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  • Ovid Technologies (Wolters Kluwer Health)  (14)
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  • 1
    Online Resource
    Online Resource
    Severe coronary artery spasm can be associated with hyperthyroidism
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Coronary Artery Disease Vol. 16, No. 3 ( 2005-05), p. 135-139
    Details
    In: Coronary Artery Disease, Ovid Technologies (Wolters Kluwer Health), Vol. 16, No. 3 ( 2005-05), p. 135-139
    Type of Medium: Online Resource
    ISSN: 0954-6928
    URL: Article
    DOI: 10.1097/00019501-200505000-00001
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 2042449-8
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  • 2
    Online Resource
    Online Resource
    Comparative Effects of Diet and Statin on NO Bioactivity and Matrix Metalloproteinases in Hypercholesterolemic Patients With Coronary Artery Disease
    Ovid Technologies (Wolters Kluwer Health) ; 2002
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 22, No. 9 ( 2002-09)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 22, No. 9 ( 2002-09)
    Abstract: Objective— We investigated the effects of statin compared with the American Heart Association (AHA) Step I Diet on lipoproteins, vasomotor function, tumor necrosis factor (TNF)-α, and serological markers of plaque stability. Furthermore, we investigated the mechanism of regulation suggested by experimental studies. Methods and Results— For 14 weeks, we administered AHA diet+placebo and AHA diet+simvastatin (20 mg daily) to 31 and 32 randomly selected patients with coronary artery disease, respectively. Compared with diet alone, simvastatin significantly improved the percent flow-mediated dilator response to hyperemia from 3.37±2.28% to 5.89±2.35% ( P 〈 0.001) and lowered plasma levels of C-reactive protein from 0.48 to 0.10 mg/dL ( P 〈 0.001), TNF-α from 3.38 to 2.79 pg/mL ( P 〈 0.001), total matrix metalloproteinase (MMP)-9 from 36 to 28 ng/mL ( P =0.006), and tissue inhibitor of matrix metalloproteinase-1 from 80±30 to 74±23 ng/mL ( P =0.041), and simvastatin lowered to a greater extent MMP-9 activity (from 71 to 52 ng/mL, P =0.006) and MMP-9 activity/tissue inhibitor of matrix metalloproteinase-1 ratios ( P =0.018), although this difference did not reach statistical significance. There were significant correlations between the degree of changes in TNF-α and the degree of changes in MMP-9 activity ( r =0.424, P =0.016). However, no significant correlations between lipoprotein levels or flow-mediated dilation percentages and levels of plaque stability markers were determined (−0.208≤ r ≤0.243). Conclusions— Simvastatin reduced serological markers of inflammation and plaque stability, independent of lipoprotein changes.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/01.ATV.0000030997.02059.BB
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2002
    detail.hit.zdb_id: 1494427-3
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  • 3
    Online Resource
    Online Resource
    Circulating S‐Glutathionylated cMyBP‐C as a Biomarker for Cardiac Diastolic Dysfunction
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Journal of the American Heart Association Vol. 11, No. 11 ( 2022-06-07)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 11, No. 11 ( 2022-06-07)
    Abstract: cMyBP‐C (Cardiac myosin binding protein‐C) regulates cardiac contraction and relaxation. Previously, we demonstrated that elevated myocardial S‐glutathionylation of cMyBP‐C correlates with diastolic dysfunction (DD) in animal models. In this study, we tested whether circulating S‐glutathionylated cMyBP‐C would be a biomarker for DD. Methods and Results Humans, African Green monkeys, and mice had DD determined by echocardiography. Blood samples were acquired and analyzed for S‐glutathionylated cMyBP‐C by immunoprecipitation. Circulating S‐glutathionylated cMyBP‐C in human participants with DD (n=24) was elevated (1.46±0.13‐fold, P =0.014) when compared with the non‐DD controls (n=13). Similarly, circulating S‐glutathionylated cMyBP‐C was upregulated by 2.13±0.47‐fold ( P =0.047) in DD monkeys (n=6), and by 1.49 (1.22–2.06)‐fold ( P =0.031) in DD mice (n=5) compared with the respective non‐DD controls. Circulating S‐glutathionylated cMyBP‐C was positively correlated with DD in humans. Conclusions Circulating S‐glutathionylated cMyBP‐C was elevated in humans, monkeys, and mice with DD. S‐glutathionylated cMyBP‐C may represent a novel biomarker for the presence of DD.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.122.025295
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2653953-6
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  • 4
    Online Resource
    Online Resource
    Abstract 540: Magnesium Improves Cardiac Diastolic Function by Modulating Mitochondria
