High Angiotensin II concentrations relative to sodium excretion were associated with significantly greater left ventricular mass (318 vs 257 g, P<0.02) in patients with essential hypertension.
Cross-Sectional (n=68)
In patients with essential hypertension, impaired suppression of the renin-angiotensin system relative to sodium excretion is associated with increased left ventricular hypertrophy.
Absolute Event Rate: 318% vs 257%
p-value: p=<0.02
BACKGROUND: Urinary sodium excretion and angiotensin II (Ang II), which are linked in a physiological feedback mechanism, have both been described to be blood pressure-independent determinants of left ventricular hypertrophy in essential hypertension. We conducted a study to investigate the interaction of sodium excretion with Ang II and its potential impact on myocardial hypertrophy. METHODS AND RESULTS: Sixty-eight patients (46 men and 22 women; mean age, 52 +/- 10 years) with untreated World Health Organization stage I to II essential hypertension were examined in a cross-sectional study. Left ventricular structure and function (two-dimensionally guided M-mode echocardiography), dietary sodium intake (as estimated by 24-hour urinary sodium excretion), and noninvasive ambulatory blood pressure over 24 hours (Spacelab 90207) were determined in parallel with plasma renin activity and plasma Ang II and serum aldosterone concentrations (radioimmunoassay). Twenty-four-hour urinary sodium excretion emerged as a strong correlate of relative wall thickness independent of 24-hour ambulatory blood pressure (partial r = .49, P < .001). Ang II concentrations were weakly correlated with septal wall thickness (r = .27, P < .05) and left ventricular mass (r = .25, P < .05). Patients with high Ang II concentrations in relation to sodium excretion had a greater left ventricular mass (318 +/- 77 versus 257 +/- 54 g, P < .02), posterior wall thickness (11.8 +/- 1.9 versus 10.5 +/- 0.8 mm, P < .02), and septal wall thickness (13.6 +/- 1.8 versus 11.9 +/- 1.3 mm, P < .01) than those with "relatively low" Ang II levels in relation to sodium excretion. CONCLUSIONS: Impaired suppression of the renin-Ang II system appeared to act as a stimulus for myocardial hypertrophy in hypertensive patients.
Schmieder et al. (Sun,) conducted a cross-sectional in Essential hypertension (n=68). High Angiotensin II concentrations relative to sodium excretion vs. Relatively low Angiotensin II concentrations relative to sodium excretion was evaluated on Left ventricular mass (g) (p=<0.02). High Angiotensin II concentrations relative to sodium excretion were associated with significantly greater left ventricular mass (318 vs 257 g, P<0.02) in patients with essential hypertension.