ArticleAmerican journal of physiology. Heart and circulatory physiology2014
Ultrastructural and cellular basis for the development of abnormal myocardial mechanics during the transition from hypertension to heart failure.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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59 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
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- Left ventricular and atrial myocardial strain in heart failure with preserved ejection fraction: the evidence so far and prospects for phenotyping strategy.Cardiovascular ultrasound · 2024Review
- Heart Failure with Preserved Ejection Fraction: The Pathophysiological Mechanisms behind the Clinical Phenotypes and the Therapeutic Approach.International journal of molecular sciences · 2024Review
- Blood pressure per the 2017 ACC/AHA and 2018 ESC/ESH guidelines and heart failure risk: the Suita Study.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Left Atrial Strain and the Risk of Atrial Arrhythmias From Extended Ambulatory Cardiac Monitoring: MESA.Journal of the American Heart Association · 2022Article
- Glucose dysregulation and subclinical cardiac dysfunction in older adults: The Cardiovascular Health Study.Cardiovascular diabetology · 2022Article
- Adverse cardiac mechanics and incident coronary heart disease in the Cardiovascular Health Study.Heart (British Cardiac Society) · 2022Article
- Multi-Scale Computational Modeling of Spatial Calcium Handling From Nanodomain to Whole-Heart: Overview and Perspectives.Frontiers in physiology · 2022Review
- High salt intake damages myocardial viability and induces cardiac remodelingFrontiers in cardiovascular medicine · 2022Article
- Association Between Myocardial Strain and Frailty in CHS.Circulation. Cardiovascular imaging · 2021Article
- Role of t-tubule remodeling on mechanisms of abnormal calcium release during heart failure development in canine ventricle.American journal of physiology. Heart and circulatory physiology · 2021Article
- Phosphatidylinositol-4,5-Bisphosphate Binding to Amphiphysin-II Modulates T-Tubule Remodeling: Implications for Heart Failure.Frontiers in physiology · 2021Article
- The Physiology and Pathophysiology of T-Tubules in the Heart.Frontiers in physiology · 2021Review
- The Mechanism Actions of Astragaloside IV Prevents the Progression of Hypertensive Heart Disease Based on Network Pharmacology and Experimental Pharmacology.Frontiers in pharmacology · 2021Article
- Article
- Characterization of cardiac mechanics and incident atrial fibrillation in participants of the Cardiovascular Health Study.JCI insight · 2020Article
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Authors and funding
23 authors at 1 institution in 1 country.
Funding
Abstract
Although the development of abnormal myocardial mechanics represents a key step during the transition from hypertension to overt heart failure (HF), the underlying ultrastructural and cellular basis of abnormal myocardial mechanics remains unclear. We therefore investigated how changes in transverse (T)-tubule organization and the resulting altered intracellular Ca(2+) cycling in large cell populations underlie the development of abnormal myocardial mechanics in a model of chronic hypertension. Hearts from spontaneously hypertensive rats (SHRs; n = 72) were studied at different ages and stages of hypertensive heart disease and early HF and were compared with age-matched control (Wistar-Kyoto) rats (n = 34). Echocardiography, including tissue Doppler and speckle-tracking analysis, was performed just before euthanization, after which T-tubule organization and Ca(2+) transients were studied using confocal microscopy. In SHRs, abnormalities in myocardial mechanics occurred early in response to hypertension, before the development of overt systolic dysfunction and HF. Reduced longitudinal, circumferential, and radial strain as well as reduced tissue Doppler early diastolic tissue velocities occurred in concert with T-tubule disorganization and impaired Ca(2+) cycling, all of which preceded the development of cardiac fibrosis. The time to peak of intracellular Ca(2+) transients was slowed due to T-tubule disruption, providing a link between declining cell ultrastructure and abnormal myocardial mechanics. In conclusion, subclinical abnormalities in myocardial mechanics occur early in response to hypertension and coincide with the development of T-tubule disorganization and impaired intracellular Ca(2+) cycling. These changes occur before the development of significant cardiac fibrosis and precede the development of overt cardiac dysfunction and HF.
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