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  1. Article ; Online: Symptomatic bradyarrhythmias in the athlete-Underlying mechanisms and treatments.

    Al-Othman, Sami / Boyett, Mark R / Morris, Gwilym M / Malhotra, Aneil / Mesirca, Pietro / Mangoni, Matteo E / D'Souza, Alicia

    Heart rhythm

    2024  

    Abstract: Bradyarrhythmias including sinus bradycardia and atrioventricular (AV) block are frequently encountered in endurance athletes especially at night. While these are well tolerated by the young athlete, there is evidence that generally from the fifth decade ...

    Abstract Bradyarrhythmias including sinus bradycardia and atrioventricular (AV) block are frequently encountered in endurance athletes especially at night. While these are well tolerated by the young athlete, there is evidence that generally from the fifth decade of life onward, such arrhythmias can degenerate into pathological symptomatic bradycardia requiring pacemaker therapy. For many years, athletic bradycardia and AV block have been attributed to high vagal tone, but work from our group has questioned this widely held assumption and demonstrated a role for intrinsic electrophysiological remodeling of the sinus node and the AV node. In this article, we argue that bradyarrhythmias in the veteran athlete arise from the cumulative effects of exercise training, the circadian rhythm and aging on the electrical activity of the nodes. We consider contemporary strategies for the treatment of symptomatic bradyarrhythmias in athletes and highlight potential therapies resulting from our evolving mechanistic understanding of this phenomenon.
    Language English
    Publishing date 2024-02-28
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2229357-7
    ISSN 1556-3871 ; 1547-5271
    ISSN (online) 1556-3871
    ISSN 1547-5271
    DOI 10.1016/j.hrthm.2024.02.050
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Clinical Experience of the Efficacy and Safety of Low-dose Tolvaptan Therapy in a UK Tertiary Oncology Setting.

    Chatzimavridou-Grigoriadou, Victoria / Al-Othman, Sami / Brabant, Georg / Kyriacou, Angelos / King, Jennifer / Blackhall, Fiona / Trainer, Peter J / Higham, Claire E

    The Journal of clinical endocrinology and metabolism

    2021  Volume 106, Issue 11, Page(s) e4766–e4775

    Abstract: Context: In patients with cancer, hyponatremia is associated with increased morbidity and mortality and can delay systemic therapy.: Objective: To assess the safety and efficacy of low-dose tolvaptan (7.5 mg) for hospitalized, adult patients with ... ...

    Abstract Context: In patients with cancer, hyponatremia is associated with increased morbidity and mortality and can delay systemic therapy.
    Objective: To assess the safety and efficacy of low-dose tolvaptan (7.5 mg) for hospitalized, adult patients with hyponatremia due to syndrome of inappropriate antidiuresis (SIAD), and coexisting malignancy.
    Methods: Retrospective evaluation in a tertiary cancer center.
    Results: Fifty-five patients with mean baseline serum sodium (sNa) 117.9 ± 4.6 mmol/L were included. In total, 90.9% had severe hyponatremia (sNa < 125 mmol/L). Mean age was 65.1 ± 9.3 years. Following an initial dose of tolvaptan 7.5 mg, median (range) increase in sNa observed at 24 hours was 9 (1-19) mmol/L. Within 1 week, 39 patients (70.9%) reached sNa ≥ 130 mmol/L and 48 (87.3%) had sNa rise of ≥5 mmol/L within 48 hours. No severe adverse events were reported. Thirty-three (60%) and 17 (30.9%) patients experienced sNa rise of ≥8 and ≥12 mmol/L/24 hours, respectively. The rate of sNa correction in the first 24 hours was significantly higher among participants that continued fluid restriction after tolvaptan administration (median [quantiles]: 14 [9-16] versus 8 [5-11] mmol/L, P = .036). Moreover, in the over-rapid correction cohort (≥12 mmol/L/24 hours) demeclocycline was appropriately discontinued only in 60% compared with 91.7% of the remaining participants (P = .047). Lower creatinine was predictive of higher sNa correction rate within 24 hours (P = .01).
    Conclusion: In the largest series to date, although low-dose tolvaptan was demonstrated to be effective in correcting hyponatremia due to SIAD in cancer patients, a significant proportion experienced over-rapid correction. Concurrent administration of demeclocycline and/or fluid restriction must be avoided due to the increased risk of over-rapid correction.
    MeSH term(s) Aged ; Antidiuretic Hormone Receptor Antagonists/therapeutic use ; Female ; Follow-Up Studies ; Humans ; Hyponatremia/drug therapy ; Hyponatremia/etiology ; Hyponatremia/pathology ; Male ; Neoplasms/complications ; Prognosis ; Retrospective Studies ; Tolvaptan/therapeutic use
    Chemical Substances Antidiuretic Hormone Receptor Antagonists ; Tolvaptan (21G72T1950)
    Language English
    Publishing date 2021-02-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3029-6
    ISSN 1945-7197 ; 0021-972X
    ISSN (online) 1945-7197
    ISSN 0021-972X
    DOI 10.1210/clinem/dgab131
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Cardiac GR Mediates the Diurnal Rhythm in Ventricular Arrhythmia Susceptibility.

