Hypertensive patients with left ventricular hypertrophy had significantly higher plasma renin activity and serum aldosterone levels than controls, both correlating with LV mass index (P<0.001).
Case-Control (n=191)
Do markers of the renin-angiotensin-aldosterone system, sympathetic nervous system, glucose homeostasis, and leptin correlate with left ventricular mass in hypertensive patients?
Plasma renin activity and serum aldosterone levels are elevated in hypertensive patients with left ventricular hypertrophy and correlate with LV mass index, suggesting RAAS activation plays a nonhemodynamic role in LVH development.
Effect estimate: r = 0.44 for PRA and r = 0.27 for aldosterone
p-value: p=<0.001
OBJECTIVES: Several neurohormonal systems have been suggested to stimulate myocardial cell growth, and thus take part in the development of left ventricular (LV) hypertrophy. We studied associations between LV mass and markers of the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system, glucose homeostasis and leptin. DESIGN: A total of 115 hypertensive patients with LV hypertrophy and two age- and gender-matched control groups consisting of 38 hypertensive patients without LV hypertrophy and 38 normotensive subjects were included. We examined determinants of the RAAS, plasma levels and 24-h urinary excretions of noradrenaline and adrenaline, plasma proinsulin, insulin, glucose, leptin and LV mass by echocardiography. RESULTS: Plasma renin activity (PRA) and serum aldosterone were higher (both P < 0.001) in the LV hypertrophy group than in patients without LV hypertrophy and normotensive subjects (1.0 +/- 0.8, 0.2 +/- 0.2 and 0.2 +/- 0.2 ng mL(-1) h(-1), and 327 +/- 126, 269 +/- 146 and 221 +/- 80 pmol L(-1), respectively). PRA and aldosterone both related (P < 0.001) to LV mass index (r = 0.44 and 0.27, respectively). Catecholamine levels and excretions were similar in all three groups and did not relate to LV mass index. Proinsulin, insulin and leptin levels were all elevated in the hypertensive patients (P < 0.01), but proinsulin, insulin, insulin sensitivity (by the homeostasis model assessment) and leptin did not relate to LV geometry, when indexed for body size. CONCLUSIONS: Plasma renin activity and serum aldosterone levels are elevated in hypertensive LV hypertrophy and relate to LV mass index. In addition to blood pressure, activation of the RAAS may be an important nonhaemodynamic mechanism in the control of LV hypertrophy.
Malmqvist et al. (Tue,) conducted a case-control in Hypertension with left ventricular hypertrophy (n=191). Hypertension with left ventricular hypertrophy vs. Hypertensive patients without left ventricular hypertrophy and normotensive subjects was evaluated on Plasma renin activity and serum aldosterone levels and their correlation with left ventricular mass index (r = 0.44 for PRA and r = 0.27 for aldosterone, p=<0.001). Hypertensive patients with left ventricular hypertrophy had significantly higher plasma renin activity and serum aldosterone levels than controls, both correlating with LV mass index (P<0.001).