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Quantitative assessment of myocardial stiffness is crucial to understand and evaluate cardiac biomechanics and function. Despite the recent progresses of ultrasonic shear wave elastography, quantitative evaluation of myocardial stiffness still remains a challenge because of strong elastic anisotropy. In this paper we introduce a smart ultrasound approach for non-invasive real-time quantification of shear wave velocity (SWV) and elastic fractional anisotropy (FA) in locally transverse isotropic elastic medium such as the myocardium. The approach relies on a simultaneous multidirectional evaluation of the SWV without a prior knowledge of the fiber orientation. We demonstrated that it can quantify accurately SWV in the range of 1.5 to 6 m/s in transverse isotropic medium (FA < 0.7) using numerical simulations. Experimental validation was performed on calibrated phantoms and anisotropic ex vivo tissues. A mean absolute error of 0.22 m/s was found when compared to gold standard measurements. Finally, in vivo feasibility of myocardial anisotropic stiffness assessment was evaluated in four healthy volunteers on the antero-septo basal segment and on anterior free wall of the right ventricle (RV) in end-diastole. A mean longitudinal SWV of 1.08 ± 0.20 m/s was measured on the RV wall and 1.74 ± 0.51 m/s on the septal wall with a good intra-volunteer reproducibility (±0.18 m/s). This approach has the potential to become a clinical tool for the quantitative evaluation of myocardial stiffness and diastolic function.
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http://dx.doi.org/10.1109/TBME.2021.3087039 | DOI Listing |
Rev Cardiovasc Med
August 2025
Department of Nephrology, Akron Nephrology Associates at Cleveland Clinic Akron General Medical Center, Akron, OH 44302, USA.
Cardiovascular assessments in children and adolescents with hypertension are essential for detecting early signs of organ damage and guiding timely interventions. The pathophysiology of pediatric hypertension involves a complex interplay of arterial stiffness, endothelial dysfunction, metabolic disturbances, activation of the renin-angiotensin-aldosterone system, and immune dysregulation. These mechanisms collectively contribute to target organ damage, particularly in the cardiovascular system.
View Article and Find Full Text PDFSci Adv
September 2025
School of Engineering and Materials Science, Queen Mary University of London, UK.
During heart disease, the cardiac extracellular matrix (ECM) undergoes a structural and mechanical transformation. Cardiomyocytes sense the mechanical properties of their environment, leading to phenotypic remodeling. A critical component of the ECM mechanosensing machinery, including the protein talin, is organized at the cardiomyocyte costamere.
View Article and Find Full Text PDFFront Cardiovasc Med
August 2025
Department of Biomedical Engineering, Thorax Center Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands.
Atherosclerotic plaque rupture can lead to thrombotic cardiovascular events such as stroke and myocardial infarction. Computational models have shown that microcalcifications (calcified particles with a diameter < 50 μm) in the atherosclerotic plaque cap can increase cap tissue stresses and consequently contribute to plaque rupture. Microcalcification characteristics, such as particle size and volume fraction, have been implicated to affect cap stresses.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
September 2025
Department of Medicine, Center for the Prevention of Cardiovascular Disease, New York University School of Medicine. (M.S.G., J.S.B.).
Background: The underlying mechanisms of atherosclerosis and strategies for identifying high cardiovascular risk in psoriasis are incompletely understood. Platelet activity is increased in psoriasis and induces vascular dysfunction. We investigated the platelet phenotype and platelet transcriptome as one potential mechanism to explain cardiovascular risk in psoriasis.
View Article and Find Full Text PDFEur Heart J
September 2025
Institute of Molecular and Translational Therapeutic Strategies, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Heart failure with preserved ejection fraction (HFpEF) accounts for nearly half of all heart failure cases and is characterized by phenotypical heterogeneity with a high prevalence of multiple, often overlapping cardiometabolic disorders. Comorbidities such as hypertension, obesity, or diabetes are present in many HFpEF patients and are hypothesized to contribute to adverse cardiac remodelling and myocardial fibrosis through a variety of haemodynamic and metabolic impairments, with nearly half of all HFpEF patients exhibiting left ventricular (LV) hypertrophy or concentric remodelling. Myocardial fibrosis and its surrogate changes in LV structure and geometry lead to functional impairments such as increased diastolic stiffness and elevated filling pressures and are associated with reduced exercise tolerance and poor prognosis in patients with HFpEF.
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