ABSTRACT
Purpose: Left ventricular (LV) replacement fibrosis is a marker of adverse cardiac events in hypertrophic cardiomyopathy (HCM). We aimed to assess the efficacy of the feature-tracking cardiac magnetic resonance (FT-CMR) in the detection of LV replacement fibrosis. Material and methods: Fifty-one patients with HCM (51% female, mean age = 21 ± 5.2 years) and significant myocardial hypertrophy, who underwent CMR between February 2018 and December 2019 were enrolled. Functional and 3D FT-CMR parameters were measured. LV global longitudinal strain, global radial strain (GRS), and global circumferential strain (GCS) were recorded. The percentage of enhanced myocardial mass was calculated. Univariate and multivariate regression analyses were performed to determine the predictors of fibrosis. A p-value of less than 0.05 was considered significant. Results: The mean enhanced mass percentage was 15.2 ± 10.53%. Among LV volumetric parameters, end-systolic and end-diastolic volume indices predicted fibrosis (fitness [F] = 8.11 and p = 0.006 vs. F = 6.6 and p = 0.012, correspondingly). The univariate linear regression demonstrated that GCS and GRS predicted total enhanced mass (%) (F = 12.29 and p = 0.001 vs. F = 7.92 and p = 0.007, respectively). After the inclusion of all volumetric and deformation parameters, the multivariate analysis identified the model of a combination of LV end-diastolic volume index (LV EDVI) and LV GCS as a robust predictor of the fibrosis percentage (F = 8.86 and p = 0.005). Conclusions: Non-contrast CMR parameters including LV GCS and LV EDVI are valuable markers of replacement fibrosis in HCM patients with notable myocardial hypertrophy.
ABSTRACT
Iron-overload cardiomyopathy is the principal cause of mortality in thalassemia. Via feature-tracking cardiac magnetic resonance (FT-CMR), we investigated alterations in cardiac deformation with the progression in myocardial iron overload (MIO). We enrolled 154 patients with thalassemia (50.64% male, mean age = 32.19 ± 9.79 years) referred for MIO assessment and 28 controls (50% male, mean age = 31.07 ± 4.35 years). Functional, strain, and T2* values were assessed in 4 study groups: no MIO (T2* > 20), mild-to-moderate MIO (T2* = 10-20), severe MIO (T2* < 10), and healthy controls. The recorded strain values were compared between the groups. The study groups were statistically significantly different vis-à-vis left ventricular (LV) global longitudinal strain (GLS) (F [3, 178] = 20.30), LV global radial strain (GRS) (F [3, 178] = 11.61), right ventricular (RV) GLS (F [3, 178]) = 5.32), RV global circumferential strain (GCS) (F [3, 178] = 26.02), and RVGRS (F [3, 178] = 16.86) (Ps < 0.005). The post hoc test revealed that LVGLS, RVGCS, and RVGRS were different between patients with thalassemia but without MIO and the control group (Ps < 0.001). A significant difference in LVGLS and LVGRS was detected between the T2* > 20 and 10 ≤ T2* ≤ 20 groups (Ps < 0.05). The multivariate logistic regression analysis depicted LVGRS as the most robust predictor of MIO (T2* ≤ 20) (odds ratio = 0.920, 95% CI 0.886 to 0.955), which predicted MIO with a cutoff point of 31.16% or less (sensitivity = 62% and specificity = 80.77%). Biventricular FT-CMR values are impaired in patients with thalassemia even without MIO. With MIO progression, LV strain values are the first ones to be undermined. Notably, functional CMR indices are jeopardized late, only after severe iron deposition.
