Confusion may exist at the time of postmortem examination as to whether the diseased heart is dilated, hypertrophied, or both. Ventricular dilatation and ventricular hypertrophy were therefore evaluated by cardiac partition techniques in 441 subjects at autopsy to determine their relationship. Specific weight and surface area of each ventricle were obtained and patients were divided into categories of disease. Wall thickness measurements, a parameter routinely used in the ordinary autopsy, were found to be unreliable in defining hypertrophy. Ventricular surface area (an index of dilatation) was highly correlated with ventricular weight in most disease categories. Exceptions were cardiomyopathy and aortic stenosis, in which hypertrophy predominated. We conclude from these data that dilatation and hypertrophy occur proportionately in the postmortem heart in most disease categories except in cardiomyopathy and aortic stenosis. These findings clarify the relationship of dilatation and hypertrophy at the time of autopsy in most cases. Therefore, uncertainty as to whether cardiac dilatation or hypertrophy is present or which predominates is usually related to the inability to assess these states critically at the time of autopsy when the ordinary pathological methods are used.
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http://dx.doi.org/10.1002/clc.4960110505 | DOI Listing |
Genes (Basel)
January 2025
Institute of Clinical Medicine, V.N. Vinogradov Faculty Therapeutic Clinic, I.M. Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia.
Background: Myocardial disease is an important component of the wide field of cardiovascular disease. However, the phenomenon of multiple myocardial diseases in a single patient remains understudied.
Aim: To investigate the prevalence and impact of myocarditis in patients with genetic cardiomyopathies and to evaluate the outcomes of myocarditis treatment in the context of cardiomyopathies.
Diagnostics (Basel)
January 2025
Cardiology Department, Coimbra Hospital and University Center, 3004-561 Coimbra, Portugal.
Hypertrophic cardiomyopathy (HCM) is a heterogeneous cardiac disease and one of its major challenges is the limited accuracy in stratifying the risk of sudden cardiac death (SCD). Positron emission tomography (PET), through the evaluation of myocardial blood flow (MBF) and metabolism using fluorodeoxyglucose (FDG) uptake, can reveal microvascular dysfunction, ischemia, and increased metabolic demands in the hypertrophied myocardium. These abnormalities are linked to several factors influencing disease progression, including arrhythmia development, ventricular dilation, and myocardial fibrosis.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
January 2025
Metabolic and Immune Diseases Department, Biomedical Research Institute Sols-Morreale (IIBM), National Research Council (CSIC), Autonoma University of Madrid, Spain (T.A.-G., S.M.-T., R.C.-M., S.U.-B., S.M.-P.).
Background: Hypoxia is associated with the onset of cardiovascular diseases including cardiac hypertrophy and pulmonary hypertension. HIF2 (hypoxia-inducible factor 2) signaling in the endothelium mediates pulmonary arterial remodeling and subsequent elevation of the right ventricular systolic pressure during chronic hypoxia. Thus, novel therapeutic opportunities for pulmonary hypertension based on specific HIF2 inhibitors have been proposed.
View Article and Find Full Text PDFJ Physiol Sci
January 2025
Experimental Physiology and Biochemistry Laboratory. Physical Education and Sport Center, Federal University of Espirito Santo, Vitoria, Brazil. Electronic address:
Background/objectives: Myocardial infarction (MI) frequently leads to cardiac remodeling and failure with impaired life quality, playing an important role in cardiovascular deaths. Although physical exercise is a well-recognized effective non-pharmacological therapy for cardiovascular diseases, the effects of strength training (ST) on the structural and functional aspects of cardiac remodeling need to be further documented. In this study, we aimed to investigate the role of a linear block ST protocol in the rat model of MI.
View Article and Find Full Text PDFSci Adv
January 2025
Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Protein homeostasis is crucial for maintaining cardiomyocyte (CM) function. Disruption of proteostasis results in accumulation of protein aggregates causing cardiac pathologies such as hypertrophy, dilated cardiomyopathy (DCM), and heart failure. Here, we identify ubiquitin-specific peptidase 5 (USP5) as a critical determinant of protein quality control (PQC) in CM.
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