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  • Ovid Technologies (Wolters Kluwer Health)  (18)
Materialart
Verlag/Herausgeber
  • Ovid Technologies (Wolters Kluwer Health)  (18)
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Erscheinungszeitraum
Fachgebiete(RVK)
  • 11
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 47, No. 10 ( 2016-10), p. 2582-2588
    Kurzfassung: The discrimination between paroxysmal and sustained (persistent or permanent) atrial fibrillation (AF) has not been considered in the approach to secondary stroke prevention. We aimed to assess the differences in clinical outcomes between mostly anticoagulated patients with sustained and paroxysmal AF who had previous ischemic stroke or transient ischemic attack. Methods— Using data from 1192 nonvalvular AF patients with acute ischemic stroke or transient ischemic attack who were registered in the SAMURAI-NVAF study (Stroke Management With Urgent Risk-Factor Assessment and Improvement-Nonvalvular AF; a prospective, multicenter, observational study), we divided patients into those with paroxysmal AF and those with sustained AF. We compared clinical outcomes between the 2 groups. Results— The median follow-up period was 1.8 (interquartile range, 0.93–2.0) years. Of the 1192 patients, 758 (336 women; 77.9±9.9 years old) and 434 (191 women; 77.3±10.0 years old) were assigned to the sustained AF group and paroxysmal AF groups, respectively. After adjusting for sex, age, previous anticoagulation, and initial National Institutes of Health Stroke Scale score, sustained AF was negatively associated with 3-month independence (multivariable-adjusted odds ratio, 0.61; 95% confidence interval, 0.43–0.87; P =0.006). The annual rate of stroke or systemic embolism was 8.3 and 4.6 per 100 person-years, respectively (multivariable-adjusted hazard ratio, 1.95; 95% confidence interval, 1.26–3.14) and that of major bleeding events was 3.4 and 3.1, respectively (hazard ratio, 1.13; 95% confidence interval, 0.63–2.08). Conclusions— Among patients with previous ischemic stroke or transient ischemic attack, those with sustained AF had a higher risk of stroke or systemic embolism compared with those with paroxysmal AF. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01581502.
    Materialart: Online-Ressource
    ISSN: 0039-2499 , 1524-4628
    RVK:
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2016
    ZDB Id: 1467823-8
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 12
    Online-Ressource
    Online-Ressource
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Hypertension Vol. 41, No. 3 ( 2003-03), p. 512-518
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 41, No. 3 ( 2003-03), p. 512-518
    Kurzfassung: We investigated whether adrenomedullin (AM) participates in the pathophysiology during the transition from left ventricular hypertrophy (LVH) to heart failure (HF). We used the Dahl salt-sensitive (DS) rat model, in which systemic hypertension causes LVH at the age of 11 weeks, followed by HF at the age of 18 weeks. Two molecular forms of AM levels in the plasma and myocardium at the LVH stage were significantly elevated compared with those in controls, and they were further increased at the HF stage. Interestingly, the LV tissue AM-mature/AM-total ratio was higher only in the HF group than in controls and LVH. The LV tissue AM-mature/AM-total ratio, AM-mature, and AM-total concentrations had close relations with the LV weight/body weight ( r =0.72, r =0.79, and r =0.70, respectively; all P 〈 0.001). AM gene expression was significantly increased at the LVH stage and was further increased at the HF stage. Furthermore, gene expression of AM receptor system components such as calcitonin receptor–like receptor (CRLR), receptor activity–modified protein 2 (RAMP2), and RAMP3 were significantly increased at the stage of LVH and HF. Regarding other neurohumoral factors, plasma renin and aldosterone levels were not increased at the LVH stage but were increased at the HF stage, whereas atrial natriuretic peptide was increased in both the plasma and myocardium at the LVH stage and was further increased at the HF stage. These results suggest that induction of the cardiac AM system, including the ligand, receptor, and amidating activity, may modulate pathophysiology during the transition from LVH to HF in this model.
