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  • Ovid Technologies (Wolters Kluwer Health)  (10)
  • 1
    Online Resource
    Online Resource
    No Clinical Benefit of Intramuscular Delivery of Bone Marrow-derived Mononuclear Cells in Nonreconstructable Peripheral Arterial Disease : Results of a Phase-III Randomized-controlled Trial
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Annals of Surgery Vol. 268, No. 5 ( 2018-11), p. 756-761
    Details
    In: Annals of Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 268, No. 5 ( 2018-11), p. 756-761
    Abstract: Prospects for no-option, end-stage peripheral artery disease (PAD) patients remain poor. Although results from open and semiblinded studies fuel hope for cell-based strategies in no-option patients, so far conclusions from the available placebo-controlled studies are not supportive. With the intention to end the remaining controversy with regard to cell therapy for PAD we conducted a confirmatory, double-blinded randomized placebo-controlled phase 3 trial. Study Design: This randomized controlled trial was registered (NCT00539266). Inclusion criteria included stable or progressive disabling PAD, no imminent need for amputation, absent accepted options for revascularization. Diabetic disease was an exclusion criterion. Bone marrow (500–700 mL) was harvested and bone marrow-derived mononuclear cells were concentrated to 40 mL. Concentrated cells or placebo (diluted blood) were intramuscularly injected at 40 locations of the calf muscle. Results: Fifty-four patients (mean (sd) age 58.2 (14.2) yrs, 58% males) were randomized. Twenty-eight patients received BM-MNCs, 26 placebo. Baseline criteria were similar in the 2 groups. No significant differences were observed for the primary (number of amputations, (pain free) walking distance) and secondary outcome parameters (ankle brachial index, pain scores, quality of life (SF-36)). Discussion: This fully blinded replication trial of autologous BM-MNC fails to confirm a benefit for cell therapy in no-option PAD patients, consequently BM-MNC therapy should not be offered as a clinical treatment. Apparent contrasting conclusions from open and controlled studies underscore the importance of a controlled trial design in evaluating cell-based interventions in PAD.
    Type of Medium: Online Resource
    ISSN: 0003-4932 , 1528-1140
    URL: Article
    DOI: 10.1097/SLA.0000000000002896
    RVK:
    XA 23900
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2641023-0
    detail.hit.zdb_id: 2002200-1
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  • 2
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    Extent of Coronary Artery Disease in Patients With Stenotic Bicuspid Versus Tricuspid Aortic Valves
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Journal of the American Heart Association Vol. 10, No. 12 ( 2021-06-15)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 10, No. 12 ( 2021-06-15)
    Abstract: Bicuspid aortic valve (BAV) is the most common congenital cardiac malformation, which is often complicated by aortic valve stenosis (AoS). In tricuspid aortic valve (TAV), AoS strongly associates with coronary artery disease (CAD) with common pathophysiological factors. Yet, it remains unclear whether AoS in patients with BAV is also associated with CAD. This study investigated the association between the aortic valve morphological features and the extent of CAD. Methods and Results A single‐center study was performed, including all patients who underwent an aortic valve replacement attributable to AoS between 2006 and 2019. Coronary sclerosis was graded on preoperative coronary angiographies using the coronary artery greater even than scoring method, which divides the coronaries in 28 segments and scores nonobstructive (20%–49% sclerosis) and obstructive coronary sclerosis ( 〉 49% sclerosis) in each segment. Multivariate analyses were performed, controlling for age, sex, and CAD risk factors. A total of 1296 patients (931 TAV and 365 BAV) were included, resulting in 548 matched patients. Patients with TAV exhibited more CAD risk factors (odds ratio [OR], 2.66; 95% CI, 1.79–3.96; P 〈 0.001). Patients with BAV had lower coronary artery greater even than 20 (1.61±2.35 versus 3.60±2.79) and coronary artery greater even than 50 (1.24±2.43 versus 3.37±3.49) scores ( P 〈 0.001), even after correcting for CAD risk factors ( P 〈 0.001). Patients with TAV more often needed concomitant coronary revascularization (OR, 3.50; 95% CI, 2.42–5.06; P 〈 0.001). Conclusions Patients with BAV who are undergoing surgery for AoS carry a lower cardiovascular risk profile, correlating with less coronary sclerosis and a lower incidence of concomitant coronary revascularization compared with patients with TAV.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.120.020080
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2653953-6
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  • 3
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    Parallel Murine and Human Aortic Wall Genomics Reveals Metabolic Reprogramming as Key Driver of Abdominal Aortic Aneurysm Progression
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Journal of the American Heart Association Vol. 10, No. 17 ( 2021-09-07)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 10, No. 17 ( 2021-09-07)
