# Cardiomyopathies: Temporal Review and Genetic Determination

**Authors:** Gaetano Thiene, Stefania Rizzo, Cristina Basso

PMC · DOI: 10.3390/biomedicines13102470 · Biomedicines · 2025-10-10

## TL;DR

This paper reviews the history and genetic causes of cardiomyopathies, including newly recognized electrical dysfunction types.

## Contribution

The paper expands the definition of cardiomyopathies to include electrical dysfunction without structural changes, emphasizing genetic factors.

## Key findings

- Cardiomyopathies now include electrical disorders like channellopathies.
- Genetic background and gene therapy are key areas of focus in modern cardiomyopathy research.

## Abstract

Cardiomyopathies are a heterogeneous group of diseases of the myocardium associated with dysfunction, with or without a structural substrate. They are frequently genetically determined. The dysfunction may be mechanical, both of the systole and diastole, or electrical, including arrhythmias or conduction disorders. Originally, only dilated, hypertrophic, restrictive–obliterative and arrhythmogenic dysfunctions were considered cardiomyopathies. Nowadays, since dysfunction can also be electric, disorders affected by electrical dysfunction without a structural substrate can be regarded as cardiomyopathies as well. This is the case of channellopathies and ryanodine receptors. This paper is a review of the history of cardiomyopathies, including the issues of their classification and nomination, genetic background and gene therapy.

## Linked entities

- **Diseases:** cardiomyopathies (MONDO:0004994)

## Full-text entities

- **Diseases:** arrhythmogenic dysfunctions (MESH:D019571), Cardiomyopathies (MESH:D009202), arrhythmias or conduction disorders (MESH:D001145), diseases of the myocardium (MESH:D017682), hypertrophic (MESH:D002312), dysfunction (MESH:D006331)

## Full text

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## Figures

26 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12561973/full.md

## References

39 references — full list in the complete paper: https://tomesphere.com/paper/PMC12561973/full.md

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Source: https://tomesphere.com/paper/PMC12561973