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  • Ovid Technologies (Wolters Kluwer Health)  (32)
  • 1
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    Features and Outcomes of Histologically Proven Myocarditis With Fulminant Presentation
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Vol. 146, No. 19 ( 2022-11-08), p. 1425-1433
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 146, No. 19 ( 2022-11-08), p. 1425-1433
    Abstract: Fulminant myocarditis presentation (FMP) is a rare and severe presentation of myocarditis. The natural history of FMP and its clinical features associated with poor outcomes are incompletely understood because there is a lack of generalizable evidence. Methods: This multicenter retrospective cohort study included patients hospitalized with histologically proven myocarditis who underwent catecholamine or mechanical support from 235 cardiovascular training hospitals across Japan between April 2012 and March 2017. Clinical features and the prognostic predictors of death or heart transplantation within 90 days on the basis of clinical and pathologic findings were determined using the Kaplan-Meier method, log-rank test, and Cox regression analysis. Results: This study included 344 patients with histologically proven FMP (median age, 54 years; 40% female). The median follow-up was 600 days (interquartile range, 36 to 1599 days) and the cumulative risk of death or heart transplantation at 90 days was 29% (n=98). Results from multivariable Cox regression analysis showed that older age, nonsinus rhythm, low left ventricular wall motion ( 〈 40%) on admission, and ventricular tachycardia or fibrillation on admission day were associated with worse 90-day survival. Severe histologic damage (damaged cardiomyocytes comprising ≥50% of the total cardiomyocytes) was associated with a worse 90-day prognosis in patients with lymphocytic myocarditis. Conclusions: The results from analyses of data from this multicenter registry demonstrated that patients with FMP are at a higher risk of death or heart transplantation in real-world settings. These observations inform which clinical and pathologic findings may be useful for prognostication in FMP. Registration: URL: https://www.umin.ac.jp/ctr ; Unique identifier: UMIN000039763.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.121.058869
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1466401-X
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  • 2
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    Lowering Uric Acid May Improve Prognosis in Patients With Hyperuricemia and Heart Failure With Preserved Ejection Fraction
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Journal of the American Heart Association Vol. 11, No. 19 ( 2022-10-04)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 11, No. 19 ( 2022-10-04)
    Abstract: An association between uric acid (UA) and cardiovascular diseases, including heart failure (HF), has been reported. However, whether UA is a causal risk factor for HF is controversial. In particular, the prognostic value of lowering UA in patients with HF with preserved ejection fraction (HFpEF) is unclear. Methods and Results We enrolled patients with HFpEF from the PURSUIT‐HFpEF (Prospective Multicenter Observational Study of Patients With Heart Failure With Preserved Ejection Fraction) registry. We investigated whether UA was correlated with the composite events, including all‐cause mortality and HF rehospitalization, in patients with hyperuricemia and HFpEF (UA 〉 7.0 mg/dL). Additionally, we evaluated whether lowering UA for 1 year (≥1.0 mg/dL) in them reduced mortality or HF rehospitalization. We finally analyzed 464 patients with hyperuricemia. In multivariable Cox regression analysis, UA was an independent determinant of composite death and rehospitalization (hazard ratio [HR] , 1.15 [95% CI, 1.03–1.27], P =0.015). We divided them into groups with severe and mild hyperuricemia according to median estimated value of serum UA (8.3 mg/dL). Cox proportional hazards models revealed the incidence of all‐cause mortality was significantly higher in the group with severe hyperuricemia than in the group with mild hyperuricemia (HR, 1.73 [95% CI, 1.19–2.25], P =0.004). The incidence of all‐cause mortality was significantly decreased in the group with lowering UA compared with the group with nonlowering UA (HR, 1.71 [95% CI, 1.02–2.86], P =0.041). The incidence of urate‐lowering therapy tended to be higher in the group with lowering UA than in the group with nonlowering UA (34.9% versus 24.6%, P =0.06). Conclusions UA is a predictor for the composite of all‐cause death and HF rehospitalization in patients with hyperuricemia and HFpEF. In these patients, lowering UA, including the use of urate‐lowering therapy, may improve prognosis.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.122.026301
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2653953-6
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  • 3
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    Cardiovascular Prognosis in Drug-Resistant Hypertension Stratified by 24-Hour Ambulatory Blood Pressure: The JAMP Study