    Abstract: While numerous interventions effectively interfered with abdominal aortic aneurysm (AAA) formation/progression in preclinical models, none of the successes translated into clinical success. Hence, a systematic exploration of parallel and divergent processes in clinical AAA disease and its 2 primary models (the porcine pancreatic elastase and angiotensin‐II infusion [AngII] murine model) was performed to identify mechanisms relevant for aneurysm disease. Methods and Results This study combines Movat staining and pathway analysis for histological and genomic comparisons between clinical disease and its models. The impact of a notable genomic signal for metabolic reprogramming was tested in a rescue trial (AngII model) evaluating the impact of 1‐(4‐pyridinyl)‐3‐(2‐quinolinyl)‐2‐propen‐1‐one (PFK15)‐mediated interference with main glycolytic switch PFKFB3. Histological evaluation characterized the AngII model as a dissection model that is accompanied by adventitial fibrosis. The porcine pancreatic elastase model showed a transient inflammatory response and aortic dilatation, followed by stabilization and fibrosis. Normalization of the genomic responses at day 14 confirmed the self‐limiting nature of the porcine pancreatic elastase model. Clear parallel genomic responses with activated adaptive immune responses, and particularly strong signals for metabolic switching were observed in human AAA and the AngII model. Rescue intervention with the glycolysis inhibitor PFK15 in the AngII model showed that interference with the glycolytic switching quenches aneurysm formation. Conclusions Despite clear morphological contrasts, remarkable genomic parallels exist for clinical AAA disease and the AngII model. The metabolic response appears causatively involved in AAA progression and provides a novel therapeutic target. The clear transient genomic response classifies the porcine pancreatic elastase model as a disease initiation model.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.120.020231
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
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  • 4
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    Molecular Fingerprint for Terminal Abdominal Aortic Aneurysm Disease
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Journal of the American Heart Association Vol. 6, No. 12 ( 2017-12-02)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 12 ( 2017-12-02)
    Abstract: Clinical decision making in abdominal aortic aneurysms (AAA) relies completely on diameter. At this point, improved decision tools remain an unmet medical need. Our goal was to identify changes at the molecular level specifically leading up to AAA rupture. Methods and Results Aortic wall tissue specimens were collected during open elective (e AAA ; n=31) or emergency repair of ruptured AAA (r AAA ; n=17), and gene expression was investigated using microarrays. Identified candidate genes were validated with quantitative real‐time polymerase chain reaction in an independent sample set (e AAA : n=46; r AAA : n=18). Two gene sets were identified, 1 set containing 5 genes linked to terminal progression, that is, positively associated with progression of larger AAA , and with rupture ( HILPDA , ANGPTL 4 , LOX , SRPX 2 , FCGBP ), and a second set containing 5 genes exclusively upregulated in rAAA ( ADAMTS 9 , STC 1 , GFPT 2 , GAL 3 ST 4 , CCL 4L1 ). Genes in both sets essentially associated with processes related to impaired tissue remodeling, such as angiogenesis and adipogenesis. In gene expression experiments we were able to show that upregulated gene expression for identified candidate genes is unique for AAA . Functionally, the selected upregulated factors converge at processes coordinated by the canonical HIF ‐1α signaling pathway and are highly expressed in fibroblasts but not inflammatory cells of the aneurysmatic wall. Histological quantification of angiogenesis and exploration of the HIF ‐1α network in r AAA versus e AAA shows enhanced microvessel density but also clear activation of the HIF ‐1α network in r AAA . Conclusions Our study shows a specific molecular fingerprint for terminal AAA disease. These changes appear to converge at activation of HIF ‐1α signaling in mesenchymal cells. Aspects of this cascade might represent targets for rupture risk assessment.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.117.006798
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
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  • 5
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    Systematic Evaluation of the Cellular Innate Immune Response During the Process of Human Atherosclerosis
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Journal of the American Heart Association Vol. 5, No. 6 ( 2016-06-13)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 5, No. 6 ( 2016-06-13)