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Circulation Research Vol. 123, No. Suppl_1 ( 2018-08-03)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 123, No. Suppl_1 ( 2018-08-03)
    Abstract: Rationale: A diet rich in saturated fat has been found to induce diabetes mellitus (DM) accompanied by myocardial mitochondrial dysfunction, insulin resistance, and magnesium (Mg) deficiency. The most prominent characteristic of diabetic cardiomyopathy is cardiac diastolic dysfunction (DD). Mg supplementation improves the heart rate variability and arterial elasticity in chronic heart failure. Recently, we have reported that mitochondrial reactive oxygen species (mitoROS) play a critical role in the progress of DD and diastolic heart failure. Therefore, we hypothesized that Mg supplementation would benefit diastolic function by improving mitochondrial function. Methods and Results: High fat diet (HFD)-induced diabetic mouse hearts showed cardiac DD with increased E/e’ (45±2 in DM mice vs. 32±2 in control mice), increased left ventricular diastolic volume (LVDV, 80±1 μL in DM vs. 61±4 μL in control), and increased incidence of DD (9 of 10 mice in DM vs 1 of 10 mice in control; P 〈 0.05 for all). DM mice also showed decreased plasma Mg concentration (0.80±0.04 mmol/L in DM vs. 0.98±0.03 mmol/L in control, P 〈 0.05). Ventricular cardiomyocytes isolated from DM mice exhibited decreased mitochondrial ATP production (75±11% of control), a 1.7±0.2-fold increase in mitoROS, significantly depolarized mitochondrial membrane potential, and mitochondrial Ca 2+ overload (3.7±1.3-fold; P 〈 0.05 vs. control for all). Dietary Mg administration (50 mg/mL, ≈6-8 g/kg/day) for 6 weeks corrected all these parameters with increased plasma Mg concentration (1.5±0.1 mmol/L), improved cardiac diastolic function (E/e’ 37±1; LVDV 54±5 μL; LVPWT 0.77±0.02 mm; the incidence of DD, 2 of 10 mice; P 〈 0.05 vs. DM for all). Mitochondrial function was improved significantly by Mg with increased ATP production, decreased mitoROS, repolarized mitochondrial membrane potential, and decreased mitochondrial Ca 2+ overload in DM mice. Conclusion: These results indicate that Mg supplementation improved mitochondrial function, reduced oxidative stress, and prevented diastolic dysfunction in DM.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.123.suppl_1.540
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 1467838-X
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  • 5
    Online Resource
    Online Resource
    Ranolazine Improves Cardiac Diastolic Dysfunction Through Modulation of Myofilament Calcium Sensitivity
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Research Vol. 110, No. 6 ( 2012-03-16), p. 841-850
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 110, No. 6 ( 2012-03-16), p. 841-850
    Abstract: Previously, we demonstrated that a deoxycorticosterone acetate (DOCA)-salt hypertensive mouse model produces cardiac oxidative stress and diastolic dysfunction with preserved systolic function. Oxidative stress has been shown to increase late inward sodium current (I Na ), reducing the net cytosolic Ca 2+ efflux. Objective: Oxidative stress in the DOCA-salt model may increase late I Na , resulting in diastolic dysfunction amenable to treatment with ranolazine. Methods and Results: Echocardiography detected evidence of diastolic dysfunction in hypertensive mice that improved after treatment with ranolazine (E/E′:sham, 31.9±2.8, sham+ranolazine, 30.2±1.9, DOCA-salt, 41.8±2.6, and DOCA-salt+ranolazine, 31.9±2.6; P =0.018). The end-diastolic pressure-volume relationship slope was elevated in DOCA-salt mice, improving to sham levels with treatment (sham, 0.16±0.01 versus sham+ranolazine, 0.18±0.01 versus DOCA-salt, 0.23±0.2 versus DOCA-salt+ranolazine, 0.17±0.0 1 mm Hg/L; P 〈 0.005). DOCA-salt myocytes demonstrated impaired relaxation, τ, improving with ranolazine (DOCA-salt, 0.18±0.02, DOCA-salt+ranolazine, 0.13±0.01, sham, 0.11±0.01, sham+ranolazine, 0.09±0.02 seconds; P =0.0004). Neither late I Na nor the Ca 2+ transients were different from sham myocytes. Detergent extracted fiber bundles from DOCA-salt hearts demonstrated increased myofilament response to Ca 2+ with glutathionylation of myosin binding protein C. Treatment with ranolazine ameliorated the Ca 2+ response and cross-bridge kinetics. Conclusions: Diastolic dysfunction could be reversed by ranolazine, probably resulting from a direct effect on myofilaments, indicating that cardiac oxidative stress may mediate diastolic dysfunction through altering the contractile apparatus.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.111.258251
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 1467838-X
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  • 6
    Online Resource
    Online Resource
    A0407 Astragaloside IV Reduces Cardiac Oxidation and Improves Left Ventricular Diastolic Dysfunction
