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Updated: May 5, 2026

Ultrasonic Assessment of Myocardial Microstructure
Published on: January 14, 2014
Electrocardiographic, echocardiographic and ventriculographic characterization of hypertrophic non-obstructive
Insights
Hypertrophic cardiomyopathy (HCM) presents in various forms, including apical hypertrophy. While genetics play a role, environmental factors also influence myocardial hypertrophy, with specific patterns linked to distinct ECG abnormalities.
Area of Science:
- Cardiology
- Genetics
- Internal Medicine
Background:
- Hypertrophic cardiomyopathy (HCM) encompasses diverse morphological patterns, including apical hypertrophy (AH) and asymmetrical septal hypertrophy (ASH).
- While genetic factors underpin HCM, non-genetic influences like hypertension and aging contribute to myocardial hypertrophy, particularly in HNCM.
- Distinguishing between different HCM morphologies is crucial for understanding disease mechanisms and clinical presentation.
Purpose of the Study:
- To differentiate the etiological and morphological characteristics of different patterns of hypertrophic cardiomyopathy (HCM).
- To investigate the relationship between specific hypertrophic patterns and electrocardiographic (ECG) abnormalities.
- To clarify the role of genetic versus environmental factors in the development of myocardial hypertrophy.
Main Methods:
- Comparative analysis of clinical and etiological features of different HCM subtypes (HNCM, HOCM, ASH, apical hypertrophy).
- Correlation of specific left ventricular hypertrophy patterns with characteristic ECG findings.
- Review of existing literature on the pathophysiology of myocardial hypertrophy in response to various stimuli.
Main Results:
- HNCM exhibits more diffuse hypertrophy than HOCM, though both share genetic origins.
- Apical hypertrophy is specifically associated with characteristic ECG abnormalities, including giant negative T waves and high QRS voltage.
- Abnormal Q waves and left axis deviation suggest marked septal hypertrophy and potential conduction disturbances.
Conclusions:
- Apical hypertrophy is a distinct morphological pattern in HCM with specific ECG markers, differentiating it from other forms.
- While genetics are fundamental, HNCM development involves abnormal myocardial response to stimuli like hypertension and aging.
- ECG findings provide valuable insights into localized hypertrophy and septal involvement in HCM.
Abstract:
HNCM tends to have more diffuse or generalized hypertrophy than HOCM, although these two types are not fundamentally different in aetiology (genetic). Extreme ASH is primarily related to a hereditary factor while HNCM, including apical hypertrophy, seems to be based on an abnormal disposition to produce myocardial hypertrophy in response to endogenous or exogenous stimulation such as catecholamines, chronic anoxia, hypertension or even aging. Hypertension by itself, however, can not be a cause of apical hypertrophy. The configuration of left ventricular hypertrophy in HCM can be divided roughly into several patterns: ASH, apical, postero-inferior, generalized or diffuse types, etc. ASH is not an essential morphology for HNCM. Apical hypertrophy is the only specific hypertrophic pattern which shows characteristic ECG abnormalities (giant negative T waves and high QRS voltage in left precordial leads). Inverted T waves combined with high QRS voltage tends to be a reflection of a localized hypertrophic portion in the left ventricular free wall. Abnormal Q waves associated with left axis deviation usually suggest marked septal hypertrophy. They seem to be related to conduction disturbances in myopathic septum.
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