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Role of late gadolinium enhancement cardiovascular magnetic resonance in the risk stratification of hypertrophic cardiomyopathy
  1. Tevfik F Ismail1,2,
  2. Andrew Jabbour1,2,
  3. Ankur Gulati1,
  4. Amy Mallorie1,2,
  5. Sadaf Raza1,2,
  6. Thomas E Cowling1,2,
  7. Bibek Das1,2,
  8. Jahanzaib Khwaja1,2,
  9. Francisco D Alpendurada1,
  10. Ricardo Wage1,
  11. Michael Roughton3,
  12. William J McKenna4,
  13. James C Moon4,
  14. Amanda Varnava5,
  15. Carl Shakespeare1,6,
  16. Martin R Cowie1,2,
  17. Stuart A Cook1,2,
  18. Perry Elliott4,
  19. Rory O'Hanlon1,
  20. Dudley J Pennell1,2,
  21. Sanjay K Prasad1,2
  1. 1Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital, London, UK
  2. 2Imperial College London, London, UK
  3. 3R-Squared Statistics, London, UK
  4. 4Institute of Cardiovascular Science, University College London, London, UK
  5. 5West Hertfordshire Hospitals NHS Trust, Hertfordshire, UK
  6. 6Department of Cardiology, South London Healthcare NHS Trust, London, UK
  1. Correspondence to Professor Dudley J Pennell, Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK; d.pennell{at}ic.ac.uk

Abstract

Objective Myocardial fibrosis identified by late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) in patients with hypertrophic cardiomyopathy (HCM) is associated with adverse cardiovascular events, but its value as an independent risk factor for sudden cardiac death (SCD) is unknown. We investigated the role of LGE-CMR in the risk stratification of HCM.

Methods We conducted a prospective cohort study in a tertiary referral centre. Consecutive patients with HCM (n=711, median age 56.3 years, IQR 46.7–66.6; 70.0% male) underwent LGE-CMR and were followed for a median 3.5 years. The primary end point was SCD or aborted SCD.

Results Overall, 471 patients (66.2%) had myocardial fibrosis (median 5.9% of left ventricular mass, IQR: 2.2–13.3). Twenty-two (3.1%) reached the primary end point. The extent but not the presence of fibrosis was a significant univariable predictor of the primary end point (HR per 5% LGE: 1.24, 95% CI 1.06 to 1.45; p=0.007 and HR for LGE: 2.69, 95% CI 0.91 to 7.97; p=0.073, respectively). However, on multivariable analysis, only LV-EF remained statistically significant (HR: 0.92, 95% CI 0.89 to 0.95; p<0.001). For the secondary outcome of cardiovascular mortality/aborted SCD, the presence and the amount of fibrosis were significant predictors on univariable but not multivariable analysis after adjusting for LV-EF and non-sustained ventricular tachycardia.

Conclusions The amount of myocardial fibrosis was a strong univariable predictor of SCD risk. However, this effect was not maintained after adjusting for LV-EF. Further work is required to elucidate the interrelationship between fibrosis and traditional predictors of outcome in HCM.

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