Key result
CT-derived ECV correlated well with CMR-ECV (31.25% vs 30.88%; r=0.68, P<0.001) and showed comparable discrimination for high-risk HCM (AUC 0.748 vs 0.714, P=0.65).
Why the study?
CMR-derived extracellular volume is an established marker of myocardial fibrosis in HCM, but limited availability and contraindications restrict its widespread use. Cardiac CT-derived ECV is a potential alternative requiring evaluation of its agreement with CMR-ECV and diagnostic performance for fibrosis quantification and high-risk stratification.
Does cardiac CT-derived extracellular volume provide comparable agreement and diagnostic performance to CMR-derived extracellular volume for myocardial fibrosis quantification and high-risk stratification in patients with genetically confirmed hypertrophic cardiomyopathy?
Observational (n=32)
Does cardiac CT-derived extracellular volume provide comparable agreement and diagnostic performance to CMR-derived extracellular volume for myocardial fibrosis quantification and high-risk stratification in patients with genetically confirmed hypertrophic cardiomyopathy?
Cardiac CT-derived extracellular volume demonstrates good agreement with CMR-derived ECV and comparable discrimination for high-risk stratification in hypertrophic cardiomyopathy, offering a viable alternative when CMR is unavailable or contraindicated.
Background Cardiac magnetic resonance (CMR)–derived extracellular volume (ECV) is an established marker of myocardial fibrosis in hypertrophic cardiomyopathy (HCM). However, limited availability and contraindications restrict its widespread use. Cardiac CT–derived ECV (CT-ECV) has emerged as a potential alternative. Purpose To assess the agreement between CT-ECV and CMR-ECV, and to evaluate the diagnostic performance of CT-ECV for myocardial fibrosis quantification and high-risk stratification in HCM. Methods Thirty-two genetically confirmed HCM patients who underwent both cardiac CT and CMR within one month (September 2024–June 2025) were retrospectively analysed. CT-ECV was calculated using non-contrast, contrast-enhanced and delayed-phase images. CMR-ECV was derived from T1 mapping. Segmental analyses were performed at basal, mid-ventricular and apical levels. Interobserver reproducibility of CT-ECV was assessed using intraclass correlation coefficients. Agreement was evaluated using paired t-tests, Pearson correlation and Bland–Altman analyses. High-risk status was defined as late gadolinium enhancement ≥15%. Receiver operating characteristic analysis assessed discrimination for high-risk identification. Results Among 32 patients (65.6% male; mean age 40.1 ± 14.4 years), no significant difference was observed between CT-ECV and CMR-ECV (31.25 ± 5.07% vs. 30.88 ± 4.35%, P = 0.582). CT-ECV correlated significantly with CMR-ECV overall (r = 0.68, P < 0.001) and at basal (r = 0.51), mid-ventricular (r = 0.69) and apical levels (r = 0.69; all P ≤ 0.003). For identification of high-risk patients, the area under the curve was 0.748 for CT-ECV and 0.714 for CMR-ECV (P = 0.65). Conclusions CT-derived ECV demonstrates good agreement with CMR-derived ECV in HCM and provides comparable performance for fibrosis quantification and high-risk stratification. CT-ECV may represent a practical and accessible alternative when CMR is unavailable or contraindicated.figure 1figure 2
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Chen et al. (2026) conducted an observational in Hypertrophic cardiomyopathy (n=32). Cardiac CT-derived extracellular volume (CT-ECV) vs. CMR-derived extracellular volume (CMR-ECV) was evaluated on Agreement with CMR-ECV and diagnostic performance (AUC) for identifying high-risk status (late gadolinium enhancement ≥15%) (r 0.68; AUC 0.748 vs 0.714, p=<0.001 for correlation; 0.582 for mean difference; 0.65 for AUC comparison). CT-derived ECV correlated well with CMR-ECV (31.25% vs 30.88%; r=0.68, P<0.001) and showed comparable discrimination for high-risk HCM (AUC 0.748 vs 0.714, P=0.65).
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