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Hypertension Vol. 78, No. 6 ( 2021-12), p. 1781-1790
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 78, No. 6 ( 2021-12), p. 1781-1790
    Abstract: Resistant hypertension is an important cardiovascular risk factor. This analysis of the JAMP study (Japan Ambulatory Blood Pressure Monitoring Prospective) data investigated the effects of uncontrolled resistant hypertension diagnosed using ambulatory blood pressure (BP) monitoring on the risk of heart failure (HF) and overall cardiovascular events. The JAMP study patients with hypertension and no HF history were included. They had true resistant hypertension (24-hour BP ≥130/80 mm Hg), pseudoresistant hypertension (24-hour BP 〈 130/80 mm Hg), well-controlled nonresistant hypertension (24-hour BP 〈 130/80 mm Hg), or uncontrolled nonresistant hypertension (24-hour BP ≥130/80 mm Hg). The primary end point was total cardiovascular events, including atherosclerotic cardiovascular disease (fatal/nonfatal stroke and fatal/nonfatal coronary artery disease), and HF. During 4.5±2.4 years of follow-up the overall incidence per 1000 person-years was 10.1 for total cardiovascular disease, 4.1 for stroke, 3.5 for coronary artery disease, and 2.6 for HF. The adjusted risk of total cardiovascular and HF events was significantly increased in patients with true resistant versus controlled nonresistant hypertension (hazard ratio, 1.66 [95% CI, 1.12–2.48] ; P =0.012 and 2.24 [95% CI, 1.17–4.30]; P =0.015, respectively) and versus uncontrolled nonresistant hypertension (1.51 [1.03–2.20]; P =0.034 and 3.03 [1.58–5.83]; P 〈 0.001, respectively). The findings were robust in a sensitivity analysis using a slightly different definition of resistant hypertension. True resistant hypertension diagnosed using ambulatory BP monitoring is a significant independent risk factor for cardiovascular disease events, especially for HF. This highlights the importance of diagnosing and effectively treating resistant hypertension. Registration: URL: https://www.umin.ac.jp/ctr ; Unique identifier: UMIN000020377.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.121.18198
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2094210-2
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  • 4
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    Abstract 1211: Hif-1α In T Cells Pathway Plays A Crucial Role In The Progression Of Arteriosclerosis And Artery Intimal Thickening
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Vol. 116, No. suppl_16 ( 2007-10-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 116, No. suppl_16 ( 2007-10-16)
    Abstract: Background and Objective T cell-mediated inflammatory process is involved in arteriosclerosis and vascular remodeling. Hypoxia-inducible factor-1 (HIF-1) is a transcription factor and regulates the gene expressions in response to hypoxia in order to maintain physiological oxygen homeostasis. In the previous annual meeting, we showed that arterial cuff injury caused prominent neointimal and adventitial hyperplasia in Hif-1α-deficient mice compared to that of the control mice. The object of the present study is to reveal how the function of HIF-1α in T cells contributes to the vascular remodeling. Methods and Results T cell-specific Hif-1α-deficient mice were generated using a Cre-LoxP technology. Vascular remodeling was characterized 4 weeks after femoral arterial injury induced by an external vascular polyethylene cuff model. Morphological and histological studies showed that the cuff placement caused prominent neointimal and adventitial hyperplasia in Hif-1α-deficient mice compared to that of the control mice, and that infiltration of mononuclear cells at the adventitia was remarkably increased in the mutant mice. Hif-1α-deficient T cells were normally generated in the thymus and their distribution in the spleen and lymph nodes was unimpaired. However, number of peripheral Hif-1α-deficient T cells was significantly increased compared to the control. In the in vitro culture condition, Hif-1α-deficient T cells exhibited significant more increases of IL2 production and proliferation upon stimulation with anti-CD3/anti-CD28 antibodies compared to the controls. In addition, productions of 2,4,6-trinitrophenol (TNP)-KLH antigen-specific antibodies, including IgG1, IgG2b and IgG2c, were more enhanced in the mutant mice after stimulation of the antigen. Conclusions HIF-1α in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury, serving as a negative regulator of T cell-mediated immune response.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.116.suppl_16.II_246
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
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  • 5
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    Abstract 4203: Diastolic Wall Strain Can Noninvasively Predict Hemodynamic Deterioration Unassociated with Systolic Dysfunction in Hypertensive Hearts
