Left ventricular hypertrophy in normotensive individuals: Stimuli and prognostic significance
Diabetes Mellitus, Type 2
Hypertrophy, Left Ventricular
Left ventricular (LV) weight is physiologically determined by the interaction between inherited and hemodynamic factors. During body growth, the initially close relation between body size and LV mass becomes more variable with increasing age because of the superimposition of hemodynamic, hormonal, and environmental factors that increase LV load. Normal LV weight is therefore the consequence of the physiological interplay of all these stimuli. When physiological levels of preprogrammed LV load are exceeded, LV hypertrophy develops. Apparently normal individuals may present with relative LV hypertrophy as a consequence of stimuli such as genetic proneness to increase the number or size of cardiocytes and/or to increase LV load; exaggerated caloric intake, leading to overweight or overt obesity; unbalanced sodium intake; and increased arterial stiffness. Each of these influences may increase LV mass to levels that increase cardiovascular risk, independently of the presence of arterial hypertension. There is evidence that increase in LV mass is indeed an earlier sign of cardiovascular impairment than clinically detectable high blood pressure levels in offspring of hypertensive parents, in children with exaggerated blood pressure response to physical effort, and in otherwise normal adults. Whether LV mass represents the biological signal of increased reactivity and strength of the cardiovascular system to many stimuli or is the pure consequence of a primary alteration of cardiac loading conditions, hidden to traditional clinic examination, needs to be clarified.