Correlation of Electrocardiographic Changes and Myocardial Fibrosis in Patients With Hypertrophic Cardiomyopathy Detected by Cardiac Magnetic Resonance Imaging

Abstract

Despite several electrophysiologic and pathologic studies, the cause of electrocardiographic (ECG) changes in patients with hypertrophic cardiomyopathy (HCM) remains unclear. Late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) imaging can detect myocardial fibrosis. We aimed to assess the relationship between ECG findings and LGE in such patients. Myocardial LGE may be associated with ECG changes in HCM. Seventy consecutive patients with HCM (mean age, 55.5 ± 10.7 years; 47 males) underwent CMR and 12-lead ECG. The subjects were divided into 3 groups according to the type of hypertrophy: the asymmetric septal hypertrophy group (ASH group, n = 31), the apical hypertrophy group (AP group, n = 22), and concentric hypertrophy group (CH group, n = 17). The transmural and segmental extent, pattern, and location of myocardial LGE were assessed and analyzed in relation to ECG changes. All of the subjects showed some degree of LGE on CMR. The AP group showed significantly higher prevalence of negative T-wave (P = 0.028) and deep negative T-wave inversion (P = 0.001) than the ASH and CH groups. The total volume of LGE did not show any significant association with ECG changes. LGE detected at the interventricular septum was associated with increased QRS duration (P = 0.009) and was found in 94% of the ASH group, 59% of the AP group, and 77% of the CH group. LGE at the apex of the heart was present in 32% of the ASH group, 73% of the AP group, and 35% of the CH group and was also associated with negative T-wave (P = 0.006) and deep negative T-wave inversion (P = 0.018). Multifocal LGE lesions were associated with increased QRS duration (P = 0.039) as opposed to single nodular or patchy pattern of presence. The location of myocardial LGE in HCM shows significant association with various ECG changes. This may be useful information for initially evaluating subjects with HCM and adds pathophysiological insight into understanding ECG changes in myocardial diseases that cannot be explained otherwise.