Abstract :
In hypertensive patients, the presence of LV hypertrophy (LVH) is an independent predictor of morbidity and mortality. The mechanisms of LVH on the systolic and diastolic ventricular function is multifactorial. From the physiologic point of view, the “appropriateness” of cardiac hypertrophy to ventricular pressure load plays an important role. Stress represents the force per unit of cross-sectional area of the ventricular wall expressed in dynes/cm2. Wall stress is calculated by the Laplace equation: σ = p • r / d, where P = intracavitary pressure, R = radius of the LV cavity, and D = wall thickness. In the untreated hypertensive patient, LVH has a dual cardiovascular effect. Initially, the LVH compensates for the abnormal wall stress. Since the end-diastolic volume remains unchanged, the mass-to-volume ratio increase. This represents an “appropriate” response to increase pressure load. Later on the curse, both ventricular mass and volume increase, whereas wall thickness remains unchanged, or increases only modestly. This leads to ventricular dilation with constancy or even decrease in the mass-to-volume ratio representing an “inappropriate” response to ventricular pressure load. In the treated patient, the effect on LV mass and function is variable depending upon the drug class used, the adequacy of the blood pressure control, the length of treatment, the degree of LVH (when present), the status of ventricular function at the time of intervention, and very importantly, the presence and extent of LVH regression. In conclusion, systolic wall stress is an important parameter in assessing the degree and appropriateness of cardiac hypertrophy in hypertensive patients. It is unknown the effect of LVH regression on wall stress, systolic and diastolic function
