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  • 1
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 12, No. 13 ( 2023-07-04)
    Abstract: Little is known about the impact of transcatheter mitral valve edge‐to‐edge repair on changes in left ventricular ejection fraction (LVEF) and the effect of an acute reduction in LVEF on prognosis. We aimed to assess changes in LVEF after transcatheter mitral valve edge‐to‐edge repair for both primary and secondary mitral regurgitation (PMR and SMR, respectively), identify rates and predictors of LVEF reduction, and estimate its impact on prognosis. Methods and Results In this international multicenter registry, patients with both PMR and SMR undergoing transcatheter mitral valve edge‐to‐edge repair were included. We assessed rates of acute LVEF reduction (LVEFR), defined as an acute relative decrease of 〉 15% in LVEF, its impact on all‐cause mortality, major adverse cardiac event (composite end point of all‐cause death, mitral valve surgery, and residual mitral regurgitation grade ≥2), and LVEF at 12 months, as well as predictors for LVEFR. Of 2534 patients included (727 with PMR, and 1807 with SMR), 469 (18.5%) developed LVEFR. Patients with PMR were older (79.0±9.2 versus 71.8±8.9 years; P 〈 0.001) and had higher mean LVEF (54.8±14.0% versus 32.7±10.4%; P 〈 0.001) at baseline. After 6 to 12 months (median, 9.9 months; interquartile range, 7.8–11.9 months), LVEF was significantly lower in patients with PMR (53.0% versus 56.0%; P 〈 0.001) but not in patients with SMR. The 1‐year mortality was higher in patients with PMR with LVEFR (16.9% versus 9.7%; P 〈 0.001) but not in those with SMR ( P =0.236). LVEF at baseline (odds ratio, 1.03 [95% CI, 1.01–1.05]; P =0.002) was predictive of LVEFR for patients with PMR, but not those with SMR ( P =0.092). Conclusions Reduction in LVEF is not uncommon after transcatheter mitral valve edge‐to‐edge repair and is correlated with worsened prognosis in patients with PMR but not patients with SMR. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT05311163.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2653953-6
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  • 2
    In: Journal of Cardiovascular Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 10 ( 2020-10), p. 751-758
    Abstract: Limited real-world data are available regarding the outcome of patients treated with inappropriate dose of nonvitamin-K antagonist oral anticoagulants (NOACs). Objective To assess the prevalence and factors associated with inappropriate dose prescription of NOACs and to evaluate adverse events that come from this inappropriate prescription. Methods Single-center multidisciplinary registry including nonvalvular atrial fibrillation patients treated with NOACs. Based on guidelines criteria for dose reduction, two subcohorts were defined as treated with appropriate or inappropriate NOACs dose. Primary efficacy endpoint was 2-year rate of thromboembolic events. Primary safety endpoint was 2-year rate of major bleeding. Event-free survival curves among groups were compared using Cox–Mantel test. Results A total of 760 nonvalvular atrial fibrillation patients were included; 32% patients were treated with dabigatran, 34% with apixaban, 24% with rivaroxaban and 10% with edoxaban. An inappropriate dose was prescribed in 96 patients (12.6%), and in most cases (68%) it was too low. Rivaroxaban (15%) and apixaban (18.5%) were the most frequently prescribed with an inappropriate dose. Patients treated with an inappropriate dose were elderly people, with low-creatinine clearance value, who had experienced previous bleeding and with a high CHADS2 VASc score. In 2 years, a trend for higher numbers of thromboembolic events (5.2 vs. 3.3%, P  = 0.348) and less major bleeding (2.1 vs. 4.2%, P  = 0.316) has been observed in patients with inappropriate NOACs prescriptions. Conclusion Nearly 13% of patients were treated with an inappropriate dose of NOACs, in this single-center study. A trend for higher numbers of thromboembolic events was observed in these patients. The results should be considered as hypothesis generating.
    Type of Medium: Online Resource
    ISSN: 1558-2027 , 1558-2035
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
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  • 3
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 76, No. 2 ( 2020-08)
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2094210-2
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  • 4
    In: Retina, Ovid Technologies (Wolters Kluwer Health), Vol. 37, No. 8 ( 2017-08), p. 1581-1590
    Abstract: To evaluate differences in the visual phenotype and natural history of Usher syndrome caused by mutations in MYO7A or USH2A , the most commonly affected genes of Usher syndrome Type I (USH1) and Type II (USH2), respectively. Methods: Eighty-eight patients with a clinical diagnosis of USH1 (26 patients) or USH2 (62 patients) were retrospectively evaluated. Of these, 48 patients had 2 disease-causing mutations in MYO7A (10 USH1 patients), USH2A (33 USH2 patients), and other USH (5 patients) genes. Clinical investigation included best-corrected visual acuity, Goldmann visual field, fundus photography, electroretinography, and audiologic and vestibular assessments. Longitudinal analysis was performed over a median follow-up time of 3.5 years. Results: Patients carrying mutations in MYO7A had a younger age of onset of hearing and visual impairments than those carrying mutations in USH2A , leading to an earlier diagnosis of the disease in the former patients. Longitudinal analysis showed that visual acuity and visual field decreased more rapidly in subjects carrying MYO7A mutations than in those carrying USH2A mutations (mean annual exponential rates of decline of 3.92 vs. 3.44% and of 8.52 vs. 4.97%, respectively), and the former patients reached legal blindness on average 15 years earlier than the latter. Conclusion: The current study confirmed a more severe progression of the retinal disease in USH1 patients rather than in USH2 patients. Furthermore, most visual symptoms (i.e., night blindness, visual acuity worsening) occurred at an earlier age in USH1 patients carrying mutations in MYO7A .
