ArticleJournal of molecular and cellular cardiology2017
Myocardial relaxation is accelerated by fast stretch, not reduced afterload.
Article in Journal of molecular and cellular cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Simple and Practical Way of Assessing Diastolic Function: Diastolic Heart Failure Revisited.Korean circulation journal · 2025Review
- Strain rate of stretch affects crossbridge detachment during relaxation of intact cardiac trabeculae.PloS one · 2024Article
- Mechanical Control of Relaxation using Intact Cardiac Trabeculae.Journal of visualized experiments : JoVE · 2023Article
- Molecular regulation of stretch activation.American journal of physiology. Cell physiology · 2022Article
- Pressing physiology to move our understanding of cytosolic calcium dynamics.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2022Review
- Effect of Myosin Isoforms on Cardiac Muscle Twitch of Mice, Rats and Humans.International journal of molecular sciences · 2022Article
- FiberSim: A flexible open-source model of myofilament-level contraction.Biophysical journal · 2022Article
- Inorganic phosphate accelerates cardiac myofilament relaxation in response to lengthening.Frontiers in physiology · 2022Article
- Preparing Excitable Cardiac Papillary Muscle and Cardiac Slices for Functional Analyses.Frontiers in physiology · 2022Article
- Reduced preload increases Mechanical Control (strain-rate dependence) of Relaxation by modifying myosin kinetics.Archives of biochemistry and biophysics · 2021Article
- Contraction-relaxation coupling is unaltered by exercise training and infarction in isolated canine myocardium.The Journal of general physiology · 2021Article
- Novel insights into sarcomere regulatory systems control of cardiac thin filament activation.The Journal of general physiology · 2021Article
- Multiscale modeling of twitch contractions in cardiac trabeculae.The Journal of general physiology · 2021Article
- Making waves: A proposed new role for myosin-binding protein C in regulating oscillatory contractions in vertebrate striated muscle.The Journal of general physiology · 2021Article
- Fast-relaxing cardiomyocytes exert a dominant role in the relaxation behavior of heterogeneous myocardium.Archives of biochemistry and biophysics · 2021Article
- Need for Speed: The Importance of Physiological Strain Rates in Determining Myocardial Stiffness.Frontiers in physiology · 2021Article
- Enhancing diastolic function by strain-dependent detachment of cardiac myosin crossbridges.The Journal of general physiology · 2020Article
- Move quickly to detach: Strain rate-dependent myosin detachment and cardiac relaxation.The Journal of general physiology · 2020Article
- Left ventricular vortex and intraventricular pressure difference in dogs under various loading conditions.American journal of physiology. Heart and circulatory physiology · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Fast relaxation of cross-bridge generated force in the myocardium facilitates efficient diastolic function. Recently published research studying mechanisms that modulate the relaxation rate has focused on molecular factors. Mechanical factors have received less attention since the 1980s when seminal work established the theory that reducing afterload accelerates the relaxation rate. Clinical trials using afterload reducing drugs, partially based on this theory, have thus far failed to improve outcomes for patients with diastolic dysfunction. Therefore, we reevaluated the protocols that suggest reducing afterload accelerates the relaxation rate and identified that myocardial relengthening was a potential confounding factor. We hypothesized that the speed of myocardial relengthening at end systole (end systolic strain rate), and not afterload, modulates relaxation rate and tested this hypothesis using electrically-stimulated trabeculae from mice, rats, and humans. We used load-clamp techniques to vary afterload and end systolic strain rate independently. Our data show that the rate of relaxation increases monotonically with end systolic strain rate but is not altered by afterload. Computer simulations mimic this behavior and suggest that fast relengthening quickens relaxation by accelerating the detachment of cross-bridges. The relationship between relaxation rate and strain rate is novel and upends the prevailing theory that afterload modifies relaxation. In conclusion, myocardial relaxation is mechanically modified by the rate of stretch at end systole. The rate of myocardial relengthening at end systole may be a new diagnostic indicator or target for treatment of diastolic dysfunction.
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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.