J Díez1, C Laviades. 1. Department of Medicine, University of Zaragoza, Spain.
Abstract
BACKGROUND: Preliminary studies have shown that patients with essential hypertension and left ventricular hypertrophy have an excess of circulating insulin-like growth factor-1 (IGF-1). In addition, an association has been found between the decrease in IGF-1 after antihypertensive treatment and regression of left ventricular hypertrophy. OBJECTIVES: To determine whether the effect of angiotensin converting enzyme (ACE) inhibitors on left ventricular hypertrophy in patients with essential hypertension is related to ACE inhibitor effects on IGF-1 levels. PATIENTS AND METHODS: The relationship between echocardiographically determined left ventricular hypertrophy and plasma IGF-1 levels was investigated in 87 patients with essential hypertension before and after 6 months of randomly allocated treatment with captopril (n = 30), lisinopril (n = 37) or quinapril (n = 20). The control group consisted of 30 age- and sex-matched normotensive subjects without left ventricular hypertrophy. RESULTS:Baseline IGF-1 levels were higher in hypertensive patients than in normotensive controls (280 +/- 21 versus 240 +/- 15 ng/ml, means +/- SEM, P < 0.02). IGF-1 levels were higher in hypertensive patients with left ventricular hypertrophy (n = 25, 316 +/- 41 ng/ml) than in those without left ventricular hypertrophy (n = 62, 242 +/- 16 ng/ml, P < 0.05). There was a direct correlation between baseline IGF-1 and left ventricular mass in the hypertensive patients (r = 0.365, P < 0.001). All three ACE inhibitors caused similar reductions in IGF-1 levels, the left ventricular mass index and blood pressure after the treatment period. The effect of ACE inhibition on mean blood pressure was similar in patients with (-13%) and without (-12%) a regression of left ventricular hypertrophy. The mean change in IGF-1 levels with treatment was more pronounced in those patients in whom left ventricular hypertrophy regressed (-25 versus -12%). CONCLUSIONS: These results indicate that circulating IGF-1 levels are increased in essential hypertension. Furthermore, there is an association between high IGF-1 levels and left ventricular hypertrophy in hypertensive patients. Our findings suggest that the ability of ACE inhibitors to induce regression of hypertensive cardiac hypertrophy may be related to their ability to normalize IGF-1 and also supports the view that ACE inhibition affects left ventricular mass through pathways other than blood pressure reduction.
RCT Entities:
BACKGROUND: Preliminary studies have shown that patients with essential hypertension and left ventricular hypertrophy have an excess of circulating insulin-like growth factor-1 (IGF-1). In addition, an association has been found between the decrease in IGF-1 after antihypertensive treatment and regression of left ventricular hypertrophy. OBJECTIVES: To determine whether the effect of angiotensin converting enzyme (ACE) inhibitors on left ventricular hypertrophy in patients with essential hypertension is related to ACE inhibitor effects on IGF-1 levels. PATIENTS AND METHODS: The relationship between echocardiographically determined left ventricular hypertrophy and plasma IGF-1 levels was investigated in 87 patients with essential hypertension before and after 6 months of randomly allocated treatment with captopril (n = 30), lisinopril (n = 37) or quinapril (n = 20). The control group consisted of 30 age- and sex-matched normotensive subjects without left ventricular hypertrophy. RESULTS: Baseline IGF-1 levels were higher in hypertensivepatients than in normotensive controls (280 +/- 21 versus 240 +/- 15 ng/ml, means +/- SEM, P < 0.02). IGF-1 levels were higher in hypertensivepatients with left ventricular hypertrophy (n = 25, 316 +/- 41 ng/ml) than in those without left ventricular hypertrophy (n = 62, 242 +/- 16 ng/ml, P < 0.05). There was a direct correlation between baseline IGF-1 and left ventricular mass in the hypertensivepatients (r = 0.365, P < 0.001). All three ACE inhibitors caused similar reductions in IGF-1 levels, the left ventricular mass index and blood pressure after the treatment period. The effect of ACE inhibition on mean blood pressure was similar in patients with (-13%) and without (-12%) a regression of left ventricular hypertrophy. The mean change in IGF-1 levels with treatment was more pronounced in those patients in whom left ventricular hypertrophy regressed (-25 versus -12%). CONCLUSIONS: These results indicate that circulating IGF-1 levels are increased in essential hypertension. Furthermore, there is an association between high IGF-1 levels and left ventricular hypertrophy in hypertensivepatients. Our findings suggest that the ability of ACE inhibitors to induce regression of hypertensive cardiac hypertrophy may be related to their ability to normalize IGF-1 and also supports the view that ACE inhibition affects left ventricular mass through pathways other than blood pressure reduction.