Artificial Intelligence-Derived Myocardial Fibrosis on Cardiac Magnetic Resonance for Prognosis in Cardiomyopathy: A Systematic Review of a Sparse Evidence Base.
Authors
Affiliations (5)
Affiliations (5)
- Division of Cardiothoracic Imaging, Department of Radiology and Imaging Sciences, Emory University, Atlanta, GA, USA. Electronic address: [email protected].
- Ziauddin University, Karachi, Pakistan.
- Department of Medicine, Jinnah Sindh Medical University, Karachi, Pakistan.
- Division of Cardiothoracic Imaging, Department of Radiology, Mayo Clinic, Phoenix, AZ, USA.
- Division of Cardiothoracic Imaging, Department of Radiology and Imaging Sciences, Emory University, Atlanta, GA, USA.
Abstract
Myocardial fibrosis on cardiovascular magnetic resonance (CMR), assessed by late gadolinium enhancement (LGE) and parametric mapping, is an established predictor of adverse events in cardiomyopathy. We assessed whether artificial intelligence (AI) quantification of fibrosis adds independent prognostic value. We searched six databases, a clinical-trials register, and a preprint server from inception to 13 June 2026. Eligible studies used AI to generate a fibrosis marker in adults with ischemic or nonischemic cardiomyopathy, with covariate-adjusted outcomes over ≥12 months. Risk of bias was assessed using PROBAST, PROBAST+AI, and QUIPS. Fewer than three comparable studies precluded meta-analysis; certainty was rated using GRADE. Of 448 records (381 after de-duplication), 18 full texts were reviewed and two included, one peer-reviewed and one preprint. In an ischemic-cardiomyopathy registry (Ghanbari et al.; n = 216 analytic, 26 events), AI-derived dense LGE scar predicted arrhythmic events (univariable hazard ratio [HR] 2.35, 95% CI 1.33-4.15), and AI-derived but not manual scar improved discrimination beyond guideline criteria (area under the curve 0.63 to 0.68; p = 0.02). In a nonischemic dilated-cardiomyopathy preprint (Kim et al.; n = 347, 119 events), automated extracellular volume ≥30% predicted cardiovascular death or heart-failure hospitalization (adjusted HR 2.00, 95% CI 1.32-3.03). Both were at high risk of bias, with data-derived thresholds and no external validation. Across only two studies, AI-derived fibrosis was independently associated with adverse cardiovascular events, but its added value over manual quantification remains unproven. Certainty was very low. The evidence base is sparse and not yet ready for clinical use.