ReviewPflugers Archiv : European journal of physiology2011
Electromechanical coupling in the cardiac myocyte; stretch-arrhythmia feedback.
Review in Pflugers Archiv : European journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Investigating PKD2 deficiency-associated cardiomyopathies using hESC-cardiomyocytes and bioengineered 3D ventricular cardiac tissue strips.Cell death & disease · 2026Article
- Abnormal Mechanics Relate to Myocardial Fibrosis and Ventricular Arrhythmias in Patients With Mitral Valve Prolapse.Circulation. Cardiovascular imaging · 2023Article
- An autonomously swimming biohybrid fish designed with human cardiac biophysics.Science (New York, N.Y.) · 2022Article
- A Fully-Coupled Electro-Mechanical Whole-Heart Computational Model: Influence of Cardiac Contraction on the ECG.Frontiers in physiology · 2021Article
- Arrhythmogenic Current Generation by Myofilament-Triggered CaBiophysical journal · 2019Article
- Caveolae in ventricular myocytes are required for stretch-dependent conduction slowing.Journal of molecular and cellular cardiology · 2014Article
- Polycystins and partners: proposed role in mechanosensitivity.The Journal of physiology · 2014Review
- Mitochondria and arrhythmias.Free radical biology & medicine · 2014Review
- SERCA2a gene therapy in heart failure: an anti-arrhythmic positive inotrope.British journal of pharmacology · 2014Review
- Impaired contractile function due to decreased cardiac myosin binding protein C content in the sarcomere.American journal of physiology. Heart and circulatory physiology · 2013Article
- Myocardial twitch duration and the dependence of oxygen consumption on pressure-volume area: experiments and modelling.The Journal of physiology · 2012Article
- Functional cardiac tissue engineering.Regenerative medicine · 2012Review
- The cytoskeleton and the cellular transduction of mechanical strain in the heart: a special issue.Pflugers Archiv : European journal of physiology · 2011Article
- Electrophysiological and contractile function of cardiomyocytes derived from human embryonic stem cells.Progress in biophysics and molecular biologyReview
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The macroscopic hallmarks of the normal heartbeat are rapid onset of contraction and rapid relaxation and an inotropic response to both increased end diastolic volume and increased heart rate. At the microscopic level, the calcium ion (Ca(2+)) plays a crucial role in normal cardiac contraction. This paper reviews the cycle of Ca(2+) fluxes during the normal heartbeat, which underlie the coupling between excitation and contraction (ECC) and permit a highly synchronized action of cardiac sarcomeres. Length dependence of the response of the regulatory sarcomeric proteins mediates the Frank-Starling Law of the heart. However, Ca(2+) transport may go astray in heart disease and both jeopardize the exquisite mechanism of systole and diastole and triggering arrhythmias. The interplay between weakened and strong segments in nonuniform cardiac muscle may further lead to mechanoelectric feedback-or reverse excitation contraction coupling (RECC) mediating an early diastolic Ca(2+) transient caused by the rapid force decrease during the relaxation phase. These rapid force changes in nonuniform muscle may cause arrhythmogenic Ca(2+) waves to propagate by activation of neighbouring SR by diffusing Ca(2+) ions.
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What OpenQuestion holds
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.