# Dataset on cardiac structural and functional parameters in TMAO-challenged mouse

## TL;DR

This paper provides a dataset on how TMAO, a gut metabolite, affects heart structure and function in mice, offering tools for further research into its role in cardiovascular disease.

## Contribution

The dataset includes original echocardiography files for reprocessing, enabling customizable and transparent analyses of TMAO-induced cardiac effects.

## Key findings

- TMAO-challenged mice showed altered cardiac functional parameters compared to controls.
- The dataset includes high-resolution images and CSV reports for detailed cardiac assessments.
- Original echocardiography files are provided to allow reproducible and tailored data analysis.

## Abstract

Trimethylamine-N-oxide (TMAO) is a gut-derived metabolite formed from dietary choline and l-carnitine, known to impede cholesterol metabolism and is implicated in the pathogenesis of thrombosis and atherosclerosis, contributing to the etiology of cardiovascular diseases. We present a dataset derived from an experimental study designed to elucidate the cardiotoxic effects of TMAO. This dataset encompasses echocardiographic assessments from two cohorts of mice: one subjected to a 6-week regimen of 20 mg/kg/day TMAO injections (n = 16) and a control group (n = 18). Each subject's echocardiographic dataset comprises six high-resolution TIFF images, capturing both B-type and M-mode views in standard echocardiographic planes, along with two additional M-mode images enriched with analysed cardiac functional data. Complementing these images, a CSV-formatted report details critical cardiac parameters, including heart rate, ejection fraction, and fractional shortening, among others. In a novel approach to enhance data integrity and permit tailored analyses, we provide the original output files from the echocardiography apparatus, which researchers can reprocess using dedicated analysis software. This dataset is anticipated to be instrumental in advancing our understanding of the mechanistic links between TMAO exposure and cardiac dysfunction.