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Original article
Global longitudinal strain is associated with heart failure outcomes in hypertrophic cardiomyopathy
  1. Patricia Reant1,2,
  2. Mariana Mirabel1,3,
  3. Guy Lloyd1,
  4. Jérôme Peyrou2,
  5. Jose-Maria Lopez Ayala1,
  6. Shaughan Dickie1,
  7. Heeraj Bulluck1,
  8. Gabriella Captur1,
  9. Stefania Rosmini1,
  10. Oliver Guttmann1,
  11. Camelia Demetrescu1,
  12. Antonis Pantazis1,
  13. Maite Tome-Esteban1,
  14. James C Moon1,
  15. Stephane Lafitte2,
  16. William J McKenna1
  1. 1Inherited Cardiac Disease Unit, The Heart Hospital; Institute of Cardiovascular Science, University College London, London, UK
  2. 2University of Bordeaux, CHU de Bordeaux, Bordeaux, France
  3. 3Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Paris, France
  1. Correspondence to Dr Patricia Reant, Hopital Cardiologique Haut-Leveque, Pessac 33600, France; patricia.reant{at}chu-bordeaux.fr

Abstract

Objective We hypothesised that abnormal global longitudinal strain (GLS) would predict outcome in hypertrophic cardiomyopathy (HCM) better than current echocardiographic measures.

Methods Retrospective analysis of risk markers in relation to outcomes in 472 patients with HCM at a single tertiary institution (2006–2012). Exclusion criteria were left ventricular (LV) hypertrophy of other origin, patients in atrial fibrillation, lost to follow-up and insufficient image quality to perform strain analysis. Standardised echocardiogram recordings were reviewed and standard variables and LV GLS were measured. The primary end-point included all cardiac deaths, appropriate defibrillator shocks and heart failure (HF) admissions. The secondary end-point was death by HF and admissions related to HF.

Results Mean age was 50.0±15.0 years; 322 (68%) were men. At a median of 4.3 years (IQR 0.1–7.8) follow-up, 21 (4.4%) patients experienced cardiovascular death: 6 (1.3%) died from HF, 13 (2.7%) had sudden cardiac death and 2 (0.4%) died secondary to stroke. Four (0.8%) patients experienced appropriate defibrillator shock, and 13 (2.7%) were admitted for HF. On multivariate Fine–Gray proportional hazard analyses, GLS was significantly associated with the primary end-point (HR=0.90, 95% CI 0.83 to 0.98, p=0.018) independently of age, maximal provoked LV outflow-tract gradient and LV end-systolic volume. Moreover, GLS was particularly associated with the secondary end-point (HR=0.82, 95% CI 0.75 to 0.90, p<0.0001) independently of age, previous atrial fibrillation, New York Heart Association (NYHA) class III–IV, LV end-systolic volume, E/E′, and outflow-tract gradient. Survival curves confirmed that GLS was associated with HF events (GLS <15.6%, p=0.0035).

Conclusions In patients with HCM, reduced GLS is an independent factor associated with poor cardiac outcomes, and particularly HF outcomes.

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