    Abstract: The concept of innate immunity is well recognized within the spectrum of atherosclerosis, which is primarily dictated by macrophages. Although current insights to this process are largely based on murine models, there are fundamental differences in the atherosclerotic microenvironment and associated inflammatory response relative to humans. In this light, we characterized the cellular aspects of innate immune response in normal, nonprogressive, and progressive human atherosclerotic plaques. Methods and Results A systematic analysis of innate immune response was performed on 110 well‐characterized human perirenal aortic plaques with immunostaining for specific macrophage subtypes (M1 and M2 lineage) and their activation markers, neopterin and human leukocyte antigen–antigen D related ( HLA ‐ DR), together with dendritic cells (DCs), natural killer ( NK ) cells, mast cells, neutrophils, and eosinophils. Normal aortae were devoid of low‐density lipoprotein, macrophages, DCs, NK cells, mast cells, eosinophils, and neutrophils. Early, atherosclerotic lesions exhibited heterogeneous populations of ( CD 68 + ) macrophages, whereby 25% were double positive “M1” ( CD 68 + / inducible nitric oxide synthase [ iNOS ] + / CD 163 − ), 13% “M2” double positive ( CD 68 + / iNOS − / CD 163 + ), and 17% triple positive for (M1) iNOS (M2)/ CD 163 and CD 68, with the remaining (≈40%) only stained for CD 68. Progressive fibroatheromatous lesions, including vulnerable plaques, showed increasing numbers of NK cells and fascin‐positive cells mainly localized to the media and adventitia whereas the M1/M2 ratio and level of macrophage activation ( HLA ‐ DR and neopterin) remained unchanged. On the contrary, stabilized (fibrotic) plaques showed a marked reduction in macrophages and cell activation with a concomitant decrease in NK cells, DCs, and neutrophils. Conclusions Macrophage “M1” and “M2” subsets, together with fascin‐positive DCs, are strongly associated with progressive and vulnerable atherosclerotic disease of human aorta. The observations here support a more complex theory of macrophage heterogeneity than the existing paradigm predicated on murine data and further indicate the involvement of (poorly defined) macrophage subtypes or greater dynamic range of macrophage plasticity than previously considered.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.115.002860
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
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  • 6
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    Impaired Collagen Biosynthesis and Cross‐linking in Aorta of Patients With Bicuspid Aortic Valve
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Journal of the American Heart Association Vol. 2, No. 1 ( 2013-01-23)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 2, No. 1 ( 2013-01-23)
    Abstract: Patients with bicuspid aortic valve ( BAV ) have an increased risk of developing ascending aortic aneurysm. In the present study, collagen homeostasis in nondilated and dilated aorta segments from patients with BAV was studied, with normal and dilated aortas from tricuspid aortic valve ( TAV ) patients as reference. Methods and Results Ascending aortas from 56 patients were used for biochemical and morphological analyses of collagen. mRNA expression was analyzed in 109 patients. Collagen turnover rates were similar in nondilated and dilated aortas of BAV patients, showing that aneurysmal formation in BAV is, in contrast to TAV , not associated with an increased collagen turnover. However, BAV in general was associated with an increased aortic collagen turnover compared with nondilated aortas of TAV patients. Importantly, the ratio of hydroxylysyl pyridinoline (HP) to lysyl pyridinoline (LP), 2 distinct forms of collagen cross‐linking, was lower in dilated aortas from patients with BAV , which suggests that BAV is associated with a defect in the posttranslational collagen modification. This suggests a deficiency at the level of lysyl hydroxylase ( PLOD 1 ), which was confirmed by mRNA and protein analyses that showed reduced PLOD 1 expression but normal lysyl oxidase expression in dilated aortas from patients with BAV . This suggests that impaired collagen cross‐linking in BAV patients may be attributed to changes in the expression and/or activity of PLOD 1 . Conclusions Our results demonstrate an impaired biosynthesis and posttranslational modification of collagen in aortas of patients with BAV , which may explain the increased aortic aneurysm formation in BAV patients.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.112.000034
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
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  • 7
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    Vitamin E Status in Preterm Infants: Assessment by Plasma and Erythrocyte Vitamin E-Lipid Ratios and Hemolysis Tests
    Ovid Technologies (Wolters Kluwer Health) ; 1998
    In:  Journal of Pediatric Gastroenterology & Nutrition Vol. 26, No. 1 ( 1998-01), p. 73-79
    Details
    In: Journal of Pediatric Gastroenterology &amp Nutrition, Ovid Technologies (Wolters Kluwer Health), Vol. 26, No. 1 ( 1998-01), p. 73-79
    Type of Medium: Online Resource
    ISSN: 0277-2116
    URL: Article
    DOI: 10.1097/00005176-199801000-00013
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1998
    detail.hit.zdb_id: 2078835-6
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  • 8
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    Response to the Comment on “Long-term Prognosis After Elective Abdominal Aortic Aneurysm Repair is Poor in Women and Men”
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Annals of Surgery Vol. 274, No. 6 ( 2021-12), p. e858-
    Details
    In: Annals of Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 274, No. 6 ( 2021-12), p. e858-
    Type of Medium: Online Resource
    ISSN: 0003-4932 , 1528-1140
    URL: Article
    DOI: 10.1097/SLA.0000000000004688
    RVK:
    XA 23900
