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Link of nonhemodynamic factors to hemodynamic determinants of left ventricular hypertrophy
G de Simone1, F Pasanisi, F Contaldo
1Department of Clinical and Experimental Medicine, Federico II University Hospital School of Medicine, Naples, Italy. simogi@unina.it
Insights
Left ventricular hypertrophy (LVH) is influenced by hemodynamic load, but non-hemodynamic factors like gender and body size also play a role. Inappropriately high LVH indicates advanced pathological changes and high cardiovascular risk.
Area of Science:
- Cardiology
- Physiology
- Molecular Biology
Background:
- Hemodynamic load is considered the primary stimulus for left ventricular hypertrophy (LVH).
- Non-hemodynamic factors including genotype, gender, and body size also contribute to molecular changes leading to increased left ventricular mass.
- These factors can influence loading conditions, thereby regulating LVH progression.
Purpose of the Study:
- To evaluate echocardiographic left ventricular mass in relation to individual gender, body size, and hemodynamic load.
- To identify left ventricular mass values that are inappropriately high for specific individual characteristics.
- To understand the association of inappropriately high left ventricular mass with cardiovascular risk phenotypes.
Main Methods:
- Analysis of measurable factors: gender, body size, and hemodynamic load.
- Evaluation of echocardiographic left ventricular mass as a deviation from expected levels.
- Assessment of cardiovascular risk phenotypes associated with elevated left ventricular mass.
Main Results:
- Inappropriately high left ventricular mass, relative to gender, body size, and hemodynamic load, is linked to a high cardiovascular risk phenotype.
- This association persists even in the absence of arterial hypertension.
- Inappropriately high left ventricular mass represents a pathological stage beyond compensatory needs.
Conclusions:
- Left ventricular mass assessment should consider individual gender, body size, and hemodynamic load.
- Inappropriately high left ventricular mass is a significant indicator of cardiovascular risk.
- The development of inappropriate left ventricular mass involves prolonged activity of mediators like proto-oncogenes, growth factors, neurohormones, and cytokines, leading to detrimental myocardial structural changes.
Abstract:
Despite current evidence suggesting that hemodynamic load is the fundamental stimulus to begin the sequence of biological events leading to the development of left ventricular hypertrophy, genotype, gender, body size, and less easily recognizable environmental factors may contribute to generate the cascade of molecular changes that eventually yield the increase in protein synthesis needed to increase left ventricular mass. However, even nonhemodynamic factors such as gender and body size eventually regulate the growth of left ventricular mass by at least in part influencing loading conditions. Consideration of measurable factors, such as gender, body size, and hemodynamic load, allows evaluation of individual echocardiographic left ventricular mass as the deviation from the level that would be required to face a gender-specific hemodynamic load at a given body size. Values of left ventricular mass that are inappropriately high for individual gender, body size, and hemodynamic load are associated with a high cardiovascular risk phenotype, even independent of the presence of arterial hypertension. Thus, the condition of inappropriately high left ventricular mass may be recognized as a more advanced stage of pathological structural changes initially induced by overload, going beyond the compensatory needs. The biological process that yields inappropriate left ventricular mass is probably linked to the protracted activity over time of biological mediators of left ventricular hypertrophy, such as proto-oncogenes and other growth factors, neurohormones, and cytokines, inducing structural modifications that initially compensate imposed overload but eventually change the structure of myocardial tissue and the composition of motor units.