Twelve-lead electrocardiography, a traditional component in evaluations of patients with hypertrophic cardiomyopathy (HC), is often regarded as a marker for the magnitude of left ventricular(LV) hypertrophy, which in turn has been linked to sudden death risk. To determine whether electrocardiographic(ECG) patterns have clinical utility by accurately reflecting phenotypic expression or predicting clinical outcome, voltages and patterns were compared with LV wall thicknesses assessed by echocardiography and with clinical outcomes in 448 consecutive patients with HC. Significant but relatively weak correlations were evident between maximum LV wall thickness and ECG voltage: r=0.295(p< 0.01) for the sum of R-and S-wave voltages in all 12 leads, r=0.254(p< 0.01)for the maximum R or S wave in any lead, and r=0.210(p< 0.01) for the sum of SV1(or SV2) and RV5(or RV6). Of 55 patients with extreme LV hypertrophy(LV wall thickness ≥30 mm), only 24(44%) showed greatly increased ECG voltage≥30 mm in any lead. Of 102 patients with outflow gradients≥30 mm Hg at rest, only 43(42%) had ECG voltage ≥30 mm in any lead. Normal ECG results were uncommonly associated with HC-related death(1 of 40 patients, 2.5%) but had similar prevalence in surviving patients(17 of 376 patients, 4.5%; p=NS). In conclusion, in HC, 12-lead ECG voltages are not a reliable clinical marker for the magnitude of LV hypertrophy or outflow obstruction. Diverse ECG patterns, consistent with heterogenous expression of this disease, did not predict HC-related death. Scalar electrocardiography has selective but limited power in routine clinical assessments of patients with HC. Twelve-lead electrocardiography, a traditional component in evaluations of patients with hypertrophic cardiomyopathy (HC), is often considered as a marker for the magnitude of left ventricular (LV) hypertrophy, which in turn has been linked to sudden death risk. electrocardiographic (ECG) patterns have clinical utility by accurately reflecting phenotypic expression or predicting clinical outcome, voltages and patterns were compared with LV wall thicknesses assessed by echocardiography and with clinical outcomes in 448 consecutive patients with HC. Significant but relatively weak correlations were clearly between maximum For the sum of R-and S-wave voltages in all 12 leads, r = 0.254 (p <0.01) for the maximum R or S wave in any lead, Of 55 patients with extreme LV hypertrophy (LV wall thickness ≥30 mm), only 24 (44%) were used for the sum of SV1 (or SV2) and RV5 (or RV6) ECG voltage≥30 Of 102 patients with outflow gradients ≥ 30 mm Hg at rest, only 43 (42%) had ECG voltage ≥ 30 mm in any lead. Normal ECG results were uncommonly associated with HC-related death (1 of 40 patients , 2.5%) but had similar prevalence in surviving patients (17 of 376 patients, 4.5%; p = NS). In conclusion, in HC, 12-lead ECG voltages are not a reliable clinical marker for the magnitude of LV hypertrophy or outflow obstruction. Diverse ECG patterns, consistent with heterogenous expression of this disease, did not predict HC-related death. Scalar electrocardiography has selective but limited power in routine clinical assessments of patients with HC.