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Unravelling the grey zone: cardiac MRI volume to wall mass ratio to differentiate hypertrophic cardiomyopathy and the athlete's heart
  1. Tim Luijkx1,
  2. Maarten J Cramer2,
  3. Constantinus F Buckens1,3,
  4. Abbas Zaidi4,
  5. Rienk Rienks2,5,
  6. Arend Mosterd2,3,6,
  7. Niek HJ Prakken1,
  8. Barbara Dijkman2,
  9. Willem PThM Mali1,
  10. Birgitta K Velthuis1
  1. 1Department of Radiology, University Medical Center Utrecht, Utrecht, The Netherlands
  2. 2Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands
  3. 3Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands
  4. 4Department of Cardiovascular Sciences, St George's, University of London, London, UK
  5. 5Department of Cardiology, Central Military Hospital, Utrecht, The Netherlands
  6. 6Department of Cardiology, Meander Medical Center, Amersfoort, The Netherlands
  1. Correspondence to Dr T Luijkx, Department of Radiology, Room E 01.132, University Medical Center Utrecht, Heidelberglaan 100, Utrecht 3584 CX, The Netherlands; tluijkx{at}gmail.com

Abstract

Background Differentiating physiological left ventricular hypertrophy (LVH) in athletes from pathological hypertrophic cardiomyopathy (HCM) can be challenging. This study assesses the ability of cardiac MRI (CMR) to distinguish between physiological LVH (so-called athlete's heart) and HCM.

Methods 45 patients with HCM (71% men and 20% athletic) and 734 healthy control participants (60% men and 75% athletic) underwent CMR. Quantitative ventricular parameters were used for multivariate logistic regression with age, gender, sport status and left ventricular (LV) end-diastolic volume (EDV) to ED ventricular wall mass (EDM) ratio as covariates. A second model added the LV EDV : right ventricular (RV) EDV ratio. The performance of the model was subsequently tested.

Results LV EDM was greater in patients with HCM (74 g/m2) compared with healthy athletes/non-athletes (53/41 g/m2), while LV EDV was largest in athletes (114 ml/m2) as compared with non-athletes (94 ml/m2) and patients with HCM (88 ml/m2). The LV EDV : EDM ratio was significantly lower in patients with HCM compared with healthy controls and athletes (1.30/2.39/2.25, p<0.05). The LV EDV : RV EDV ratio was significantly greater in patients with HCM (1.10) than in healthy participants (non-athletes/athletes 0.94/0.93). The regression model resulted in high sensitivity and specificity levels in all and borderline-LVH participants (as defined by septal wall thickness). Corresponding areas under the receiver operator characteristic (ROC) curves were 0.995 (all participants) and 0.992 (borderline-LVH participants only). Adding the LV EDV : RV EDV ratio yielded no additional improvement.

Conclusions A model incorporating the LV EDV : EDM ratio can help distinguish HCM from physiological hypertrophy in athletes. This also applies to cases with borderline LVH, which present the greatest diagnostic challenge in clinical practice.

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