Link of nonhemodynamic factors to hemodynamic determinants of left ventricular hypertrophy

Despite current evidence suggesting that hemodynamic load is the fundamenta l stimulus to begin the sequence of biological events leading to the develo pment of left ventricular hypertrophy, genotype, gender, body size, and les s 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 nonhemody namic factors such as gender and body size eventually regulate the growth o f left ventricular mass by at least in part influencing loading conditions. Consideration of measurable factors, such as gender, body size, and hemody namic load, allows evaluation of individual echocardiographic left ventricu lar mass as the deviation from the level that would be required to face a g ender-specific hemodynamic load at a given body size. Values of left ventri cular mass that are inappropriately high for individual gender, body size, and hemodynamic load are associated with a high cardiovascular risk phenoty pe, even independent of the presence of arterial hypertension. Thus, the co ndition 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 th at yields inappropriate left ventricular mass is probably linked to the pro tracted activity over time of biological mediators cf left ventricular hype rtrophy, such as proto-oncogenes and other growth factors, neurohormones, a nd cytokines, inducing structural modifications that initially compensate i mposed overload but eventually change the structure of myocardial tissue an d the composition of motor units.