correlation of identified mutations with cardiac phenotype. RESULTS Refined locus mapping revealed SCN5A, encoding
the cardiac sodium channel, as a candidate gene. Mutation scans identified
a missense mutation (D1275N) that cosegregated with an age-dependent, variably
expressed phenotype of DCM, atrial fibrillation, impaired automaticity, and
conduction delay. In the DCM cohort, additional missense (T220I, R814W, D1595H)
and truncation (2550-2551insTG) SCN5A mutations,
segregating with cardiac disease or arising de novo, were discovered in unrelated
probands. Among individuals with an SCN5A mutation
27% had early features of DCM (mean age at diagnosis, 20.3 years), 38% had
DCM (mean age at diagnosis, 47.9 years), and 43% had atrial fibrillation (mean
age at diagnosis, 27.8 years). CONCLUSIONS Heritable SCN5A defects are associated with susceptibility to early-onset
DCM and atrial fibrillation. Similar or even identical mutations may lead
to heart failure, arrhythmia, or both.
•There is little evidence guiding management of fracture related infections; reports indicate treatment failure up to 60%.•Failure of initial infection treatment can be associated with poor outcomes ...including prolonged salvage or limb amputation.•In our cohort, 35% of patients failed initial surgical management, necessitating return to the operating room.•Predictive factors for failure were polymicrobial infections, open IIIB/IIIC fractures, and removal of implant.•Associated risk factors for failure included overweight and obesity.
Infection after fracture fixation is a potentially devastating outcome, and surgical management is frequently unsuccessful at clearing these infections. The purpose of this study is to determine if factors can be identified that are associated with treatment failure after operative management of a deep surgical site infection.
We retrospectively reviewed the billing system at a Level I trauma center between March 2006 and December 2015. We identified 451 patients treated for deep surgical site infection after fracture fixation at our center. A multivariate regression analysis was then performed to evaluate for factors associated with treatment failure.
Mean follow-up was 2.3 years. One hundred fifty-six patients (35%) failed initial surgical management. Risk factors associated with treatment failure included initial culture results positive for polymicrobial organisms (odds ratio OR, 1.6; 95% confidence interval CI, 1.0–2.4), removal of implants (OR, 1.9; 95% CI, 1.2–2.9), or Gustilo-Anderson IIIB/IIIC injury (OR, 2.0; 95% CI, 1.1–3.7). Increased body mass index and fulfilling the criteria to have a methicillin-resistant Staphylococcus aureus (MRSA) nasal swab screening showed a trend toward increased risk of failure.
Treatment failure after deep surgical site infection was relatively common. Three distinct factors (polymicrobial infection, removal of implants, and IIIB/C fracture) were associated with failure to eradicate the infection in the first series of surgeries and antibiotics. These data might help guide clinicians as they counsel patients on the risk of treatment failure and might focus efforts to improve treatment toward patients at higher risk of treatment failure.
The pannexin family of channels consists of three members-pannexin-1 (Panx1), pannexin-2 (Panx2), and pannexin-3 (Panx3) that enable the exchange of metabolites and signaling molecules between ...intracellular and extracellular compartments. Pannexin-mediated release of intracellular ATP into the extracellular space has been tied to a number of cellular activities, primarily through the activity of type P2 purinergic receptors. Previous work indicates that the opening of Panx1 channels and activation of purinergic receptors by extracellular ATP may cause inflammation and apoptosis. In the CNS (central nervous system) and PNS (peripheral nervous system), coupled pannexin, and P2 functions have been linked to peripheral sensitization (pain) pathways. Purinergic pathways are also essential for other critical processes in the PNS, including myelination and neurite outgrowth. However, whether such pathways are pannexin-dependent remains to be determined. In this study, we use a Panx1 knockout mouse model and pharmacological inhibitors of the Panx1 and the ATP-mediated signaling pathway to fill gaps in our understanding of Panx1 localization in peripheral nerves, roles for Panx1 in axonal outgrowth and myelination, and neurite extension. Our data show that Panx1 is localized to axonal, myelin, and vascular compartments of the peripheral nerves. Knockout of Panx1 gene significantly increased axonal caliber
and axonal growth rate in cultured dorsal root ganglia (DRG) neurons. Furthermore, genetic knockout of Panx1 or inhibition of components of purinergic signaling, by treatment with probenecid and apyrase, resulted in denser axonal outgrowth from cultured DRG explants compared to untreated wild-types. Our findings suggest that Panx1 regulates axonal growth in the peripheral nervous system.
Background: Scaphoid fractures progress to nonunion rates of up to 15% when non-displaced, and are even more frequent when the fracture is displaced. Standard treatment in these cases is surgery; ...however, individuals unable to undergo this operation, or for those who wish to try more conservative measures, there may be benefit from nonoperative options. Of these, low-intensity pulsed ultrasound (LIPUS) has been shown to improve fracture nonunion healing. The purpose of this study was to perform a comprehensive meta-analysis of relevant literature to determine success of the use of LIPUS for treatment of scaphoid nonunion. Methods: Utilizing PubMed, Embase, and Ovid databases, we performed a literature search using key terms for scaphoid nonunions. A total of 686 studies met initial search criteria. Studies reporting fewer than 5 cases, those not published in English, those not related to LIPUS nonoperative scaphoid nonunion treatment, and those without sufficient data were excluded. Five studies met these criteria, and statistical analysis was performed to determine overall union rates. Results: The use of LIPUS on 166 nonunions reported a mean healing index of 78.6%. The average time to union following LIPUS treatment was 4.2 months. Conclusions: While surgical intervention is still the standard, our results show that LIPUS may serve as a nonoperative alternative to scaphoid nonunion in certain cases. The results are encouraging in which these challenging fracture a nonunions can heal without further surgical intervention in the majority of patients.
