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Find video protocols related to scientific articles indexed in Pubmed.
Granulocyte colony-stimulating factor therapy for stem cell mobilization following anterior wall myocardial infarction: the CAPITAL STEM MI randomized trial.
CMAJ
PUBLISHED: 06-16-2014
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Small studies have yielded divergent results for administration of granulocyte colony-stimulating factor (G-CSF) after acute myocardial infarction. Adequately powered studies involving patients with at least moderate left ventricular dysfunction are lacking.
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Endovascular cooling catheter related thrombosis in patients undergoing therapeutic hypothermia for out of hospital cardiac arrest.
Resuscitation
PUBLISHED: 05-20-2014
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Therapeutic hypothermia improves neurologic outcome and survival in patients following out-of-hospital cardiac arrest (OHCA). Endovascular cooling devices are commonly used to rapidly achieve and maintain hypothermia. The use of these devices may be associated with catheter related thrombosis. The objective of this study was to determine the risk of catheter related thrombosis associated with the use of an endovascular cooling catheter in patients referred for therapeutic hypothermia following OHCA.
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A comparative pharmacodynamic study of ticagrelor versus clopidogrel and ticagrelor in patients undergoing primary percutaneous coronary intervention: the CAPITAL RELOAD study.
PLoS ONE
PUBLISHED: 01-01-2014
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In patients undergoing primary percutaneous coronary intervention (PPCI) ticagrelor is superior to clopidogrel in reducing cardiovascular events. This study sought to evaluate the effect of clopidogrel pretreatment on the pharmacodynamics of ticagrelor in patients undergoing PPCI.
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Glycogen Synthase Kinase-3? Inhibition Augments Diabetic Endothelial Progenitor Cell Abundance and Functionality via Cathepsin B: a Novel Therapeutic Opportunity for Arterial Repair.
Diabetes
PUBLISHED: 12-02-2013
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Progenitor cell therapy is hindered in patients with diabetes mellitus (DM) due to cellular senescence. Glycogen synthase kinase 3? (GSK3?) activity is increased in DM potentially exacerbating impaired cell based therapies. Thus, we aimed to determine if and how GSK3? inhibitors (GSKi) can improve therapeutic efficacy of endothelial progenitor cells (EPC) from patients with DM. Patients with DM had fewer EPCs and increased rates of apoptosis. DM-EPCs also exhibited higher levels of GSK3? activity resulting in increased levels of phosphorylated ?-catenin. Proteomic profiling of DM EPCs treated with GSKi identified 37 non-redundant, differentially regulated proteins. Cathepsin B (cathB) was subsequently confirmed to be differentially regulated and showed 40% less baseline activity in DM-EPCs - an effect reversed by GSKi treatment. Finally, in vivo efficacy of cell based therapy was assessed in a xenotransplant femoral wire injury mouse model. Administration of DM EPCs reduced the intima:media - an effect that was further augmented when DM EPCs were pre-treated with GSKi, yet absent when cathB was antagonized. In DM, increased basal GSK3? activity contributes to accelerated EPC cellular senescence - an effect reversed by small molecule antagonism of GSK3? which enhances cell based therapy following vascular injury.
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Heat shock protein 27 attenuates neointima formation and accelerates reendothelialization after arterial injury and stent implantation: importance of vascular endothelial growth factor up-regulation.
FASEB J.
