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Increased plasma aldosterone-to-renin ratio is associated with impaired left ventricular longitudinal functional reserve in patients with uncomplicated hypertension.

Choi EY, Ha JW, Yoon SJ, Shim CY, Seo HS, Park S, Ko YG, Kang SM, Choi D, Rim SJ, Jang Y, Chung N

Cardiology Division, Yonsei Cardiovascular Center and Cardiovascular Research Institute, Yonsei University College of Medicine, Seoul, South Korea.

Relative aldosterone excess is associated with endothelial dysfunction and higher incidence of end organ damage. We sought to investigate whether plasma aldosterone-to-renin ratio (ARR) is associated with left ventricular (LV) longitudinal function reserve to exercise in patients with controlled hypertension. In the patients with controlled and uncomplicated hypertension without overt LV hypertrophy, plasma aldosterone concentrations (ng/dL) and renin activities (ng/mL/h) were measured. Then 28 consecutive patients with higher ARR (group II, ARR > or = 30, 55 +/- 10 years) and 56 age- and sex-matched patients with lower ARR (group I, ARR < 30) underwent supine bicycle exercise echocardiography. Despite similar 24-hour blood pressure, LV mass index was significantly higher in group II (91.1 +/- 16.4 vs 101.7 +/- 18.2 g/m(2), P = .008). Early diastolic and systolic mitral annular velocity (E' and S', cm/s) at 50-W exercise was significantly lower in group II compared with group I (9.91 +/- 1.66 vs 8.67 +/- 1.65 cm/s, P = .002; 9.52 +/- 1.71 vs 8.46 +/- 1.79, P = .010, respectively) despite similar resting values. Longitudinal diastolic functional reserve at 25-W and 50-W exercise, defined as DeltaE' (change from resting E', cm/s) of group II was significantly lower than that of group I (2.60 +/- 1.42 vs 1.85 +/- 1.44 cm/s, P = .016; 3.40 +/- 1.48 vs 2.36 +/- 1.43 cm/s, P = .003, respectively). In conclusion, in patients with hypertension without overt LV hypertrophy, increased ARR is associated with increased LV mass, and impaired LV longitudinal functional reserve during exercise.

Published 3 March 2008 in J Am Soc Echocardiogr, 21(3): 251-6.
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