ArticleScience translational medicine2015
Pacemaker-induced transient asynchrony suppresses heart failure progression.
Article in Science translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04159454 (Pacemaker Induced Transient Dyssynchrony for Treating Heart Failure), which is not on this map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Pacemaker Induced Transient Dyssynchrony for Treating Heart Failure (PITA-HF): Feasibility, Safety, and Tolerability
Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
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- Poly(Glutamic Acid-Lysine) Hydrogels with Alternating Sequence Resist the Foreign Body Response in Rodents and Non-Human Primates.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- EMD-57033 Augments the Contractility in Porcine Myocardium by Promoting the Activation of Myosin in Thick Filaments.International journal of molecular sciences · 2022Article
- GSK-3β Localizes to the Cardiac Z-Disc to Maintain Length Dependent Activation.Circulation research · 2022Article
- Myofibril orientation as a metric for characterizing heart disease.Biophysical journal · 2022Article
- Answer ALS, a large-scale resource for sporadic and familial ALS combining clinical and multi-omics data from induced pluripotent cell lines.Nature neuroscience · 2022Article
- Myofilament glycation in diabetes reduces contractility by inhibiting tropomyosin movement, is rescued by cMyBPC domains.Journal of molecular and cellular cardiology · 2022Article
- An integrated multi-omic analysis of iPSC-derived motor neurons from C9ORF72 ALS patients.iScience · 2021Article
- Therapeutic targeting of BAG3: considering its complexity in cancer and heart disease.The Journal of clinical investigation · 2021Review
- Cardiomyocyte contractile impairment in heart failure results from reduced BAG3-mediated sarcomeric protein turnover.Nature communications · 2021Article
- Advances in the role and mechanism of BAG3 in dilated cardiomyopathy.Heart failure reviews · 2021Review
- Precision wearable accelerometer contact microphones for longitudinal monitoring of mechano-acoustic cardiopulmonary signals.NPJ digital medicine · 2020Article
- Cardiac Resynchronisation Therapy and Cellular Bioenergetics: Effects Beyond Chamber Mechanics.European cardiology · 2019Review
- Chronic Atrial and Ventricular Pacing in the Mouse.Circulation. Heart failure · 2019Article
- Adverse Consequences of Right Ventricular Apical Pacing and Novel Strategies to Optimize Left Ventricular Systolic and Diastolic Function.Current cardiology reviews · 2019Review
- A Miniaturized, Programmable Pacemaker for Long-Term Studies in the Mouse.Circulation research · 2018Article
- Diabetes with heart failure increases methylglyoxal modifications in the sarcomere, which inhibit function.JCI insight · 2018Article
- Article
- Right Ventricular Myofilament Functional Differences in Humans With Systemic Sclerosis-Associated Versus Idiopathic Pulmonary Arterial Hypertension.Circulation · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
Uncoordinated contraction from electromechanical delay worsens heart failure pathophysiology and prognosis, but restoring coordination with biventricular pacing, known as cardiac resynchronization therapy (CRT), improves both. However, not every patient qualifies for CRT. We show that heart failure with synchronous contraction is improved by inducing dyssynchrony for 6 hours daily by right ventricular pacing using an intracardiac pacing device, in a process we call pacemaker-induced transient asynchrony (PITA). In dogs with heart failure induced by 6 weeks of atrial tachypacing, PITA (starting on week 3) suppressed progressive cardiac dilation as well as chamber and myocyte dysfunction. PITA enhanced β-adrenergic responsiveness in vivo and normalized it in myocytes. Myofilament calcium response declined in dogs with synchronous heart failure, which was accompanied by sarcomere disarray and generation of myofibers with severely reduced function, and these changes were absent in PITA-treated hearts. The benefits of PITA were not replicated when the same number of right ventricular paced beats was randomly distributed throughout the day, indicating that continuity of dyssynchrony exposure is necessary to trigger the beneficial biological response upon resynchronization. These results suggest that PITA could bring the benefits of CRT to the many heart failure patients with synchronous contraction who are not CRT candidates.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.