    Tikhomirov, Roman / Oakley, Robert H / Anderson, Cali / Xiang, Yirong / Al-Othman, Sami / Smith, Matthew / Yaar, Sana / Torre, Eleonora / Li, Jianying / Wilson, Leslie R / Goulding, David R / Donaldson, Ian / Harno, Erika / Soattin, Luca / Shiels, Holly A / Morris, Gwilym M / Zhang, Henggui / Boyett, Mark R / Cidlowski, John A /
    Mesirca, Pietro / Mangoni, Matteo E / D'Souza, Alicia

    Circulation research

    2024  Volume 134, Issue 10, Page(s) 1306–1326

    Abstract: Background: Ventricular arrhythmias (VAs) demonstrate a prominent day-night rhythm, commonly presenting in the morning. Transcriptional rhythms in cardiac ion channels accompany this phenomenon, but their role in the morning vulnerability to VAs and the ...

    Abstract Background: Ventricular arrhythmias (VAs) demonstrate a prominent day-night rhythm, commonly presenting in the morning. Transcriptional rhythms in cardiac ion channels accompany this phenomenon, but their role in the morning vulnerability to VAs and the underlying mechanisms are not understood. We investigated the recruitment of transcription factors that underpins transcriptional rhythms in ion channels and assessed whether this mechanism was pertinent to the heart's intrinsic diurnal susceptibility to VA.
    Methods and results: Assay for transposase-accessible chromatin with sequencing performed in mouse ventricular myocyte nuclei at the beginning of the animals' inactive (ZT0) and active (ZT12) periods revealed differentially accessible chromatin sites annotating to rhythmically transcribed ion channels and distinct transcription factor binding motifs in these regions. Notably, motif enrichment for the glucocorticoid receptor (GR; transcriptional effector of corticosteroid signaling) in open chromatin profiles at ZT12 was observed, in line with the well-recognized ZT12 peak in circulating corticosteroids. Molecular, electrophysiological, and in silico biophysically-detailed modeling approaches demonstrated GR-mediated transcriptional control of ion channels (including
    Conclusions: Our study registers a day-night rhythm in chromatin accessibility that accompanies diurnal cycles in ventricular myocytes. Our approaches directly implicate the cardiac GR in the myocyte excitability rhythm and mechanistically link the ZT12 surge in glucocorticoids to intrinsic VA propensity at this time.
    MeSH term(s) Animals ; Circadian Rhythm ; Receptors, Glucocorticoid/metabolism ; Receptors, Glucocorticoid/genetics ; Mice ; Myocytes, Cardiac/metabolism ; Male ; Arrhythmias, Cardiac/metabolism ; Arrhythmias, Cardiac/physiopathology ; Arrhythmias, Cardiac/genetics ; Mice, Inbred C57BL ; NAV1.5 Voltage-Gated Sodium Channel/metabolism ; NAV1.5 Voltage-Gated Sodium Channel/genetics ; Connexin 43/metabolism ; Connexin 43/genetics ; Mice, Knockout ; Action Potentials
    Chemical Substances Receptors, Glucocorticoid ; Scn5a protein, mouse ; NAV1.5 Voltage-Gated Sodium Channel ; GJA1 protein, mouse ; Connexin 43
    Language English
    Publishing date 2024-03-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.123.323464
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Proteomics couples electrical remodelling to inflammation in a murine model of heart failure with sinus node dysfunction.

    Kahnert, Konstantin / Soattin, Luca / Mills, Robert W / Wilson, Claire / Maurya, Svetlana / Sorrentino, Andrea / Al-Othman, Sami / Tikhomirov, Roman / van de Vegte, Yordi J / Hansen, Finn B / Achter, Jonathan / Hu, Wei / Zi, Min / Smith, Matthew / van der Harst, Pim / Olesen, Morten S / Olsen, Kristine Boisen / Banner, Jytte / Jensen, Thomas H L /
    Zhang, Henggui / Boyett, Mark R / D'Souza, Alicia / Lundby, Alicia

    Cardiovascular research

    2024  

    Abstract: Aims: In patients with heart failure (HF), concomitant sinus node dysfunction (SND) is an important predictor of mortality, yet its molecular underpinnings are poorly understood. Using proteomics, this study aimed to dissect the protein and ... ...

    Abstract Aims: In patients with heart failure (HF), concomitant sinus node dysfunction (SND) is an important predictor of mortality, yet its molecular underpinnings are poorly understood. Using proteomics, this study aimed to dissect the protein and phosphorylation remodelling within the sinus node in an animal model of HF with concurrent SND.
    Methods and results: We acquired deep sinus node proteomes and phosphoproteomes in mice with heart failure and SND and report extensive remodelling. Intersecting the measured (phospho)proteome changes with human genomics pharmacovigilance data, highlighted downregulated proteins involved in electrical activity such as the pacemaker ion channel, Hcn4. We confirmed the importance of ion channel downregulation for sinus node physiology using computer modelling. Guided by the proteomics data, we hypothesized that an inflammatory response may drive the electrophysiological remodeling underlying SND in heart failure. In support of this, experimentally induced inflammation downregulated Hcn4 and slowed pacemaking in the isolated sinus node. From the proteomics data we identified proinflammatory cytokine-like protein galectin-3 as a potential target to mitigate the effect. Indeed, in vivo suppression of galectin-3 in the animal model of heart failure prevented SND.
    Conclusion: Collectively, we outline the protein and phosphorylation remodeling of SND in heart failure, we highlight a role for inflammation in electrophysiological remodelling of the sinus node, and we present galectin-3 signalling as a target to ameliorate SND in heart failure.
    Language English
    Publishing date 2024-04-25
    Publishing country England
    Document type Journal Article
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvae054
    Database MEDical Literature Analysis and Retrieval System OnLINE

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