337Value of feature tracking cardiovascular magnetic resonance imaging in detecting genotype-positive hypertrophic cardiomyopathy
Year: 2019
Type: article
Study design: Observational Study
Abstract: Background/Introduction: Since the phenotypic expression of Hypertrophic Cardiomyopathy (HCM) is variable and some patients express only mild left ventricular hypertrophy (LVH), the differentiation between genotype-positive HCM and genotype-negative causes of LVH can be challenging. Myocardial deformation imaging can detect early contractile dysfunction, and may therefore be usable in HCM. Purpose: This cross-sectional study assesses the ability of feature tracking cardiovascular magnetic resonance imaging (FT-CMR) to distinguish between genotype-positive and genotype-negative LVH. Methods: Monocenter study of 145 patients (27,6% females, 51,13 ± 14.29 years) who had a maximum myocardial wall thickness (MMWT) ≥13mm on good quality CMR and underwent genetic testing in the University Medical Center Utrecht. We excluded patients if no clinical information was available or if there was a history of myocardial infarction or cardiac intervention. LV endocardial contours of short axis, horizontal longitudinal axis and vertical long axis were traced using Medis QStrain software. This allowed calculation of the wall motion in longitudinal, radial and circumferential strain. The Mann-Whitney U test was used for statistical analysis. Results: No difference was found in feature tracking strain patterns in HCM genotype-positive LVH (n = 46) compared to genotype-negative (n = 99) patients with LVH. There was also no difference when comparing strain values stratified for region of hypertrophy (septal, apical or concentric LVH). However, when comparing strain values in patients with mild LVH (MMWT 13-15mm, n = 43) there was a significant difference in strain values between MYBPC3 mutation carriers (n = 7) versus MYBPC3 mutation negative patients (n = 36) [MYH7 mutation carriers n = 4, other mutation carriers n = 4, genotype negative n = 28]. This reached statistical significance for long axis global longitudinal strain (GLS) -20,64 (p = 0,045), global circumferential strain (GCS) -35,04 (p = 0,049) and global regional strain (GRS) 64,37 (p = 0,029). The short axis showed no significant difference in strain values (p = 0,062). There was also a significant difference in strain values in genotype positive patients with any MMWT between MYBPC3 mutation positive (n = 29) and carriers of other mutations (MYH7 n = 9, other n = 8) on all axis [long axis GLS -17.42 (p = 0,022), GCS -35.48 (p = 0,010), GRS 61.48 (p = 0,015), short axis GCS -29.45 (p = 0,026)]. Conclusions: FT-CMR cannot distinguish between genotype-positive or genotype-negative patients with HCM, but can help discriminate MYBPC3 mutation carriers from other patients with mild LVH (≤15mm). FT-CMR also discriminates MYBPC3 carriers in a genotype-positive cohort. These findings may point to a different pathological mechanism in MYBPC3 mutation carriers. Larger studies are necessary to investigate if FT-CMR is of value in early detection and risk stratification of genotype-positive HCM patients with mild LVH.
Institution: University Medical Center Utrecht
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2948593231