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Journal of Hypertension Vol. 36 ( 2018-10), p. e5-
    Details
    In: Journal of Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36 ( 2018-10), p. e5-
    Type of Medium: Online Resource
    ISSN: 0263-6352
    URL: Article
    DOI: 10.1097/01.hjh.0000548005.87380.b3
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2017684-3
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  • 7
    Online Resource
    Online Resource
    Abstract 11400: Circulating Glutathionylated Cardiac Myosin Binding Protein C as a Diagnostic Biomarker for Diastolic Dysfunction
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 144, No. Suppl_1 ( 2021-11-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 144, No. Suppl_1 ( 2021-11-16)
    Abstract: Introduction: Cardiac myosin binding protein-C (cMyBP-C) is a thick filament-associated protein localized to the crossbridge-containing C zones of striated muscle sarcomeres, contributing to regulate cardiac contraction and relaxation. Phosphorylation status of cMyBP-C determines cardiac function, and S-glutathionylation of cMyBP-C is increased in human heart failure (HF). In animal models, we demonstrated that elevated S-glutathionylation of cMyBP-C but not phosphorylation correlates with diastolic dysfunction (DD). Hypothesis: S-glutathionylated cMyBP-C would be a biomarker for DD. Methods: Humans, African Green monkeys, and mice with DD determined by echocardiography (E/e’ ratio 〉 X) were matched by age and gender to controls. Blood samples were acquired and analyzed for S-glutathionylated cMyBP-C by immunoblotting. Results: Circulating S-glutathionylated cMyBP-C in DD patients (N=28) was elevated (fold, 1.57± 0.12, P 〈 0.01, t-test) when compared to controls (N=16). We confirmed these results in mice and monkeys with DD demonstrated by echocardiography. In DD monkeys (N=6), the circulated S-glutathionylated cMyBP-C levels were upregulated (fold, 2.7 ± 0.57, P 〈 0.05, t-test) as compared to those in control (CTL) monkeys (N=6). Similarly, S-glutathionylated cMyBP-C was elevated (fold, 1.61 ± 0.23, P 〈 0.05, t-test) in mice with DD (N=5) as compared to controls (N=5). Conclusions: Glutathionylated cMyBP-C has been associated with DD in animal models, and circulating glutathionylated cMyBP-C was elevated in humans, monkeys, and mice with DD. Glutathionylated cMyBP-C may represent a disease-specific biomarker for the presence of DD.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.144.suppl_1.11400
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1466401-X
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  • 8
    Online Resource
    Online Resource
    Role of Mitochondrial Oxidative Stress in Glucose Tolerance, Insulin Resistance, and Cardiac Diastolic Dysfunction
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Journal of the American Heart Association Vol. 5, No. 5 ( 2016-05-06)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 5, No. 5 ( 2016-05-06)
    Abstract: Diabetes mellitus (DM) is associated with mitochondrial oxidative stress. We have shown that myocardial oxidative stress leads to diastolic dysfunction in a hypertensive mouse model. Therefore, we hypothesized that diabetes mellitus could cause diastolic dysfunction through mitochondrial oxidative stress and that a mitochondria‐targeted antioxidant (Mito TEMPO ) could prevent diastolic dysfunction in a diabetic mouse model. Methods and Results C57 BL /6J mice were fed either 60 kcal % fat diet (high‐fat diet [ HFD ]) or normal chow (control) for 8 weeks with or without concurrent Mito TEMPO administration, followed by in vivo assessment of diastolic function and ex vivo studies. HFD mice developed impaired glucose tolerance compared with the control (serum glucose=495±45 mg/dL versus 236±30 mg/dL at 60 minutes after intraperitoneal glucose injection, P 〈 0.05). Myocardial tagged cardiac magnetic resonance imaging showed significantly reduced diastolic circumferential strain (Ecc) rate in the HFD mice compared with controls (5.0±0.3 1/s versus 7.4±0.5 1/s, P 〈 0.05), indicating diastolic dysfunction in the HFD mice. Systolic function was comparable in both groups (left ventricular ejection fraction=66.4±1.4% versus 66.7±1.2%, P 〉 0.05). Mito TEMPO ‐treated HFD mice showed significant reduction in mitochondria reactive oxygen species, S ‐glutathionylation of cardiac myosin binding protein C, and diastolic dysfunction, comparable to the control. The fasting insulin levels of Mito TEMPO ‐treated HFD mice were also comparable to the controls ( P 〉 0.05). Conclusions Mito TEMPO treatment prevented insulin resistance and diastolic dysfunction, suggesting that mitochondrial oxidative stress may be involved in the pathophysiology of both conditions.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.115.003046
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2653953-6