    Materialart: Online-Ressource
    ISSN: 0194-911X , 1524-4563
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2003
    ZDB Id: 2094210-2
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 13
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 8, No. 3 ( 2019-02-05)
    Kurzfassung: We aimed to clarify associations between prior anticoagulation and short‐ or long‐term clinical outcomes in ischemic stroke or transient ischemic attack patients with nonvalvular atrial fibrillation. Methods and Results A total of 1189 ischemic stroke or transient ischemic attack patients with nonvalvular atrial fibrillation who were hospitalized within 7 days after onset were analyzed. Of these, 813 patients (68.4%) received no prior anticoagulation, 310 (26.1%) received prior warfarin treatment with an international normalized ratio ( INR ) 〈 2 on admission, 28 (2.4%) received prior warfarin treatment with an INR ≥2 on admission, and the remaining 38 (3.2%) received prior direct oral anticoagulant treatment. Prior warfarin treatment was associated with a lower risk of death or disability at 3 months compared with no prior anticoagulation ( INR 〈 2: adjusted odds ratio: 0.58; 95% CI, 0.42–0.81; P =0.001; INR ≥2: adjusted odds ratio: 0.40; 95% CI, 0.16–0.97; P =0.043) but was not associated with a lower risk of death or disability at 2 years. Prior warfarin treatment with an INR ≥2 on admission was associated with a higher risk of ischemic events within 2 years compared with no prior anticoagulation (adjusted hazard ratio: 2.94; 95% CI, 1.20–6.15; P =0.021). Conclusions Prior warfarin treatment was associated with a lower risk of death or disability at 3 months but was not associated with a lower risk of death or disability at 2 years in ischemic stroke or transient ischemic attack patients with nonvalvular atrial fibrillation. Prior warfarin treatment with an INR ≥2 on admission was associated with a higher risk of ischemic events within 2 years. Clinical Trial Registration URL : http://www.clinicaltrials.gov . Unique identifier: NCT 01581502.
    Materialart: Online-Ressource
    ISSN: 2047-9980
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2019
    ZDB Id: 2653953-6
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 14
    Online-Ressource
    Online-Ressource
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Journal of Hypertension Vol. 22, No. 9 ( 2004-09), p. 1787-1796
    In: Journal of Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 22, No. 9 ( 2004-09), p. 1787-1796
    Materialart: Online-Ressource
    ISSN: 0263-6352
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2004
    ZDB Id: 2017684-3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 15
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 8, No. 15 ( 2019-08-06)
    Kurzfassung: The aim of the present study was to investigate the efficacy and safety of antiplatelet (aspirin plus cilostazol) dual therapy for patients with noncardioembolic stroke within 48 hours of symptom onset. Methods and Results The ADS (Acute Aspirin Plus Cilostazol Dual Therapy for Non‐Cardiogenic Stroke Patients Within 48 Hours of Symptom Onset ) study is an investigator‐initiated, prospective, multicenter (34 hospitals in Japan), randomized, open‐label, and aspirin‐controlled trial. Acute stroke patients with noncardioembolic stroke within 48 hours of onset were studied. The subjects were randomly allocated to combination therapy with aspirin 81 to 200 mg plus cilostazol 200 mg (dual group) and single therapy with aspirin 81 to 200 mg (aspirin group) for 14 days. After the 14 days, all patients took the cilostazol 200 mg for 3 months. A primary efficacy outcome was defined as any one of the following occurring (neurological deterioration, symptomatic stroke recurrence, or transient ischemic attack) within 14 days. A primary safety outcome included intracerebral hemorrhage and subarachnoid hemorrhage. Between May 2011 and June 2017, 1201 patients (796 [66%] men; median age, 69 [61–77] years) randomized 1:1 to either the dual group or the aspirin group were analyzed. Initial National Institutes of Health Stroke Scale score was 2 (1–4) in both groups ( P =0.830). A primary efficacy outcome was observed in 11% in the dual group and 11% in the aspirin group ( P =0.853). A primary safety outcome occurred in 2 (0.3%) in the dual group and in 1 (0.2%) in the aspirin group ( P =0.624). Conclusions Dual antiplatelet therapy using cilostazol and aspirin was safe but did not reduce the rate of short‐term neurological worsening. Clinical Trial Registration URL : umin.ac.jp/ctr/index/htm. Unique identifier: UMIN 000004950.
    Materialart: Online-Ressource
    ISSN: 2047-9980
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2019
    ZDB Id: 2653953-6
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 16
    Online-Ressource
    Online-Ressource
    Ovid Technologies (Wolters Kluwer Health) ; 2006
    In:  Hypertension Vol. 47, No. 2 ( 2006-02), p. 265-270
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 47, No. 2 ( 2006-02), p. 265-270
    Kurzfassung: AMP-activated kinase (AMPK) is a highly conserved heterotrimeric kinase that functions as a metabolic regulator of cellular enzymes involved in carbohydrate and fat metabolism, which regulate ATP conservation and synthesis. Here, we investigated whether AMPK signaling has a role in the regulation of angiotensin II (Ang II)–induced proliferation in rat cardiac fibroblasts. Aminoimidazole-4-carboxamide-1-β-ribofuranoside (AICAR) activated AMPK in rat cardiac fibroblasts and increased Ang II–induced extracellular signal–regulated kinase 1/2 phosphorylation and activity. AICAR also increased Ang II–induced c-fos mRNA expression in the cells. [ 3 H]-thymidine and [ 3 H]-proline incorporation by cardiac fibroblasts treated with Ang II was enhanced when the cells were pretreated with AICAR. Inhibition of AMPK by small interfering RNA for AMPKα1 suppressed Ang II–induced extracellular signal–regulated kinase activity, c-fos mRNA expression, and cell proliferation. Treatment of rats with AICAR (1 mg/g body weight per day) for 1 week significantly enhanced Ang II–induced hypertrophy of the myocardium. Our findings indicate that AMPK works as a stimulator of the Ang II–induced proliferative pathway in cardiac fibroblasts. Inhibition of AMPK signaling might serve as a new therapeutic target of remodeling of the hypertrophic myocardium.
