Pathogenesis of left ventricular hypertrophy
Diabetes Mellitus, Type 2
Hypertrophy, Left Ventricular
Growth of left ventricular myocytes - left ventricular hypertrophy (LVH) - occurs physiologically from infancy to adulthood, and pathologically in response to hypertension, volume overload and LV contractile inefficiency. Consideration of these three hemodynamic stimuli to LVH explains more variability of LV mass than blood pressure alone and resolves many previously confusing observations. In addition, twin studies document heritability of LV muscle mass whereas data concerning direct stimulation of LVH by the adrenergic or renin-angiotensin systems remain inconclusive. The spectrum of stimuli to LV growth and remodelling is broadly matched to the patterns of LV geometric adaptation - concentric and eccentric LV hypertrophy and concentric LV hypertrophy - that develop in patients with hypertension, valvular heart disease, and other conditions. Further research is needed to elucidate the relative importance and specific mechanisms of the environmental and genetic factors that determine this parallelism.