Background: The clinical phenotype dilated cardiomyopathy is assumed to be the endstage of a multifactorial aetiopathogenetic pathophysiology which includes a not satisfactorily defined group of patients with inflammatory cardiomyopathy.
Methods: Within the German Competence Network Heart Failure patients with heart failure due to dilated cardiomyopathy of viral/inflammatory (DCMi/v) and nonviral/noninflammatory (DCM) aetiology were enrolled. After 1 year 237 patients (180 male/57 female) were re-examined including complete clinical work-up. The association of different clinical courses with the time from initial diagnosis of heart failure (newly: ≤ 1 year; late: > 1 year) was investigated.
Results: After 1-year-follow-up New York Heart Association (NYHA) class (by -0.48 in newly diagnosed DCM and -0.82 in newly diagnosed DCMi/v in addition to -0.24 in late diagnosed DCM and -0.17 in late diagnosed DCMi/v) as well as left ventricular ejection fraction (+14% in newly diagnosed DCM and DCMi/v and +6% in later diagnosed DCM and DCMi/v) were significantly improved in all patients. In patients with early diagnosed dilated cardiomyopathy a strong improvement of NYHA class could be demonstrated.
Conclusions: This study demonstrates for the first time a significant interaction between duration of disease, NYHA class and left ventricular ejection fraction in patients with DCM. Our results clearly demonstrate that in patients with DCM an early diagnosis within 1 year after occurrence of clinical signs is associated with a strong improvement in the clinical course, whereas late diagnosis results in a loss of change in clinical course and outcome.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/eci.12483 | DOI Listing |
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.).
Front Surg
January 2025
Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
We report a case of a patient with dilated cardiomyopathy who experienced recurrent ventricular tachycardia (VT) and multiple defibrillations following CRT-D implantation. Due to worsening cardiac function, the patient required surgical implantation of a left ventricular assist device (LVAD) as a bridge to heart transplantation. During the procedure, we used the Ensite three-dimensional mapping system to perform activation and substrate mapping of the VT targets, followed by endocardial and epicardial cryoballoon ablation of clinical VT.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!