Dilated cardiomyopathy (DCM) is an underrecognized condition with a myriad of etiologies, but it is often labeled idiopathic. However, genetic mutations are emerging as a more common cause of idiopathic DCM than previously believed. Herein, we present a case of a previously healthy 45-year-old woman who presented with three weeks of exertional dyspnea and orthopnea. An echocardiogram showed DCM with severely reduced systolic function and diastolic dysfunction. She was extensively worked up for potential etiologies of her heart failure which included HIV testing, parasite smear, viral serologies, autoimmune testing, cardiac MRI for infiltrative diseases, and coronary catheterization. She was ultimately tested for genetic mutations which revealed a 49-51 exon deletion of the dystrophin (Duchenne muscular dystrophy (DMD)) gene. This case highlights the guideline-based evaluation and management of new-onset heart failure in a healthy 45-year-old female without known predisposing risk factors or family history. It also sheds light on the expansive genetic etiologies that have only recently been identified in those with idiopathic cardiomyopathy. Further research is crucial to improve our understanding of genetic associations of cardiomyopathy.
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http://dx.doi.org/10.7759/cureus.55170 | DOI Listing |
Eur Heart J Imaging Methods Pract
January 2025
Department of Cardiology, Cardiovascular Research Institute Basel, University Hospital Basel, University of Basel, Basel, Switzerland.
Clin Genet
January 2025
Sorbonne Université- DMU BioGem-Unité Fonctionnelle de Cardiogénétique et Myogénétique Moléculaire et Cellulaire, Service de Biochimie Métabolique, APHP-Hôpital Universitaire Pitié Salpêtrière, Paris, France.
Titin truncating variants (TTNtv) are the main genetic cause of dilated cardiomyopathies (DCMs). The phenotype and prognosis of probands have been evaluated in several large cohorts. However, few data are available on intrafamilial expressivity.
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.
View Article and Find Full Text PDFArq Bras Cardiol
January 2025
Programa de Pós-Graduação em Alimentação, Nutrição e Saúde - Universidade Federal do Rio Grande do Sul, Porto Alegre, RS - Brasil.
Background: The angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism (rs4340) is associated with the pathogenesis of heart failure (HF). This polymorphism may contribute to a greater propensity for severe HF and excess weight.
Objective: To evaluate adiposity, cardiac function, and their association with ACE I/D polymorphism in HF patients.
Circ Genom Precis Med
January 2025
Department of Cardiology, Cardiovascular Research Institute Maastricht, Maastricht University, the Netherlands (S.L.V.M.S., N.J.B., M.F.G.H.M.V., V.P.M.v.E., J.A.J.V.).
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