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Abstract: This study examined whether LV diastolic wall strain (DWS) could noninvasively predict the transition to decompensated diastolic heart failure (DHF) in hypertensive hearts. Dahl salt-sensitive rats fed 0.3 % NaCl diet served as control group (group N: n=8) and those fed 8 % NaCl diet as hypertensive group (group HT: n=15). Serial Doppler echocardiographic studies were performed at age 13, 17 and 19 weeks. At 19 weeks, LV pressure was measured following the echocardiographic study. DWS was calculated as [(end-systolic thickness of LV posterior wall) - (end-diastolic thickness of LV posterior wall)]/(end-systolic thickness of LV posterior wall). Mid-wall fractional shortening (MFS) was not different between two groups at any stage. At 13 weeks (compensatory hypertrophic stage), the transmitral flow velocity curves (TMFV) represented the abnormal relaxation pattern with low E/A ratio in group HT. At 19 weeks (heart failure stage), E/A increased with the elevation of LV end-diastolic pressure and lung weight in group HT. DWS was not different between two groups at 13 weeks, however, its decrease preceded the pseudonormalization of TMFV at 17 weeks in group HT and continued until 19 weeks. The difference between the endocardial and epicardial movements is equal to that between the wall thickness at end-systole and end-diastole (a numerator of DWS). Therefore, based on the linear elastic theory, DWS is considered to decrease with increase of LV wall stiffness. We previously demonstrated that myocardial stiffness constant was elevated at age 17 weeks but not at age 13 weeks in Dahl salt-sensitive rats fed high-salt diet. The current results indicate that DWS is helpful in noninvasively predicting hemodynamic deterioration without the changes in systolic function, which is explained partly by the theory that DWS reflects LV wall stiffness. Echocardiographic Parameters and Hemodynamic Data in Control Group and Hypertensive Group
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_842-b
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
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  • 6
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    L-Carnitine prevents the development of ventricular fibrosis and heart failure with preserved ejection fraction in hypertensive heart disease
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Journal of Hypertension Vol. 30, No. 9 ( 2012-09), p. 1834-1844
    Details
    In: Journal of Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 30, No. 9 ( 2012-09), p. 1834-1844
    Type of Medium: Online Resource
    ISSN: 0263-6352
    URL: Article
    DOI: 10.1097/HJH.0b013e3283569c5a
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2017684-3
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  • 7
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    Abstract 313: Protective Effects of Iron-Restricted Food against Diabetic Nephropathy in db/db Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Hypertension Vol. 60, No. suppl_1 ( 2012-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 60, No. suppl_1 ( 2012-09)
    Abstract: Background: Iron, an essential trace metal for organisms, catalyzes highly toxic hydroxyl radical via Fenton/Haber-Weiss reaction. We recently have clarified that iron chelation prevents the development of adipocyte hypertrophy through the reduction of oxidative stress in diabetic obese mice. It is suggested that iron reduction potentiates to be beneficial effects against diabetic complications. In the present study, we investigated the protective action of iron restriction against the progression of diabetic nephropathy. METHODS: We employed and divided male db/db mice of 8 weeks old age, a model of diabetic nephropathy, into 2 groups, normal diet group (Fe 100mg/kg food; ND) and low iron diet group (Fe 10mg/kg food; LID). After 8 weeks treatment, the mice were used for analysis. Results: LID group showed the decreased renal iron content (7.5±3.0 μg/g tissue vs 5.7±0.3 μg/g tissue, ND vs LID, p 〈 0.05), serum iron concentration (213±15 μg/dL vs 157±14 μg/dL, ND vs LID, p 〈 0.05) and hemoglobin level (13.5±0.7g/dL vs 10.4±0.5g/dL, ND vs LID, p 〈 0.01). Urinary albumin excretion was significantly decreased in LID group compared to ND group (2.6±0.4mg/g·Cre vs 1.4±0.3mg/g·Cre, ND vs LID, p 〈 0.05). In histological analysis, mesangial proliferation was ameliorated in db/db mice with LID (39% vs 28%, ND vs LID, p 〈 0.05). LID reduced the deposition of collagen IV, fibronectin and desmin by 61%, 60%, and 42%, respectively, in glomeruli of db/db mice. Superoxide production, p22phox and NOX4 expression were also diminished in kidney of LID group. Conclusion: Iron restriction is suggested to prevent the development of diabetic nephropathy through the suppression of oxidative stress.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.60.suppl_1.A313
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
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  • 8
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    Abstract 371: Nitrosonifedipine, a Photodegradation Product of Nifedipine, Prevents the Progression of Diabetic Nephropathy in Type II Diabetic Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Hypertension Vol. 60, No. suppl_1 ( 2012-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 60, No. suppl_1 ( 2012-09)