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2641023-0
    detail.hit.zdb_id: 2002200-1
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  • 9
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    Extreme Diversity of the Human Vascular Mesenchymal Cell Landscape
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Journal of the American Heart Association Vol. 9, No. 23 ( 2020-12)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 9, No. 23 ( 2020-12)
    Abstract: Human mesenchymal cells are culprit factors in vascular (patho)physiology and are hallmarked by phenotypic and functional heterogeneity. At present, they are subdivided by classic umbrella terms, such as “fibroblasts,” “myofibroblasts,” “smooth muscle cells,” “fibrocytes,” “mesangial cells,” and “pericytes.” However, a discriminative marker‐based subclassification has to date not been established. Methods and Results As a first effort toward a classification scheme, a systematic literature search was performed to identify the most commonly used phenotypical and functional protein markers for characterizing and classifying vascular mesenchymal cell subpopulation(s). We next applied immunohistochemistry and immunofluorescence to inventory the expression pattern of identified markers on human aorta specimens representing early, intermediate, and end stages of human atherosclerotic disease. Included markers comprise markers for mesenchymal lineage (vimentin, FSP‐1 [fibroblast‐specific protein‐1]/S100A4, cluster of differentiation (CD) 90/thymocyte differentiation antigen 1, and FAP [fibroblast activation protein] ), contractile/non‐contractile phenotype (α‐smooth muscle actin, smooth muscle myosin heavy chain, and nonmuscle myosin heavy chain), and auxiliary contractile markers (h1‐Calponin, h‐Caldesmon, Desmin, SM22α [smooth muscle protein 22α], non‐muscle myosin heavy chain, smooth muscle myosin heavy chain, Smoothelin‐B, α‐Tropomyosin, and Telokin) or adhesion proteins (Paxillin and V inculin). Vimentin classified as the most inclusive lineage marker. Subset markers did not separate along classic lines of smooth muscle cell, myofibroblast, or fibroblast, but showed clear temporal and spatial diversity. Strong indications were found for presence of stem cells/Endothelial‐to‐Mesenchymal cell Transition and fibrocytes in specific aspects of the human atherosclerotic process. Conclusions This systematic evaluation shows a highly diverse and dynamic landscape for the human vascular mesenchymal cell population that is not captured by the classic nomenclature. Our observations stress the need for a consensus multiparameter subclass designation along the lines of the cluster of differentiation classification for leucocytes.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.120.017094
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
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  • 10
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    Long-term Prognosis After Elective Abdominal Aortic Aneurysm Repair is Poor in Women and Men : The Challenges Remain
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Annals of Surgery Vol. 272, No. 5 ( 2020-11), p. 773-778
    Details
    In: Annals of Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 272, No. 5 ( 2020-11), p. 773-778
    Abstract: To evaluate the impact of changes in elective Abdominal Aortic Aneurysm (AAA) management on life-expectancy of AAA patients. Background: Over the past decades AAA repair underwent substantial changes, that is, the introduction of EVAR and implementation of intensified cardiovascular risk management. The question rises to what extent these changes improved longevity of AAA patients. Methods: National evaluation including all 12.907 (82.7% male) patients who underwent elective AAA repair between 2001 and 2015 in Sweden. The impact of changes in AAA management was established by a time-resolved analysis based on 3 timeframes: open repair dominated period (2001–2004, n = 2483), transition period (2005–2011, n = 6230), and EVAR-first strategy period (2012–2015, n = 4194). Relative survival was used to quantify AAA-associated mortality, and to adjust for changes in life-expectancy. Results: Relative survival of electively treated AAA patients was stable and persistently compromised [4-year relative survival and 95% confidence interval: 0.87 (0.85–0.89), 0.87 (0.86–0.88), 0.89 (0.86–0.91) for the 3 periods, respectively]. Particularly alarming is the severely compromised survival of female patients (4-year relative survival females 0.78, 0.80, 0.70 vs males 0.89, 0.89, 0.91, respectively). Cardiovascular mortality remained the main cause of death (51.0%, 47.2%, 47.9%) and the proportion cardiovascular disease over non-cardiovascular disease death was stable over time. Conclusions: Changes in elective AAA management reduced short-term mortality, but failed to improve the profound long-term survival disadvantage of AAA patients. The persistent high (cardiovascular) mortality calls for further intensification of cardiovascular risk management, and a critical appraisal of the basis for the excess mortality of AAA patients.
    Type of Medium: Online Resource
    ISSN: 0003-4932 , 1528-1140
    URL: Article
    DOI: 10.1097/SLA.0000000000004182
    RVK:
    XA 23900
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2641023-0
    detail.hit.zdb_id: 2002200-1
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