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Left ventricular hypertrophy is recognized as an independent risk factor for cardiovascular morbid events. The primary mechanisms responsible for stimulating it are unknown. Epidemiological theories suggest that left ventricular hypertrophy is a continuous variable with no threshold, while morphological studies argue that it is the structure, or quality, and function of the myocardium (and therefore non-continuous), not the quantity of the myocardial mass, that poses the cardiovascular risk. Although left ventricular hypertrophy has been classically viewed as an adaptive response of the cardiovascular system to an imposed load, it has been demonstrated that haemodynamic overloading in selected hypertensive patients is not the sole determinant of left ventricular structure and function. Pathological and physiological states of left ventricular hypertrophy have been described primarily using criteria focusing on normal chamber performance and oxygen delivery as well as the reversibility of the hypertrophy once the overload is removed. Both states are also defined by the nature of the imposed load and the resulting myocardial adaptations. This review addresses the pathological and physiological states of left ventricular hypertrophy, the hypertrophy patterns, and the corresponding structural and functional characteristics, together with some of the biochemical factors thought to influence remodelling.
Richey et al. (Thu,) studied this question.