    Abstract: Diabetic nephropathy (DN) is a major microvascular complication of diabetes involving oxidative stress and endothelial damage. Nitrosonifedipine (NO-NIF) is converted from nifedipine under the light illumination. The ability of NO-NIF to block calcium channels is quite weak compared with that of nifedipine. Recently, we have demonstrated that NO-NIF reacts with unsaturated fatty acid leading to generate NO-NIF radical, which acquires radical scavenging activity. Also we have reported that NO-NIF reduces cytotoxicity of tumor necrosis factor-α (TNF-α) in cultured human glomerular endothelial cells. However, it is unclear the effects of NO-NIF on the pathogenesis related with oxidative stress, such as DN. In this study, we investigated whether NO-NIF treatment improves DN by using KKAy mice developing type II diabetes. Urinary albumin (UA) and total urinary protein (TUP) were elevated in KKAy mice (16 weeks old) compared with C57BL/6 mice, which were significantly decreased by NO-NIF treatment (30 mg/kg/day, i.p., 4 weeks) (UA; 1415.2 ± 312.5 vs 609.6 ± 151.5 μg/24hr, p 〈 0.05, TUP; 73.1 ± 11.2 vs 44.8 ± 9.4 mg/24hr, p 〈 0.05). Mesangial expansion was estimated by PAS staining. Glomerular diameter (GD) and glomerular tuft area (GTA) were extended in KKAy mice compared with C57BL/6 mice, which were significantly decreased by NO-NIF treatment (GD; 81.4 ± 2.6 vs 65.7 ± 1.9 μm, p 〈 0.05, GTA; 4198.8 ± 254.6 vs 3051.9 ± 140.4 μm2, p 〈 0.05). NO-NIF significantly suppressed urinary 8-hydroxy-20-deoxyguanosine (144.1 ± 21.4 vs 75.2 ± 11.1 ng/24hr, p 〈 0.05) in KKAy mice. Also NO-NIF reduced the elevation of reactive oxygen species in kidney of KKAy mice detected by DHE staining. However NO-NIF had no influence on SOD activity in kidney. NO-NIF significantly inhibited the mRNA expression of TNF-α in kidney of KKAy mice (2.9 ± 0.1 vs 1.9 ± 0.1 fold increase, p 〈 0.05). ICAM-1 protein expression was increased in glomeruli of KKAy mice, which was decreased by NO-NIF treatment. On the other hand, NO-NIF had no effect on glucose tolerance and systolic blood pressure (111.1 ± 2.3 vs 108.3 ± 3.3 mmHg, N.S.) in KKAy mice. These findings suggest that NO-NIF prevents the progression of DN via the attenuation of oxidative stress independent of antihypertensive or antihyperglycemic action.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.60.suppl_1.A371
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
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  • 9
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    Effects of calcium and ouabain on the release of atrial natriuretic factor
    Ovid Technologies (Wolters Kluwer Health) ; 1988
    In:  Journal of Hypertension Vol. 6, No. 4 ( 1988-12), p. 317-319
    Details
    In: Journal of Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 4 ( 1988-12), p. 317-319
    Type of Medium: Online Resource
    ISSN: 0263-6352
    URL: Article
    DOI: 10.1097/00004872-198812040-00098
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1988
    detail.hit.zdb_id: 2017684-3
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  • 10
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    Assessment of the Family History of Patients With Ulcerative Colitis at a Single Center in Japan
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Journal of Pediatric Gastroenterology & Nutrition Vol. 63, No. 5 ( 2016-11), p. 512-515
    Details
    In: Journal of Pediatric Gastroenterology & Nutrition, Ovid Technologies (Wolters Kluwer Health), Vol. 63, No. 5 ( 2016-11), p. 512-515
    Abstract: The prevalence of ulcerative colitis (UC) differs by country, which is likely due to differences in genetic factors among ethnicities. Moreover, the prevalence of pediatric UC with a family history (FH) is 4.1% in Japanese patients; its clinical course begins at an early age and is more severe. Recently, a genome-wide association study identified 3 new susceptibility loci for adult Japanese patients with UC. Methods: To assess the effects of FH in patients with UC, 60 children were enrolled. Age at diagnosis, clinical features of the initial symptoms, and family structure were assessed in patients with and without an FH. The 3 new loci were examined in patients who provided informed consent. Results: Of the patients with UC, 10 (16.7%) had an FH involving first-degree relatives, including 7 mothers, 1 father, and 2 sisters. There was a trend toward a younger age at onset in the positive FH group. There were, however, no significant differences in the clinical characteristics of the patients regardless of FH. From the genomic analyses, there were significant differences in the polymorphisms of the solute carrier family 26, member 3 (SLC26A3) between those with and without an FH. Conclusions: Although the etiology of UC remains unknown, there were no observed relation between clinical symptoms and FH. SLC26A3 may, however, contribute to the pathogenesis of UC in Japanese individuals with an FH.
    Type of Medium: Online Resource
    ISSN: 0277-2116 , 1536-4801
    URL: Article
    DOI: 10.1097/MPG.0000000000001275
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2078835-6
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