Abstract

The evidence is inescapable that even mild essential hypertension is associated with left ventricular hypertrophy, regardless of the age of the patient. Increased left ventricular afterload must play a major role in the pathogenesis of the hypertrophy; however, further proof of this awaits our improved understanding of the quantitation of afterload in the clinical setting. Other factors, including the adrenergic nervous system and blood viscosity, may play an additional role, possibly mediated through alterations in afterload or by direct myocardial action. Left ventricular hypertrophy exerts a positive benefit by normalizing wall stress in patients with hypertension. Especially in patients without coexistent coronary abnormalities, systolic function is normal and abnormalities of diastolic function are of uncertain clinical importance. Because echocardiography now provides a convenient and sensitive noninvasive means of following patients with left ventricular hypertrophy, long-term studies are now needed to document the incremental risk (or benefit) of left ventricular hypertrophy over blood pressure itself in the eventual morbidity of essential hypertension. The recognition of left ventricular hypertrophy in a patient with borderline elevation of blood pressure poses a new clinical dilemma. Should treatment be instituted based on this additional finding? In view of the data correlating stress, exercise, and mean daily blood pressure with left ventricular hypertrophy and the reduction of left ventricular mass following lowering of blood pressure, it has been our practice to treat patients with left ventricular hypertrophy more readily than those without left ventricular hypertrophy. The rationale in this approach is not that left ventricular hypertrophy per se is harmful, but rather that it indicates a greater degree of afterload than may be evident from office blood pressure measurements.

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