PUBLISHED: 10-18-2013
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Elevated serum heat shock protein 27 (HSP27) levels are atheroprotective; however, the role of HSP27 after arterial injury is unknown. Human endothelial progenitor cells (EPCs) were treated with recombinant (r)HSP27 (50 ?g/ml) or its inactive C1 terminus, and gene expression was characterized before functional studies were performed in vitro and in vivo. Vascular endothelial growth factor (VEGF) was markedly up-regulated by rHSP27 (10- and 6-fold increases in mRNA and secretion, respectively). Pretreatment of EPCs with rHSP27 resulted in a 60% reduction in reendothelialization (RE) time in a scratch assay, an effect that was blocked with VEGF-neutralizing antibodies. Mice overexpressing HSP27 demonstrated more robust mobilization of EPCs at the time of arterial injury, as well as a 67% increase in RE and a 45% reduction in neointima (NI) formation at 28 d. Implantation of rHSP27-eluting stents in rabbit carotid arteries resulted in a marked improvement in RE at 7 and 28 d and transient attenuation of NI formation by 42% at 7 d. Hence, extracellular HSP27 up-regulated VEGF and improved EPC migration in vitro. Augmented systemic or local levels of HSP27 markedly improved RE after vascular injury, an effect that is of particular relevance to the safety profile of vascular stents.-Ma, X., Hibbert, B., McNulty, M., Hu, T., Zhao, X., Ramirez, F. D., Simard, T., de Belleroche, J. S., OBrien, E. R. Heat shock protein 27 attenuates neointima formation and accelerates reendothelialization after arterial injury and stent implantation: importance of vascular endothelial growth factor up-regulation.
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Quantifying coronary artery calcification from a contrast-enhanced cardiac computed tomography angiography study.
Eur Heart J Cardiovasc Imaging
PUBLISHED: 08-13-2013
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We sought to quantify coronary artery calcium (CAC) using a single contrast-enhanced cardiac computed tomography angiography (CCTA) study. CCTA has been successfully used for the assessment of coronary artery stenoses, whereas non-contrast ECG-gated computed tomography (Standard-CAC) is commonly performed to quantify CAC. Thus each scan individually contributes to the total radiation dose.Methods resultsPatients who underwent both Standard-CAC and CCTA scans were identified. Standard-CAC images were scored using the Agatston method. CCTA scans were scored for CAC (CCTA-CAC), whereby CAC was defined as plaque with attenuation 2 SD above the mean attenuation value of the ascending aorta (HUaorta). The correlation between Standard-CAC and CCTA-CAC was determined with the slope used to derive a correction factor for the conversion of CCTA-CAC results to a Standard-CAC Agatston score (AS). To test applicability, the correction factor was assessed in a separate validation cohort of similar demographics. From April 2011 to June 2012, a derivation cohort of 92 patients was identified and analysed. An additional 47 patients were identified for the validation cohort. Correlation between Standard-CAC and CCTA-CAC was excellent (r = 0.96). The slope (y = 2.74 × CCTA-CAC score) derived correction factor from the derivation cohort was used to adjust CCTA-CAC derived scores to an AS (CCTA-CACcorrected = 2.74 × CCTA-CAC). The correction factor was applied to the validation cohort CCTA-CAC results with excellent agreement between CCTA-CACcorrected and Standard-CAC (kappa = 0.93).
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The effect of statins on circulating endothelial progenitor cells in humans: a systematic review.
J. Cardiovasc. Pharmacol.
PUBLISHED: 08-13-2013
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Numerous clinical trials have demonstrated early reductions in cardiovascular events occurring independently of the lipid-lowering effects of statins. These pleiotropic effects have been attributed to antiinflammatory properties, to atherosclerotic plaque stabilization, and more recently to mobilization of endothelial progenitor cells (EPCs). Our aim was to evaluate the evidence supporting statin-induced EPC mobilization in humans. We, therefore, performed a computerized literature search and systematic review of randomized trials to determine the effect of statin therapy and statin dosing on circulating EPC numbers. Our literature search identified 10 studies including 479 patients which met inclusion criteria with publication dates ranging from 2005 to 2011. Seven studies compared statin to nonstatin regimens whereas 3 studied low versus high-dose statin therapy. Reported increases in EPC number ranged from 25.8% to 223.5% with a median reported increase of 70.2% when compared to nonstatin regimens with 7 of 10 studies reporting significant increases. Considerable heterogeneity exists in regard to patient population, statin regimens, and the definition of an EPC within the identified studies. In conclusion, randomized studies in humans suggest that statin therapy mobilizes EPCs into the circulation. Larger randomized studies using uniform definitions are needed to definitively establish this effect.
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The evolution of coronary stents: a brief review.