    Type of Medium: Online Resource
    ISSN: 0275-004X
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2071014-8
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  • 5
    In: Retina, Ovid Technologies (Wolters Kluwer Health), Vol. 39, No. 7 ( 2019-07), p. 1399-1409
    Abstract: To investigate the natural history of Stargardt disease over a multiyear follow-up. Methods: We reviewed medical records of Stargardt disease patients, with clinical diagnosis of Stargardt disease at a single institution, which was also supported by molecular diagnosis. All patients underwent best-corrected visual acuity, fundus photography, optical coherence tomography, and full-field electroretinography. Results: The study cohort consisted of 157 Stargardt disease patients aged 30.4 ± 1.1 years. Longitudinal analysis (mean follow-up: 3 years) showed a significant worsening of best-corrected visual acuity at an average rate of 1.5 Early Treatment Diabetic Retinopathy Study letters/year ( P 〈 0.001), an enlargement of retinal pigment epithelium lesion area by optical coherence tomography at an average linear rate of 0.10 mm 2 /year ( P 〈 0.001), and a thinning of central macular thickness at a mean rate of −1.42 μ m/year ( P 〈 0.001). Survival analysis showed that patients with 2 alleles harboring likely-null variants, on average, reached most severe disease stage, i.e., legal blindness, alteration in both dark-adapted and light-adapted electroretinographic responses, and retinal pigment epithelium lesion area larger than 2.5 mm 2 significantly earlier than patients with at least one allele harboring a missense variant. Conclusion: The current longitudinal study showed a significant genotype–phenotype correlation characterization, because patients harboring 2 likely-null alleles reach a severe disease stage about 10 years earlier than patients with at least one missense allele.
    Type of Medium: Online Resource
    ISSN: 0275-004X
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2071014-8
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  • 6
    In: Coronary Artery Disease, Ovid Technologies (Wolters Kluwer Health), Vol. 32, No. 8 ( 2021-12), p. 689-697
    Abstract: Elderly constitute a high-risk subset of patients but are under-represented in clinical revascularization trials. Our aim was to investigate clinical outcomes and prognosis predictors after percutaneous coronary intervention (PCI) in this population. Methods Unrestricted consecutive patients with ≥75 years who underwent PCI from 2012 to 2015 were enrolled. The primary ischemic endpoint was the composite of 1-year myocardial infarction, definite/probable stent thrombosis and target vessel revascularization. The primary bleeding endpoint was defined according to the Bleeding Academic Research Consortium (BARC) classification as BARC ≥ 2. Results We enrolled 708 patients (mean age 80 ± 4): 14% were very elderly patients (≥85 years), 27% of patients were diabetic, 23% had chronic kidney disease (CKD), 17% atrial fibrillation and 37% presented acute coronary syndrome. The primary ischemic endpoint was reported in 67 patients (12%): 29 had myocardial infarction (5%), 25 had definite/probable stent thrombosis (4.4%) and 44 had target vessel revascularization (8%). BARC ≥ 2 bleeding was reported in 43 patients (8%). No differences were found in terms of both ischemic and bleeding events between patients with 〈 85 and ≥85 years. Three-vessel disease and use of bare metal stent were independent predictors of the primary ischemic endpoint. Triple antithrombotic therapy and CKD were the only independent predictors of BARC ≥ 2 bleedings. Conclusions In our experience, elderly patients reported reassuring efficacy and safety outcomes after PCI, even if ischemic and bleeding events were frequent. Three-vessel disease and the use of bare metal stent were the only predictors of primary ischemic endpoint. Triple antithrombotic therapy and CKD were the only predictors of BARC ≥ 2 bleedings.
    Type of Medium: Online Resource
    ISSN: 0954-6928
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2042449-8
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  • 7
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 86, No. 3 ( 2000-02-18), p. 312-318
    Abstract: Abstract —Endothelial cells are exposed to an acidotic environment in a variety of pathological and physiological conditions. However, the effect of acidosis on endothelial cell function is still largely unknown, and it was evaluated in the present study. Bovine aortic endothelial cells (BAECs) were grown in bicarbonate buffer equilibrated either with 20% CO 2 (pH 7.0, acidosis) or 5% CO 2 (pH 7.4, control). Acidosis inhibited BAEC proliferation in 10% FCS, whereas by day 7 in serum-free medium, cell number was 3-fold higher in acidotic cells than in control cells. Serum deprivation enhanced BAEC apoptosis, and apoptotic cell death was markedly inhibited by acidosis. Additionally, acidosis inhibited FCS-stimulated migration in a modified Boyden chamber assay and FCS-stimulated differentiation into capillary-like structures on reconstituted basement membrane proteins. Conditioned media from BAECs cultured for 48 hours either at pH 7.0 or pH 7.4 enhanced BAEC proliferation and migration at pH 7.4, and both effects were more marked with conditioned medium from BAECs grown in acidotic than in control conditions. Acidosis enhanced vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) mRNA expression as well as bFGF secretion, and a blocking bFGF antibody inhibited enhanced BAEC migration in response to conditioned medium from acidotic cells. These results show that acidosis protects endothelial cells from apoptosis and inhibits their proangiogenic behavior despite enhanced VEGF and bFGF mRNA expression and bFGF secretion.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 1467838-X
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