Abstract: This expert consensus paper reviews the current understanding of excessive left ventricular (LV) trabeculation, focusing specifically on cases involving the apex and inferolateral wall, often associated with a false tendon. We explore the pathophysiology of trabeculation, its variations in normal development, and its association with cardiomyopathies in both pediatric and adult populations. The paper distinguishes between normal and excessive trabeculation, highlighting the diagnostic challenges and the implications for clinical management. We aim to provide a comprehensive overview of the current literature and identify areas requiring further research.
Introduction:
The left ventricle (LV) is a complex structure with intricate internal architecture. A significant component of this architecture is the trabecular network, a meshwork of muscular strands that project into the ventricular lumen. While a degree of trabeculation is normal and contributes to efficient ventricular function, excessive trabeculation, particularly when involving specific regions like the apex and inferolateral wall, can be associated with various cardiomyopathies and potentially adverse cardiac outcomes. This paper focuses on the clinical significance of excessive LV trabeculation, particularly when observed in conjunction with a false tendon, a non-contractile fibrous band spanning the ventricular cavity.
Left Ventricular Trabeculation: Normal Anatomy and Development:
Left ventricular trabeculation is a dynamic process that begins early in fetal development. Initially, the LV myocardium is relatively smooth, but as development progresses, trabeculae develop, forming a complex network that gradually becomes more organized. The precise mechanisms regulating trabeculation are not fully understood, but they involve intricate interactions between genetic factors, signaling pathways, and mechanical forces. Normal trabeculation contributes to several crucial aspects of cardiac function:
* Increased surface area: The trabecular network significantly increases the surface area of the LV, facilitating efficient oxygen and nutrient exchange.
* Enhanced contractility: Trabeculae contribute to the overall contractile force of the LV, particularly in the apical region.
* Improved blood flow: The trabecular meshwork influences blood flow patterns within the LV, contributing to efficient ventricular filling and ejection.
* Electrical conduction: Trabeculae can play a role in the propagation of electrical impulses within the LV myocardium.
Pathophysiology of Trabeculation:
Disruptions in the normal developmental process of trabeculation can lead to excessive trabeculation or abnormal trabecular morphology. Several factors may contribute to this:
* Genetic mutations: Several genes have been implicated in the development of cardiomyopathies associated with excessive trabeculation. These mutations can affect various aspects of cardiac development, including myocyte differentiation, cell-cell adhesion, and sarcomere formation. Specific genes associated with non-compaction cardiomyopathy (NCC), a condition characterized by excessive trabeculation, are frequently cited in the literature.
* Environmental factors: While the precise role of environmental factors is less well understood, factors like hypoxia during fetal development might influence trabecular development.
* Mechanical stress: Abnormal hemodynamic forces during development or later in life can potentially influence trabecular morphology.
Left Ventricle Excessive Trabeculation:
current url：https://hebaoz.d857y.com/blog/lv-trabeculation-involving-apex-and-inferolateral-wall-and-false-cord-30074