Is cardiovascular remodeling in patients with essential hypertension related to more than high blood pressure? A LIFE substudy☆☆☆★

Abstract 

Background Blocking the renin-aldosterone-angiotensin II system has been hypothesized to induce blood pressure-dependent as well as blood pressure-independent regression of cardiovascular hypertrophy. However, the relative influence of elevated blood pressure (BP) and various neurohormonal factors on cardiovascular remodeling in hypertension is unclear. Methods In 43 untreated patients with hypertension with electrocardiographic left ventricular hypertrophy, we measured relative wall thickness and left ventricular mass index by echocardiography and by magnetic resonance imaging (n = 32), intima-media cross-sectional area, and distensibility of the common carotid arteries by ultrasound, media/lumen ratio of isolated subcutaneous resistance arteries by myography, and median 24-hour systolic BP (n = 40), serum insulin, and plasma levels of epinephrine, norepinephrine, renin, angiotensin II, aldosterone, and endothelin. Results In multiple regression analyses, left ventricular mass index by echocardiography (R² = 0.14, P < .05) and by magnetic resonance imaging (R² = 0.32, P = .001) were associated with 24-hour systolic BP, whereas relative wall thickness was associated with plasma epinephrine (R² = 0.12, P < .05) and aldosterone (R² = 0.10, P < .05). Intima-media cross-sectional area/height was associated with 24-hour systolic BP (β = 0.40) and plasma epinephrine (β = 0.43) (adjusted R² = 0.32, P < .001), whereas carotid distensibility was associated with 24-hour systolic BP (β = 0.40) and plasma angiotensin II (β = −0.41) (adjusted R² = 0.30, P < .001). Media/lumen ratio in subcutaneous resistance arteries was associated with plasma epinephrine (R² = 0.22, P < .01). Conclusion Apart from being associated with a high BP burden, cardiovascular remodeling was associated with high levels of circulating epinephrine, aldosterone, as well as angiotensin II, suggesting a beneficial effect above and beyond the effect of BP reduction when using antihypertensive agents blocking the receptors of these neurohormonal factors. (Am Heart J 2002;144:530-7.)