Cardiac MRI radiomics and texture analysis for differentiating the causes of left ventricular hypertrophy: a...

Because the causes of left ventricular hypertrophy (LVH) share a thickened-wall phenotype yet demand divergent management, from transthyretin stabilization in cardiac amyloidosis (CA) to sudden-death prevention in hypertrophic cardiomyopathy (HCM), identifying the cause is clinically decisive. Cardiac MRI radiomics and texture analysis are proposed for this differential. We asked whether this evidence supports clinically credible differentiation and whether each accuracy could be verified.

Following PRISMA-DTA, the etiological contrast was the unit of analysis. Two reviewers appraised risk of bias with QUADAS-2 and QUADAS-AI, radiomic quality with METRICS, and reporting completeness, then rated certainty with GRADE. Evidence was synthesized without meta-analysis.

Eleven studies (2019 to 2025; 91 to 621 participants, mostly retrospective, single-center) were included. By etiological contrast (studies overlapped): six HCM versus hypertensive heart disease (HHD), four CA versus HCM, one each for sarcomeric genotypes and aortic stenosis, two multiclass. A validation 2 × 2 table was reconstructable in 4 of 11 studies, only 3 from a held-out or cross-validated set; for CA versus HCM, none of 4 reported per-class counts. No study reported external geographic validation, overfitting or its high risk was evident in 8 of 11, and no contrast supported valid pooling. Certainty was very low throughout.

The evidence does not yet support clinically credible differentiation of LVH causes: every apparently high accuracy rests on internally validated, high-risk-of-bias studies of very low certainty; radiomics remains adjunctive and hypothesis-generating. Progress requires external validation, verifiable reporting, and conventional comparators; we distill existing standards into a minimum reporting set.