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[Morphological problems in cardiac hypertrophy]
1Research Laboratory for Cardiovascular Pathology, Juntendo University School of Medicine, Tokyo.
Insights
Ventricular hypertrophy, a response to hemodynamic overload, presents as volume or pressure types. Understanding these distinct cardiac adaptations is crucial for diagnosing and managing heart conditions.
Area of Science:
- Cardiovascular Physiology
- Cardiac Pathology
Context:
- Ventricular hypertrophy is a significant cardiac adaptation.
- It arises in response to hemodynamic overload, either volume or pressure.
- Idiopathic cardiomyopathies represent an exception to typical hypertrophic responses.
Purpose:
- To categorize and describe the mechanisms of ventricular hypertrophy.
- To differentiate between volume and pressure-induced cardiac remodeling.
- To elucidate the structural changes in myocardial architecture.
Summary:
- Ventricular hypertrophy is classified into volume (eccentric) and pressure (concentric) types.
- Volume hypertrophy involves ventricular dilatation and myocyte stretching, altering myocardial architecture.
- Pressure hypertrophy leads to increased myocyte mass and interventricular septum changes, potentially progressing to decompensation.
Impact:
- Provides a framework for understanding diverse hypertrophic patterns.
- Highlights the structural basis of cardiac dysfunction in response to overload.
- Informs diagnostic approaches and therapeutic strategies for heart disease.
Abstract:
Ventricular hypertrophy is categorized as (1) volume hypertrophy (eccentric hypertrophy or hypertrophy with dilatation), and (2) pressure hypertrophy (concentric hypertrophy or hypertrophy without dilatation). Hypertrophy per se is considered as a reaction to hemodynamic overload, both in occasions of excessive volume and of elevated pressure except in (idiopathic) cardiomyopathies. In patients with volume hypertrophy, some alteration of myocardial architecture is inevitable if the volume load exceeds a critical degree. Such alteration is characterized by deterioration of the median circular muscular layer of the ventricle resulting from over-stretching of the horizontally-coursing myocyte bundles. Hypertrophy of the inner oblique muscular layer of the left ventricle in cases with mitral regurgitation, and of the outer oblique muscular layer in cases with aortic regurgitation develops according to the changing configuration of the left ventricle; globular in the former, and elongated in the latter. In patients with pressure hypertrophy, there is some increase of the myocyte mass, with a disarrangement at the anterior triangle of the interventricular septum. The latter is physiologically situated at the anterior margin of the septum between the outer and median layers of both the ventricles. This seems to be a prelude to thickening of the septum and tends to hypertrophy of the free wall. A reduction in the deranged myocyte mass due to fibrosis or adiposis corresponds to arrest of the active hypertrophic process, and it may be the beginning of decompensation of cardiac function. Peculiar modes of dilatation and hypertrophy in cardiomyopathies have common denominators with those of known etiologies.(ABSTRACT TRUNCATED AT 250 WORDS)