Can J Cardiol
PUBLISHED: 05-25-2013
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Percutaneous coronary intervention is the most prevalent method for coronary artery revascularization. Initial interventions using balloon angioplasty had limited efficacy because coronary dissections, arterial recoil, and neointimal formation led to high rates of abrupt vessel closure and clinical restenosis. With the introduction of coronary stents, vascular dissections were stabilized and arterial recoil was eliminated, but neointimal accumulation remained problematic, resulting in the development of in-stent restenosis (ISR) in 20%-30% of cases. Drug-eluting stents (DESs) were developed to release antiproliferative agents at the site of arterial injury to attenuate neointimal formation. Although DESs have incrementally improved outcomes after percutaneous coronary intervention, delayed re-endothelialization and stent thrombosis remain important challenges. Herein we review the pathophysiology of ISR, stent thrombosis, and briefly summarize the clinical evidence behind first- and second-generation DESs. Moreover, we discuss advancements in our understanding of the pathogenesis of ISR and potential novel therapeutic strategies to improve clinical outcomes.
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Heat shock protein-27 attenuates foam cell formation and atherogenesis by down-regulating scavenger receptor-A expression via NF-?B signaling.
Biochim. Biophys. Acta
PUBLISHED: 02-23-2013
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Previously, we showed an inverse correlation between HSP27 serum levels and experimental atherogenesis in ApoE(-/-) mice that over-express HSP27 and speculated that the apparent binding of HSP27 to scavenger receptor-A (SR-A) was of mechanistic importance in attenuating foam cell formation. However, the nature and importance of the interplay between HSP27 and SR-A in atheroprotection remained unclear. Treatment of THP-1 macrophages with recombinant HSP27 (rHSP27) inhibited acLDL binding (-34%; p<0.005) and uptake (-38%, p<0.05). rHSP27 reduced SR-A mRNA (-39%, p=0.02), total protein (-56%, p=0.01) and cell surface (-53%, p<0.001) expression. The reduction in SR-A expression by rHSP27 was associated with a 4-fold increase in nuclear factor-kappa B (NF-?B) signaling (p<0.001 versus control), while an inhibitor of NF-?B signaling, BAY11-7082, attenuated the negative effects of rHSP27 on both SR-A expression and lipid uptake. To determine if SR-A is required for HSP27 mediated atheroprotection in vivo, ApoE(-/-) and ApoE(-/-) SR-A(-/-) mice fed with a high fat diet were treated for 3weeks with rHSP25. Compared to controls, rHSP25 therapy reduced aortic en face and aortic sinus atherosclerotic lesion size in ApoE(-/-) mice by 39% and 36% (p<0.05), respectively, but not in ApoE(-/-)SR-A(-/-) mice. In conclusion, rHSP27 diminishes SR-A expression, resulting in attenuated foam cell formation in vitro. Regulation of SR-A by HSP27 may involve the participation of NF-?B signaling. Lastly, SR-A is required for HSP27-mediated atheroprotection in vivo.
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Circulating endothelial progenitor cells in HIV infection: a systematic review.
Trends Cardiovasc. Med.
PUBLISHED: 02-08-2013
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Human Immunodeficiency Virus (HIV)-infected individuals have a cardiovascular disease risk that is almost thrice than that of their HIV-uninfected counterparts. Given the critical role of endothelial progenitor cells (EPCs) in vascular homeostasis and arterial repair postinjury, coupled with their strength as biomarkers predictive of cardiovascular events, interest has arisen in characterizing EPCs in the context of HIV infection. We conducted a systematic review of the literature to determine the current state of knowledge on EPCs in the context of HIV infection. Herein, we summarize the pertinent findings of these studies and discuss important differences in the subpopulations of EPCs examined and the methodologies used for their enumeration which likely contributed to the heterogeneity observed across studies.
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Attenuation of atherogenesis via the anti-inflammatory effects of the selective estrogen receptor beta modulator 8?-VE2.
J. Cardiovasc. Pharmacol.
PUBLISHED: 06-24-2011
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Recent studies suggest that modulation of estrogen receptor ? (ER?) may play a crucial role in maintaining vascular homeostasis. We hypothesized that selective ER? activation will attenuate atherogenesis via anti-inflammatory mechanisms.