Patent Foramen Ovale and Stroke Horton, Steven C.; Bunch, T. Jared
Mayo Clinic proceedings,
2004, 2004-Jan, 2004-1-00, 20040101, Volume:
79, Issue:
1
Journal Article
Peer reviewed
Open access
A patent foramen ovale (PFO) is a frequent remnant of embryological development with clinical importance in thromboembolism, paradoxical embolism, stroke, platypneaorthodeoxia, decompression ...sickness, and migraine headache. The proposed mechanisms of stroke with PFO include paradoxical embolization, in situ thrombosis within the canal of the PFO, associated atrial arrhythmias, and concomitant hypercoagulable states. Prospective trials using aspirin treatment to reduce recurrent stroke showed a significant recurrence of neurologic events in patients with a PFO and atrial septal aneurysm. Use of warfarin anticoagulation does not further reduce recurrent stroke rates compared with antiplatelet therapy. Both surgical and catheter-based modes of closure have been shown to decrease the rate of subsequent embolic events substantially. Successful closure, defined by transesophageal echocardiography, appears to predict freedom from subsequent embolic events. To our knowledge, no randomized trials comparing anticoagulation with surgical or catheter-based closure have been performed.
Acute osmotic fluctuations in the brain occur during a number of clinical conditions and can result in a variety of adverse neurological symptoms. Osmotic perturbation can cause changes in the ...volumes of intra- and extracellular fluid and, due to the rigidity of the skull, can alter intracranial pressure thus making it difficult to analyze purely osmotic effects in vivo. The present study aims to determine the effects of changes in osmolarity on SH-SY5Y human neuroblastoma cells in vitro, and the role of the actin-myosin network in regulating this response. Cells were exposed to hyper- or hypoosmotic media and morphological and cytoskeletal responses were recorded. Hyperosmotic shock resulted in a drop in cell body volume and planar area, a persisting shape deformation, and increases in cellular translocation. Hypoosmotic shock did not significantly alter planar area, but caused a transient increase in cell body volume and an increase in cellular translocation via the development of small protrusions rich in actin. Disruption of the actin-myosin network with latrunculin and blebbistatin resulted in changes to volume and shape regulation, and a decrease in cellular translocation. In both osmotic perturbations, no apparent disruptions to cytoskeletal integrity were observed by light microscopy. Overall, because osmotically induced changes persisted even after volume regulation occurred, it is possible that osmotic stress may play a larger role in neurological dysfunction than currently believed.
A protocol using transthoracic echocardiography was designed to diagnose the common malfunctions of patients on chronic support with a left ventricular assist device (LVAD).
Mechanical circulatory ...support, primarily with a LVAD, is increasingly used for treatment of advanced heart failure as a bridge to transplant and for long-term treatment of heart failure. The LVAD dysfunction is a recognized complication. To date, no studies have defined the role of transthoracic echocardiography in evaluating long-term mechanical complications of chronic LVAD support.
Transthoracic echocardiography was used in a protocol designed to detect the common types of mechanical malfunction. Patients were followed up with serial echocardiograms, and clinical validations were made with findings from a catheter-based protocol and inspection at the time of cardiac transplant or corrective surgery.
Thirty-two patients with 44 LVADs were followed up during a four-year period using this protocol that correctly identified 11 patients with inflow valve regurgitation, 2 with intermittent inflow conduit obstruction, 1 with severe kinking of the outflow graft, and 9 with new insufficiency of the native aortic valve.
As LVAD use for end-stage heart failure becomes widespread, and durations of support are extended, dysfunction will be increasingly prevalent. Transthoracic echocardiography provides a practical method to accurately identify the causes of mechanical dysfunction with patients on chronic LVAD support.
Purpose: Reverse total shoulder arthroplasty (RTSA) may be used to treat a variety of pathologic shoulder conditions, but complications such as scapular notching continue raise concerns. Variable ...anatomy surrounding the glenoid may have implications for future RTSA design, but at present the anatomy of the scapular neck in the human population has not been clearly defined.
Materials and Methods: 442 human scapulae from the Hamann-Todd Osteological Collection were measured for scapular neck length (SNL) and scapular neck angle (SNA). SNL was defined as the distance from the most lateral portion of the infraglenoid tubercle to the most inferolateral portion of the glenoid fossa. The SNA was measured according to Gerber et al. previously. The mean, standard deviation and ranges for SNL and SNA were calculated and compared based on sex and race, and interobserver variability was calculated.
Results: The mean SNL was 1.06 cm ± 0.33 cm (0.37-2.43 cm). Males demonstrated a larger SNL (1.08 cm ± 0.33 cm) than females (1.01 cm ± 0.32 cm) (P < 0.12), and Caucasians (1.09 cm ± 0.33 cm) demonstrated a significantly larger SNL than African-Americans (1.00 cm ± 0.32) (P < 0.01). The mean SNA was 106.7° ± 11.0° (76.9-139.4°). No significant correlation was found between SNL and SNA (Pearson Correlation Coefficient = 0.018) (P < 0.702).
Conclusion: Scapular neck length and SNA vary widely within the population but there appears to be a tendency towards increased SNL in males and Caucasians.
Clinical Relevance: The anatomy of the scapular neck may have significant implications for RTSA design, surgical planning, and reduction of associated complications.
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