The association between cardiac mr feature tracking strain and myocardial late gadolinium enhancement in patients with hypertrophic cardiomyopathy

Aim Hypertrophic cardiomyopathy (HCM) is a relatively common, heritable cardiomyopathy, and cardiac magnetic resonance (CMR) studies have been performed previously to evaluate different aspects of the disease. However, a comprehensive study, including all four cardiac chambers and analysis of left atrial (LA) function, is missing in the literature. The aim of this retrospective study was to analyze CMR-feature tracking (CMR-FT) strain parameters and atrial function of HCM patients and to investigate the association of these parameters with the amount of myocardial late gadolinium enhancement (LGE). Material and Methods In this retrospective, cross-sectional study, we analyzed the CMR images (CMRI) of 58 consecutive patients, who from February 2020 to September 2022 were diagnosed with HCM at our tertiary cardiovascular center. Patients who were younger than 18 yrs or who had moderate or severe valvular heart disease, significant coronary artery disease, previous myocardial infarction, suboptimal image quality, or with contraindication to CMR were excluded. CMRI was performed at 1.5 T with a scanner, and all scans were assessed by an experienced cardiologist and then re-assessed by an experienced radiologist. SSFP 2-, 3- and 4‑chamber, short axis views were obtained and left ventricular (LV) end-diastolic volume (EDV), end-systolic volume (ESV), ejection fraction (EF), and mass were measured. LGE images were obtained using a PSIR sequence. Native T1 and T2 mapping and post-contrast T1 map sequences were performed and each patient’s myocardial extracellular volume (ECV) was calculated. LA volume index (LAVI), LA ejection fraction (LAEF), LA coupling index (LACI) were calculated. The complete CMR analysis of each patient was performed with CVI 42 software (Circle CVi, Calgary, Canada), off-line. Results The patients were divided into two groups, HCM with LGE (n=37, 64 %) and HCM without LGE (n=21, 36 %). The average patient age in the HCM patients with LGE was 50.8±14 yrs and 47±12.9 yrs in the HCM patients without LGE. Maximum LV wall thickness and basal antero-septum thickness were significantly higher in the HCM with LGE group compared to the HCM without LGE group (14.8±3.5 mm vs 20.3±6.5 mm (p<0.001), 14.2±3.2 mm vs 17.3±6.1 mm (p=0.015), respectively). LGE was 21.9±31.7 g and 15.7±13.4 % in the HCM with LGE group. LA area (22.2±6.1 vs 28.8±11.2 cm2; p=0.015) and LAVI (28.9±10.2 vs 45.6±23.1; p-0.004) were significantly higher in the HCM with LGE group. LACI was doubled in the HCM with LGE group (0.2±0.1 vs 0.4±0.2; p<0.001). LA strain (30.4±13.2 vs 21.3±16.2; p-0.04) and LV strain (15.2±3 vs 12.2±4.5; p=0.012) were significantly decreased in the HCM with LGE group. Conclusion This study sheds light on the CMR-FT differences between HCM with and without LGE. We found a greater burden of LA volume but significantly lower LA and LV strain in the LGE patients. These findings highlight further the LA and LV remodeling in HCM. Impaired LA function appears to have physiological significance, being associated with greater LGE. While our CMR-FT findings support the progressive nature of HCM, beginning with sarcomere dysfunction to eventual fibrosis, further studies are needed to validate these results in larger cohorts and to evaluate their clinical relevance.