Adolescent Blood Pressure Variation and Ventricular Mass

BACKGROUND:

Evidence has accumulated suggesting that essential hypertension begins early in life and is potentially preventable. One possible pathogenetic mechanism implicated is a sympathetic nervous system abnormality which is manifested by increased sympathetic drive to the heart. An elevated sympathetic nervous system tone and decreased vagal inhibition is responsible for the hyperkinetic circulation seen in a significant proportion of persons with borderline essential hypertension. Exaggerated blood pressure and heart rate responses to mental stressors have been documented in normotensive children of hypertensive parents. These changes appear to involve sympathetic over-responding to fight-flight stimuli.

Increased blood pressure variability induced by stress might accelerate vascular and other changes leading to essential hypertension. Behavior and environment might chronically elevate sympathetic nervous system tone with damaging cardiovascular consequences. Stressful working conditions, defective anger management and poor interpersonal problem solving skills have been implicated in studies of stress-induced blood pressure increases. These influences may interact with diet and genetic risk to exacerbate pathophysiology. Essential hypertension risk might be reduced by modifying working and living environments and by training young persons at risk to cope with or avoid stressors that elicit defensive over-responding.

DESIGN NARRATIVE:

This longitudinal study tested two different models of sympathetic nervous system influence on the early pathophysiology of essential hypertension. The first neurogenic model was evaluated by determining whether an excessively variable or reactive blood pressure in year 1 gave rise to excessive heart growth or left ventricular hypertrophy over a two year follow-up. The second neurogenic model was evaluated by determining if higher blood pressure exacerbated by personality, stress, and dietary sodium intake led to increased left ventricular hypertrophy at follow-up.