Myocardial fibrosis progression on cardiac magnetic resonance in hypertrophic cardiomyopathy. Issue 11 (20th April 2015)

• Record Type: Journal Article
• Authors: Choi, Hong-Mi; Kim, Kyung-Hee; Lee, Joo Myung; Yoon, Yeonyee E; Lee, Seung-Pyo; Park, Eun-Ah; Lee, Whal; Kim, Yong-Jin; Cho, Goo-Yeong; Sohn, Dae-Won; Kim, Hyung-Kwan
• Is Part Of: Heart. Volume 101:Issue 11(2015)
• Page Start: 870
• Page End: 876
• Publication Date: 2015-04-20
• Subjects: Heart -- Diseases -- Treatment -- Periodicals; Cardiology -- Periodicals; 616.12
• DOI: 10.1136/heartjnl-2014-306555
• Languages: English
• ISSNs: 1355-6037

Abstract

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.