Background: 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 imaging (CMR) can detect myocardial fibrosis. We aimed to assess the relationship between ECG findings and LGE in such patients. Methods: Thirty-three consecutive patients with HCM (mean age; 55.5 짹 10.7 years, 21 male) 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=10), the apical hypertrophy group (AP group, N=13), and diffuse hypertrophy group (DH group, N=10) The transmural and segmental extent, pattern and location of myocardial LGE were assessed and analyzed in relation to ECG changes. Results: All of the subjects showed some degree of LGE on CMR. There were no specific ECG changes for each of the HCM groups. The transmural extent or 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=0.001) and ST elevation (��� 1 mm) on anterior precordial leads (p=0.015), and was found in 90% of the ASH group, 39% of the AP group, and 80% of the DH group. LGE at the apex of the heart was present in 10% of the ASH group, the 100% of AP group, and 100% of the DH group, and was also associated with ST elevation on anterior precordial leads (p=0.015). LGE at the junction of right ventricle and the interventricular septum could be seen in 60% of the ASH group, 46% of the AP group, and 70% of the DH group, and was associated with first –degree atrio-ventricular block (p=0.040). Diffuse LGE lesions were associated with increased QRS duration (p=0.015) and presence of first-degree atrio-ventricular block (p=0.011) as opposed to single nodular or patchy pattern of presence. Conclusions: 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.