In order for the conductance catheter system to accurately measure instantaneous cardiac blood volume, it is necessary to determine and remove the contribution from parallel myocardial tissue. In previous studies, the myocardium has been treated as either purely resistive or purely capacitive when developing methods to estimate the myocardial contribution. We propose that both the capacitive and the resistive properties of the myocardium are substantial, and neither should be ignored. Hence, the measured result should be labeled admittance rather than conductance. We have measured the admittance (magnitude and phase angle) of the left ventricle in the mouse, and have shown that it is measurable and increases with frequency. Further, this more accurate technique suggests that the myocardial contribution to measured admittance varies between end-systole and end-diastole, contrary to previous literature. We have tested these hypotheses both with numerical finite-element models for a mouse left ventricle constructed from magnetic resonance imaging images, and with in vivo admittance measurements in the murine left ventricle. Finally, we propose a new method to determine the instantaneous myocardial contribution to the measured left ventricular admittance that does not require saline injection or other intervention to calibrate.
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http://dx.doi.org/10.1109/TBME.2007.890732 | DOI Listing |
ESC Heart Fail
January 2025
Université de Strasbourg, Pôle d'Activité Médico-Chirurgicale Cardio-Vasculaire, Nouvel Hôpital Civil, Centre Hospitalier Universitaire, Strasbourg, France.
Background And Objectives: Initially described as a benign acute cardiomyopathy, Takotsubo syndrome has been linked to elevated mortality rates. Emerging evidence suggests that unresolved myocardial inflammation may contribute to this adverse prognosis. This study aimed to evaluate the incremental prognostic utility of C-reactive protein (CRP) in conjunction with the InterTAK prognosis score for stratifying long-term mortality in Takotsubo syndrome.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Congenital Heart Defects and Pediatric Cardiology, German Heart Center Munich, TUM University Hospital, School of Medicine & Health, Technical University of Munich, Munich, Germany.
Hypertrophic cardiomyopathy (HCM) caused by autosomal-dominant mutations in genes coding for structural sarcomeric proteins, is the most common inherited heart disease. HCM is associated with myocardial hypertrophy, fibrosis and ventricular dysfunction. Hypoxia-inducible transcription factor-1α (Hif-1α) is the central master regulators of cellular hypoxia response and associated with HCM.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Cardiovascular Sciences, Anaesthesia, Critical Care and Pain Management, University of Leicester, Leicester, United Kingdom.
Sustained pathologic myocardial hypertrophy can result in heart failure(HF); a significant health issue affecting a large section of the population worldwide. In HF there is a marked elevation in circulating levels of the peptide urotensin II(UII) but it is unclear whether this is a result of hypertrophy or whether the high levels contribute to the development of hypertrophy. The aim of this study is to investigate a role of UII and its receptor UT in the development of cardiac hypertrophy and the signalling molecules involved.
View Article and Find Full Text PDFBiol Sex Differ
January 2025
Department of Nuclear Medicine, University Hospital Zurich, Zurich, CH-8091, Switzerland.
Background: Presentations and outcomes of acute myocardial infarction (MI) differ between women and men, with the worst outcomes being reported in younger women. Mental stress induced ischemia and sympathetic activation have been suggested to play a prominent role in the pathogenesis of MI in younger women, however, the impact of sex hormones on these parameters remains unknown.
Methods: The effect of sex hormones and age on myocardial infarct size and myocardial sympathetic activity (MSA) was assessed in male and female, as well as young (4-6 months) and aged (20-22 months) FVB/N mice (n = 106, 60 gonadectomized and 46 sham-operated animals) who underwent in vivo [C]meta-hydroxyephedrine ([C]mHED) positron emission tomography (PET) and cardiac magnetic resonance (CMR) imaging 24 h after a 30 min myocardial ischemic injury.
Exp Cell Res
January 2025
Cardiovascular Center, College of Medicine, University of Cincinnati, Ohio, 45267, USA; School of Chemical and Biotechnology, SASTRA Deemed University, Tirumalaisamudram, Thanjavur, 613401, Tamil Nadu, India. Electronic address:
Multiple forms of cell death contribute significantly to cardiovascular pathologies, negatively impacting cardiac remodeling and leading to heart failure. While myocardial cell death has been associated with PM induced cardiotoxicity, the temporal dynamics of various cell death forms, such as apoptosis, ferroptosis, necroptosis, and pyroptosis, in relation to inflammatory processes, remain underexplored. This study examines the time-dependent onset and progression of these cell death pathways in the myocardium and their correlation with inflammation in a Wistar rat model.
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