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  • 9
    Online Resource
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    Role of RBM25/LUC7L3 in Abnormal Cardiac Sodium Channel Splicing Regulation in Human Heart Failure
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Circulation Vol. 124, No. 10 ( 2011-09-06), p. 1124-1131
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 124, No. 10 ( 2011-09-06), p. 1124-1131
    Abstract: Human heart failure is associated with decreased cardiac voltage-gated Na + channel current (encoded by SCN5A), and the changes have been implicated in the increased risk of sudden death in heart failure. Nevertheless, the mechanism of SCN5A downregulation is unclear. A number of human diseases are associated with alternative mRNA splicing, which has received comparatively little attention in the study of cardiac disease. Splicing factor expression profiles during human heart failure and a specific splicing pathway for SCN5A regulation were explored in this study. Methods and Results— Gene array comparisons between normal human and heart failure tissues demonstrated that 17 splicing factors, associated with all major spliceosome components, were upregulated. Two of these splicing factors, RBM25 and LUC7L3, were elevated in human heart failure tissue and mediated truncation of SCN5A mRNA in both Jurkat cells and human embryonic stem cell–derived cardiomyocytes. RBM25/LUC7L3-mediated abnormal SCN5A mRNA splicing reduced Na + channel current 91.1±9.3% to a range known to cause sudden death. Overexpression of either splicing factor resulted in an increase in truncated mRNA and a concomitant decrease in the full-length SCN5A transcript. Conclusions— Of the 17 mRNA splicing factors upregulated in heart failure, RBM25 and LUC7L3 were sufficient to explain the increase in truncated forms and the reduction in full-length Na + channel transcript. Because the reduction in channels was in the range known to be associated with sudden death, interruption of this abnormal mRNA processing may reduce arrhythmic risk in heart failure.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.111.044495
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 1466401-X
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  • 10
    Online Resource
    Online Resource
    Mitochondria Oxidative Stress, Connexin43 Remodeling, and Sudden Arrhythmic Death
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Circulation: Arrhythmia and Electrophysiology Vol. 6, No. 3 ( 2013-06), p. 623-631
    Details
    In: Circulation: Arrhythmia and Electrophysiology, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 3 ( 2013-06), p. 623-631
    Abstract: Previously, we showed that a mouse model (ACE8/8) of cardiac renin–angiotensin system activation has a high rate of spontaneous ventricular tachycardia and sudden cardiac death secondary to a reduction in connexin43 level. Angiotensin-II activation increases reactive oxygen species (ROS) production, and ACE8/8 mice show increased cardiac ROS. We sought to determine the source of ROS and whether ROS played a role in the arrhythmogenesis. Methods and Results— Wild-type and ACE8/8 mice with and without 2 weeks of treatment with L-NIO (NO synthase inhibitor), sepiapterin (precursor of tetrahydrobiopterin), MitoTEMPO (mitochondria-targeted antioxidant), TEMPOL (a general antioxidant), apocynin (nicotinamide adenine dinucleotide phosphate oxidase inhibitor), allopurinol (xanthine oxidase inhibitor), and ACE8/8 crossed with P67 dominant negative mice to inhibit the nicotinamide adenine dinucleotide phosphate oxidase were studied. Western blotting, detection of mitochondrial ROS by MitoSOX Red, electron microscopy, immunohistochemistry, fluorescent dye diffusion technique for functional assessment of connexin43, telemetry monitoring, and in vivo electrophysiology studies were performed. Treatment with MitoTEMPO reduced sudden cardiac death in ACE8/8 mice (from 74% to 18%; P 〈 0.005), decreased spontaneous ventricular premature beats, decreased ventricular tachycardia inducibility (from 90% to 17%; P 〈 0.05), diminished elevated mitochondrial ROS to the control level, prevented structural damage to mitochondria, resulted in 2.6-fold increase in connexin43 level at the gap junctions, and corrected gap junction conduction. None of the other antioxidant therapies prevented ventricular tachycardia and sudden cardiac death in ACE8/8 mice. Conclusions— Mitochondrial oxidative stress plays a central role in angiotensin II–induced gap junction remodeling and arrhythmia. Mitochondria-targeted antioxidants may be effective antiarrhythmic drugs in cases of renin–angiotensin system activation.
    Type of Medium: Online Resource
    ISSN: 1941-3149 , 1941-3084
    URL: Article
    DOI: 10.1161/CIRCEP.112.976787
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 2425487-3
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