Key result
CMR strain correlates with LV mass index and fibrosis but not VO2 peak in HCM.
Why the study?
Evaluating the relationship between CMR-derived myocardial strain and peak oxygen uptake from CPET could help assess ventricular dysfunction and its impact on functional capacity in patients with HCM.
Does CMR-derived myocardial strain correlate with functional impairment (VO₂ peak) in patients with hypertrophic cardiomyopathy?
Does CMR-derived myocardial strain correlate with functional impairment (VO₂ peak) in patients with hypertrophic cardiomyopathy?
In patients with hypertrophic cardiomyopathy, CMR-derived myocardial strain correlates with LV mass and fibrosis but does not correlate with functional exercise capacity (VO₂ peak).
Answers are grounded in this paper and cite their sources.
Strain fails to track exercise capacity in HCM despite structural links; leaves open its incremental prognostic role.
Introduction Hypertrophic cardiomyopathy (HCM) is a common hereditary condition with a wide phenotypic expression. Some individuals remain asymptomatic with a normal life expectancy, while others experience symptoms and severe cardiac events (1). Myocardial strain, assessed using cardiac magnetic resonance imaging (CMR), is a key quantitative measure of left ventricular (LV) deformation, providing valuable insights into ventricular function (2). Patients with HCM often present with both overt and subclinical LV dysfunction, along with reduced functional capacity. The relationship between myocardial strain and peak oxygen uptake (VO₂ peak) could be crucial in evaluating ventricular dysfunction and its impact on functional capacity, thereby aiding clinical management (3). Objective This study aimed to assess the association between myocardial strain and functional impairment, as measured by VO₂ peak from cardiopulmonary exercise testing (CPET) in patients with HCM. Methods A cohort of HCM patients underwent a comprehensive assessment, including transthoracic echocardiography, CMR, and CPET. CMR was performed using a 1.5-T scanner. Myocardial strain was analyzed using feature tracking, and late gadolinium enhancement (LGE) quantification was conducted with specialized cardiovascular imaging software. A linear regression model was applied to explore relationships between myocardial strain, clinical parameters, CPET data, echocardiographic findings, and CMR-derived LV metrics. Results The study included 32 HCM patients diagnosed between January 2017 and April 2023. Of these, 71% were male, with a mean age of 50 ± 15.3 years. The average LV ejection fraction was 70.8% ± 10.9%, mean myocardial strain was -12% ± 3.4%, and mean VO₂ peak was 25 ± 8 mL/kg/min. Myocardial strain was significantly associated with LGE extent (β = 9.8, p = 0.022) and indexed LV mass (β = 0.08, p = 0.001). However, no significant relationship was found between myocardial strain and VO₂ peak (β = -0.39, p = 0.358) or intraventricular pressure gradients (β = -0.001, p = 0.93). Conclusions In patients with HCM, CMR-derived myocardial strain is inversely correlated with LV mass index and the extent of myocardial fibrosis detected by LGE. These findings suggest that strain analysis is useful for assessing LV systolic function, particularly when traditional parameters remain within normal ranges. However, myocardial strain did not correlate with functional exercise capacity, as measured by CPET. Further research is needed to better understand the interaction between LV remodeling, myocardial fibrosis, and functional performance in HCM patients.
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Cantora et al. (2025) studied this question. CMR-derived myocardial strain correlates with LV mass index and fibrosis extent but not with VO2 peak in HCM patients.
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