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Pre-procedural atorvastatin mobilizes endothelial progenitor cells: clues to the salutary effects of statins on healing of stented human arteries.
PLoS ONE
PUBLISHED: 01-25-2011
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Recent clinical trials suggest an LDL-independent superiority of intensive statin therapy in reducing target vessel revascularization and peri-procedural myocardial infarctions in patients who undergo percutaneous coronary interventions (PCI). While animal studies demonstrate that statins mobilize endothelial progenitor cells (EPCs) which can enhance arterial repair and attenuate neointimal formation, the precise explanation for the clinical PCI benefits of high dose statin therapy remain elusive. Thus we serially assessed patients undergoing PCI to test the hypothesis that high dose Atorvastatin therapy initiated prior to PCI mobilizes EPCs that may be capable of enhancing arterial repair.
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Pathogenesis of neointima formation following vascular injury.
Cardiovasc Hematol Disord Drug Targets
PUBLISHED: 01-01-2011
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Revascularization remains the cornerstone of managing obstructive coronary artery disease. Although percutaneous coronary interventions involving the insertion of metal scaffolds, known as stents, has emerged as the preferred method of restoring vessel patency, as many as 30% of patients will experience a gradual re-narrowing of the lumen caused by neointima (NI) formation, resulting in a condition known as in-stent restenosis (ISR). ISR represents a significant limitation to percutaneous revascularization - however, abrogating NI formation following stent implantation has been hampered by an incomplete understanding of the pathogenesis of in-stent lesions. While numerous mechanisms have been proposed to explain the pathogenesis of ISR, data from human and animal models have yielded conflicting results. Herein, we review key studies of NI development following vascular injury with a focus on the origin of cells participating in NI formation.
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Cardiovascular complications of Salmonella enteritidis infection.
Can J Cardiol
PUBLISHED: 10-09-2010
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Salmonella has the ability to adhere to damaged endothelium, predisposing individuals to complications rarely seen with other Gram-negative organisms. Potential complications include endocarditis, infected atheroma or aneurysms, myocarditis and pericarditis. The present report describes two cases of Salmonella enteritidis-associated cardiovascular disease. Patient 1 is a young adult who presented with myopericarditis complicated by recurrent cardiac arrests following return from a tropical climate. This patient was successfully treated with a 14-day course of ciprofloxacin. Patient 2 is an elderly man who developed a pseudoaneurysm of the ascending aorta complicating S enteritidis bacteremia, and died of this complication. Recognition of potential complications of salmonellosis, especially in individuals with risk factors, is paramount in correctly diagnosing and managing these patients.
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Ventricular tachycardia following tube thoracotomy.
Europace
PUBLISHED: 06-04-2010
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Arrhythmias provoked by tube thoracotomy are a rare complication. We report a ventricular tachycardia after chest tube insertion for a device-related pneumothorax. Sinus rhythm was restored only by removal of the chest tube and insertion of a pliable pleural drain. Identification of the chest tube as an arrhythmic trigger following tube thoracotomy is essential in definitive management of refractory arrhythmias.
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Delayed re-endothelialization with rapamycin-coated stents is rescued by the addition of a glycogen synthase kinase-3beta inhibitor.
Cardiovasc. Res.
PUBLISHED: 02-17-2010
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Drug-eluting stents (DESs) reduce neointima area and in-stent restenosis but delay re-endothelialization. Recently, we demonstrated that pharmacological expansion and functional enhancement of endothelial progenitor cells (EPCs) can be achieved by treatment with a glycogen synthase kinase-3beta inhibitor (GSKi)-even for feeble cells derived from coronary artery disease patients. GSKi treatment enhanced EPC adhesion via up-regulated expression of the alpha-4 integrin, ameliorated re-endothelialization, and reduced neointima formation in denuded murine arteries. Hence, we hypothesized that GSKi-coated stents (GSs) will enhance EPC adhesion and attenuate delayed vascular healing associated with rapamycin, a key DES agent.
