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Left ventricular hypertrophy (LVH) represents a frequent observation in clinical practice. Nonetheless, the hypertrophic phenotype emerges as a common manifestation of diverse conditions, thereby presenting a diagnostic conundrum for clinicians. Differentiation among the etiologies of LVH is imperative for therapy decision-making, as different approaches must be implemented for distinct conditions, such as LVH secondary to loading changes, hypertrophic cardiomyopathy (HCM), or HCM mimics. In some instances, an erroneous or late diagnosis may lead to a progression of the underlying disease with worsening functional capacity, high morbidity and mortality. The rational use of cardiovascular multimodality imaging is of great importance when carried out in addition to a thorough clinical assessment and correlated with electrocardiographic findings, providing clues to fill the gaps, being, most of the time, the missing piece to solve this challenging puzzle. An integrative approach is of paramount importance for the evaluation of these patients, as they are often followed by several specialties, with varied systemic manifestations. Although a multidisciplinary team is needed for an optimized follow-up of these patients, the most important player in this journey is the clinician, whose mission is to bring together all the red flags and coordinate all the data for an assertive diagnosis. The objective of this review is to provide a pragmatic methodology, highlighting important clues for discriminating among the diverse conditions that result in LVH.
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http://dx.doi.org/10.36660/abc.20240529 | DOI Listing |
Int Immunopharmacol
September 2025
Department of Animal Science, College of Agricultural, Yanbian University, Yanji 133002, China; Jilin Provincial Key Laboratory of Transgenic Animal and Embryo Engineering, Yanbian University, Yanji 133002, China. Electronic address:
Objective: Long-term administration of dexamethasone (DEX) to treat severe inflammation or autoimmune disorders often result in skeletal muscle atrophy and functional decline. Exosomes facilitate intercellular communication by transferring bioactive molecules, reflecting the characteristics of their tissue of origin. Myostatin-knockout (MSTN) mice exhibit muscle hypertrophy, and their muscle-derived exosomes (KO-EXOs) retain this phenotype.
View Article and Find Full Text PDFJCI Insight
September 2025
Department of Pharmacology, University of Michigan, Ann Arbor, United States of America.
Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure. We examined how S-palmitoylation of the small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), impacts cardiomyocyte stress signaling. Mutation of the cysteine-178 palmitoylation site impaired activation of Rac1 when overexpressed in cardiomyocytes.
View Article and Find Full Text PDFOsteoarthritis Cartilage
September 2025
Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Bioengineering, University of Pittsburgh Swanson School of Engineering, Pittsburgh, PA, USA; Orland Bethel Family Musculoskeletal Research Center, University of Pittsburgh School of Med
Objective: Previous studies in our lab demonstrated that estrogen receptor-α (ERα) levels in cartilage decreased with osteoarthritis (OA). We also defined the essential role of ERα in maintaining the health of chondrocytes. However, most of the studies were conducted in vitro, and the physiological link between ERα loss and cartilage degradation has not been demonstrated using animal models.
View Article and Find Full Text PDFBiomech Model Mechanobiol
September 2025
Department of Engineering Mechanics, School of Ocean and Civil Engineering, Shanghai Jiao Tong University, Shanghai, 200240, China.
Left ventricular outflow tract obstruction (LVOTO) is a representative phenotype of obstructive hypertrophic cardiomyopathy (OHCM). Septal myectomy has been extensively demonstrated as an effective surgery for treating OHCM. However, it remains incompletely understood how the surgery would alter the mechanical and energetic states of the left ventricle (LV).
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