Cardiac magnetic resonance strain as a predictor of clinical events in hypertrophic cardiomyopathy

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Hypertrophic cardiomyopathy (HCM) is a relatively prevalent condition associated with cardiovascular death and heart failure. Several tools are currently available to identify which HCM patients are at risk of developing these events. Purpose We aimed to evaluate the association of new Tissue Tracking strain analysis by cardiac magnetic resonance (CMR) and the development of clinical events in patients with HCM. Methods We prospectively analyzed 136 consecutive patients with HCM diagnosis (established according to current clinical practice guidelines) from January 2006 to October 2017. Heart failure hospital admissions and death on follow-up were included in a combined clinical outcome. CMR studies were performed following our predefined CMR protocol for HCM with 1.5T magnets. Cine images were obtained with standard, retrospectively gated, steady-state free-precession (SSFP) sequences in 2, 3 and 4 chambers views and in 10–15 contiguous short-axis slices covering the ventricles from the base to the apex, with breath holding. The strain evaluation was performed by a commercially available Tissue Tracking analysis software, manually defining the endocardial border in short axis, 4, 3 and 2 chambers views and, after verifying adequate identification of the different structures, running the strain analysis (Figure 1, displaying myocardium identification by the strain analysis software). Results Mean follow-up was 49 ± 45 months. Mean age was 61 ± 15.33 years old (p 0.024) and 31% of patients were women (p 0.01). 20% had atrial fibrillation (p 0.154). Mean ejection fraction was 69 ± 9.21% (p 0.762) and mean HCM-SCD (hypertrophic cardiomyopathy sudden cardiac death) risk score was 2.20 ± 1.35 (p 0.885). Mean global radial systolic strain rate (GRSsr) was -1,33 ± 0.59 s-1 (p 0.083). During follow-up, 12 heart failure hospital admissions and 14 death from any cause were registered. GRSsr showed an area under de ROC curve of 0.63 (95% confidence interval -CI- 0.51 – 0.75) predicting clinical events. The value of 1.40 s−1 was selected as the best sensitivity/specificity cutoff point. Three variables (sex, age, and previous history of atrial fibrillation) were chosen (through the allsets method) and included as adjusting variables together with <1,40 s−1/≥1.40 s−1 in a multivariate Cox’s regression model (p 0.002; AIC 99.7; Harrell C index 0.82). Patients with GRSsr <1.40 s−1 showed more clinical evens on follow-up vs those with GRSsr ≥1.40 s−1 (adjusted HR 6.57; 95% CI 2.01 – 21.49; p 0.002; Figure 2, displaying Kaplan-Meier survival estimates). Conclusions A GRSsr <1.40 s−1 emerges as a novel independent predictor of worse clinical outcomes in patients with HCM and preserved ejection fraction.