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Relation of electrocardiographic patterns to phenotypic expression and clinical outcome in hypertrophic
Julia V Montgomery1, Kevin M Harris, Susan A Casey
1The Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, Minneapolis, MN, USA.
Insights
Twelve-lead electrocardiography (ECG) is not a reliable marker for left ventricular hypertrophy or outflow obstruction in hypertrophic cardiomyopathy (HC). ECG patterns do not accurately predict sudden death risk in HC patients.
Area of Science:
- Cardiology
- Medical Diagnostics
Background:
- Twelve-lead electrocardiography (ECG) is a traditional tool for evaluating hypertrophic cardiomyopathy (HC).
- ECG is often used as a marker for left ventricular (LV) hypertrophy magnitude, linked to sudden death risk.
Purpose of the Study:
- To assess the clinical utility of ECG patterns in reflecting HC phenotypic expression.
- To determine if ECG accurately predicts clinical outcomes in HC patients.
Main Methods:
- Compared ECG voltages and patterns with LV wall thickness (echocardiography) in 448 HC patients.
- Correlated ECG findings with clinical outcomes, including HC-related death.
Main Results:
- Weak correlations found between LV wall thickness and ECG voltage (r < 0.3).
- Only 44% of patients with extreme LV hypertrophy showed greatly increased ECG voltage.
- ECG patterns did not reliably predict HC-related death.
Conclusions:
- 12-lead ECG voltages are unreliable for assessing LV hypertrophy or outflow obstruction in HC.
- ECG patterns in HC are diverse and do not predict clinical outcomes like sudden death.
- Scalar electrocardiography has limited power in routine HC patient assessment.
Abstract:
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 SV(1) (or SV(2)) and RV(5) (or RV(6)). Of 55 patients with extreme LV hypertrophy (LV wall thickness > or =30 mm), only 24 (44%) showed greatly increased ECG voltage > or =30 mm in any lead. Of 102 patients with outflow gradients > or =30 mm Hg at rest, only 43 (42%) had ECG voltage > or =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 heterogeneous 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.
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