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Inhibition of endothelial progenitor cell glycogen synthase kinase-3beta results in attenuated neointima formation and enhanced re-endothelialization after arterial injury.
Cardiovasc. Res.
PUBLISHED: 05-19-2009
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Endothelial progenitor cells (EPCs) are circulating pluripotent vascular cells capable of enhancing re-endothelialization and diminishing neointima formation following arterial injury. Glycogen synthase kinase (GSK)-3beta is a protein kinase that has been implicated in the regulation of progenitor cell biology. We hypothesized that EPC abundance and function could be enhanced with the use of an inhibitor of GSK-3beta (GSKi), thereby resulting in improved arterial repair.
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Bivalirudin for primary percutaneous coronary interventions: outcome assessment in the Ottawa STEMI registry.
Circ Cardiovasc Interv
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Data from randomized trials has demonstrated the superiority of bivalirudin to glycoprotein IIb/IIIa inhibitors plus heparin in patients undergoing primary percutaneous coronary intervention. Real-world performance of bivalirudin in primary percutaneous coronary intervention and the benefit of bivalirudin over heparin remain unknown in an era of routine dual antiplatelet therapy.
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The impact of therapeutic hypothermia as adjunctive therapy in a regional primary PCI program.
Resuscitation
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Therapeutic hypothermia (TH) is associated with improved neurologic outcomes in comatose survivors of out-of-hospital cardiac arrest (OHCA). There are currently limited data on the outcomes of patients presenting with resuscitated OHCA in the setting of ST-segment elevation myocardial infarction (STEMI). We conducted a retrospective study to determine the outcomes of patients treated with TH for OHCA in a large regionalized STEMI program.
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Transradial versus transfemoral artery approach for coronary angiography and percutaneous coronary intervention in the extremely obese.
JACC Cardiovasc Interv
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This study sought to evaluate the safety and efficacy of transradial versus transfemoral access for coronary angiography and percutaneous coronary intervention in patients with a body mass index ? 40 kg/m(2).
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Infective endocarditis presenting as ST-elevation myocardial infarction: an angiographic diagnosis.
Can J Cardiol
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While systemic embolic events occur with relative frequency in infective endocarditis (IE), coronary embolization remains an uncommon cause of ST elevation myocardial infarction. Herein we report a case of ventricular fibrillation and anterior ST elevation myocardial infarction occurring in a patient initially presenting with septic shock. Angiography proved diagnostic for IE of a native bicuspid aortic valve complicated by root abscess and left anterior descending artery occlusion. Histologic examination of the embolectomy specimen from the left anterior descending artery confirmed the presence of thrombus and bacteria. The present case highlights difficulties in identifying and managing patients with coronary embolism of vegetations from IE.
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Percutaneous coronary intervention with or without on-site coronary artery bypass surgery: a systematic review and meta-analysis.
Int. J. Cardiol.
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Current American Heart Association guidelines recommend against the performance of elective or primary percutaneous coronary intervention (PCI) without on-site surgical backup (i.e. a class III and IIb recommendation respectively). Despite this, numerous centers have already implemented PCI programs with no on-site surgery backup (NSOS).
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Circulating endothelial progenitor cell levels are not reduced in HIV-infected men.
J. Infect. Dis.
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Reduced levels of endothelial progenitor cells (EPCs) have been associated with increased cardiovascular (CV) risk, but limited data are available on EPC levels in the human immunodeficiency virus (HIV)-infected population. EPCs (CD45(dim)/CD34(+)/kinase domain receptor(+)) from 36 HIV-uninfected and 30 antiretroviral therapy-naive HIV-infected men without known CV risk factors were enumerated using flow cytometry. The mean EPC levels (± standard error of the mean) were 1.4 ± 0.5 cells/?L in the HIV-infected group and 3.7 ± 2.2 cells/?L in the control group (P = .92). EPC levels were not associated with disease parameters, such as CD4 cell count or viral load. Reductions in EPC levels do not seem to explain the increased risk of CV disease among HIV-infected men.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.