ArticleJournal of biomedicine & biotechnology2010
Physiologic basis and pathophysiologic implications of the diastolic properties of the cardiac muscle.
Article in Journal of biomedicine & biotechnology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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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
4 citing papers in PubMed, 25 citations in OpenAlex.
- Untangling the prognostic value of diastolic dysfunction, NT-proBNP, and frailty in older patients with preserved left ventricular ejection fraction without valvular disease.BMC geriatrics · 2025Observational
- Human formin FHOD3-mediated actin elongation is required for sarcomere integrity in cardiomyocytes.eLife · 2025Article
- Cellular and extracellular proteomic profiling of paradoxical low-flow low-gradient aortic stenosis myocardium.Frontiers in cardiovascular medicine · 2024Article
- A guide for assessment of myocardial stiffness in health and disease.Nature cardiovascular research · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although systole was for long considered the core of cardiac function, hemodynamic performance is evenly dependent on appropriate systolic and diastolic functions. The recognition that isolated diastolic dysfunction is the major culprit for approximately fifty percent of all heart failure cases imposes a deeper understanding of its underlying mechanisms so that better diagnostic and therapeutic strategies can be designed. Risk factors leading to diastolic dysfunction affect myocardial relaxation and/or its material properties by disrupting the homeostasis of cardiomyocytes as well as their relation with surrounding matrix and vascular structures. As a consequence, slower ventricular relaxation and higher myocardial stiffness may result in higher ventricular filling pressures and in the risk of hemodynamic decompensation. Thus, determining the mechanisms of diastolic function and their implications in the pathophysiology of heart failure with normal ejection fraction has become a prominent field in basic and clinical research.
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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.