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Myocardial fibrosis progression on cardiac magnetic resonance in hypertrophic cardiomyopathy
  1. Hong-Mi Choi1,
  2. Kyung-Hee Kim2,
  3. Joo Myung Lee1,
  4. Yeonyee E Yoon1,
  5. Seung-Pyo Lee1,
  6. Eun-Ah Park3,
  7. Whal Lee3,
  8. Yong-Jin Kim1,
  9. Goo-Yeong Cho1,
  10. Dae-Won Sohn1,
  11. Hyung-Kwan Kim1
  1. 1Department of Internal Medicine, Cardiovascular Center, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Republic of Korea
  2. 2Department of Internal Medicine, Division of Cardiology, Sejong General Hospital
  3. 3Department of Radiology, Cardiovascular Section, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Republic of Korea
  1. Correspondence to Professor Hyung-Kwan Kim, Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 110-744, Republic of Korea; cardiman73{at}gmail.com or hkkim73{at}snu.ac.kr

Abstract

Objective We hypothesised that, in hypertrophic cardiomyopathy (HCM), late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) is progressive and can be predicted by baseline CMR findings and HCM phenotype.

Methods In this single-centre cohort study, 71 patients with HCM (59±13 years; 48 men) were prospectively enrolled with clinical, echocardiographic and CMR data. Two consecutive CMR scans were performed with a time interval of 582±174 days. The LGE extent was quantified as a proportion of total LV myocardium (%LGE).

Results LGE was present in 65 patients (91.5%) at the first CMR (CMR-1). In all, LGE extent was significantly increased (p<0.001). A difference in %LGE between the two CMR scans was correlated with the initial %LGE (r=0.44, p<0.001). LGE progression, defined as >4% increase in LGE at the second CMR, was present in 19 patients with non-apical HCM (36.5%), but in only one apical HCM (5.3%). Also, LGE progression rate was significantly higher in non-apical (0.15%/month) versus apical HCM (0.025%/month) (p=0.001). On the multivariate model #1 including only clinical variables (age, history of paroxysmal atrial fibrillation, LV outflow tract obstruction on echocardiography, beta-blocker use, family history of sudden death, family history of HCM, syncope, non-sustained ventricular tachycardia, rate pressure product, and HCM phenotype), only apical HCM phenotype was associated with less LGE progression (p=0.038). On the multivariate model #2 including CMR variables additional to the model #1, %LGE at CMR-1 was the only determinant for LGE progression (p=0.007). When the analysis was limited to patients with preserved EF, results remained unchanged.

Conclusions Myocardial fibrosis in HCM is a progressive phenomenon. Non-apical phenotype and a higher LGE extent at CMR-1 are both associated with greater LGE progression.

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