ReviewJournal of clinical medicine2026
Non-Dilated Left Ventricular Cardiomyopathy: Exploring the Spectrum from Phenotype to Disease Entity.
Review in Journal of clinical medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-dilated left ventricular cardiomyopathy has recently emerged as a distinct morpho-functional phenotype defined by non-ischemic left ventricular scarring or fatty replacement or by isolated global left ventricular hypokinesia without scarring in the absence of ventricular dilatation. Whether it represents a distinct biological entity or a shared phenotypic expression across cardiomyopathies remains unresolved. This narrative review examines evidence from genetics, multimodality imaging, natural history, and outcomes. Overlap with dilated and arrhythmogenic cardiomyopathies is extensive: no currently validated genetic, imaging, histological, or circulating marker uniquely identifies the phenotype, and longitudinal studies describe heterogeneous trajectories from reverse remodeling to dilated or predominantly arrhythmogenic evolution. Genetics argues in both directions, as the genes involved are shared yet their distribution differs, pro-arrhythmogenic variants being more frequent than in dilated cardiomyopathy. We propose a hypothesis-generating framework of three probable trajectories, evolving dilated cardiomyopathy, evolving arrhythmogenic cardiomyopathy, or stable non-dilated disease, integrating genotype, multiparametric cardiac magnetic resonance, longitudinal remodeling, and arrhythmic phenotype.
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