    Materialart: Online-Ressource
    ISSN: 0194-911X , 1524-4563
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2006
    ZDB Id: 2094210-2
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 17
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 42, No. 5 ( 2003-11), p. 1034-1041
    Kurzfassung: Acute administration of adrenomedullin (AM) exerts beneficial hemodynamic, renal, and neurohormonal effects in heart failure (HF). However, chronic effects of AM administration on HF remain unknown. This study sought to examine the effect of chronic infusion of AM on progression of HF in rat. Human recombinant AM was administered by osmotic minipump for 7 weeks in the HF model of Dahl salt-sensitive rats. The effect was compared with vehicle and diuretic treatment group. Chronic AM infusion significantly decreased left ventricular end-diastolic pressure, right ventricular systolic pressure, right atrial pressure, and left ventricular weight/body weight ( P 〈 0.01 for all). AM significantly attenuated the increase in circulating renin-aldosterone, endogenous rat AM, and atrial natriuretic peptide levels ( P 〈 0.01 for all). AM also inhibited the myocardial tissue levels of angiotensin II and atrial and brain natriuretic peptide ( P 〈 0.01 for all). These changes were associated with the improvement of cardiac output and systemic vascular resistance (both P 〈 0.05). Furthermore, AM improved left ventricular end-systolic elastance ( P 〈 0.01). These improvements were greater in the AM than in the diuretic group, although both drugs similarly decreased systolic blood pressure and increased urinary sodium excretion. Kaplan-Meier survival analysis showed that AM significantly prolonged survival time compared with diuretic ( P 〈 0.05) and vehicle ( P 〈 0.01) treatment groups. These results suggest that endogenous AM plays a compensatory role in HF and that chronic AM infusion attenuates progression of left ventricular dysfunction and improves survival, at least in part, through inhibition of circulating and myocardial neurohormonal activation.
    Materialart: Online-Ressource
    ISSN: 0194-911X , 1524-4563
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2003
    ZDB Id: 2094210-2
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 18
    Online-Ressource
    Online-Ressource
    Ovid Technologies (Wolters Kluwer Health) ; 2002
    In:  Hypertension Vol. 39, No. 6 ( 2002-06), p. 1077-1082
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 39, No. 6 ( 2002-06), p. 1077-1082
    Kurzfassung: The present study was designed to examine whether chronic adrenomedullin infusion has renoprotective effects in hypertensive renal failure and the mechanism by which chronic adrenomedullin infusion exerts its effects. Dahl salt-sensitive rats and Dahl salt-resistant rats were fed a high salt diet starting at 6 weeks of age. Recombinant human adrenomedullin or vehicle was infused for 7 weeks in 11-week-old Dahl salt-sensitive rats. Dahl salt-resistant rat was used as a control. After 7 weeks, untreated Dahl salt-sensitive rats were characterized by decreased kidney function, abnormal morphological findings, increased hormone levels, increased renal tissue angiotensin II levels, and altered mRNA expressions of transforming growth factor β (TGF-β) and components of the renin-angiotensin system compared with Dahl salt-resistant rats. Chronic adrenomedullin treatment significantly improved renal function (serum creatinine −87%, creatinine clearance +114%, urinary protein excretion −59%) and histological findings (glomerular injury score −54%) without changing mean arterial pressure compared with untreated Dahl salt-sensitive rats. Interestingly, long-term human adrenomedullin infusion decreased the endogenous rat adrenomedullin level (−97%) with a slight increase of human adrenomedullin level. Chronic adrenomedullin treatment also significantly inhibited the increase of plasma renin concentration (−269%), aldosterone level (−82%), and renal tissue angiotensin II levels (−60%). Furthermore, adrenomedullin infusion significantly decreased the increases of mRNA expressions of TGF-β (− 63%), angiotensin-converting enzyme (−137%), renin (−230%), and angiotensinogen (−38%) in renal cortex. These results suggest that increased endogenous adrenomedullin plays a compensatory role in chronic hypertensive renal failure and that long-term adrenomedullin infusion has renoprotective effects in this type of hypertension model, partly via inhibition of the circulating and renal renin-angiotensin system.
    Materialart: Online-Ressource
    ISSN: 0194-911X , 1524-4563
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2002
    ZDB Id: 2094210-2
    Standort Signatur Einschränkungen Verfügbarkeit
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