ObjectiveBesides arterial blood pressure, nonhemodynamic factors are known to induce cardiac hypertrophy. In Cushing's syndrome, severe ventricular hypertrophy has been linked not only to increased aortic pressure, but also to elevated plasma cortisol. The aim of this study was to examine the relationship between the cortisol/cortisone levels and left ventricular mass index (LVMI) in essential arterial hypertension with and without echocardiographic left ventricular hypertrophy (LVH).DesignEighteen untreated Caucasian patients (nine men, nine women, mean age 48 ± 6 years) with essential hypertension (163 ± 26/100 ± 14 mmHg) were enrolled. An age-matched control group of 13 subjects (seven men, six women) with normotension (121 ± 9/79 ± 7 mmHg) were enrolled also. Left ventricular dimensions were echocardiographically assessed and cortisol production evaluated by 24-h urinary free cortisol and cortisone concentrations.ResultsLVMI averaged 115 ± 31 g/m2and 24-h urinary free cortisol and cortisone were 23 ± 14 μg per 24 h and 31 ± 18 μg per 24 h. Prevalence of echocardiographic LVH was 56%. LVMI correlated significantly with 24-h urinary free cortisol (r= 0.61,P= 0.007) and cortisone (r= 0.60,P= 0.009). Patients with echocardiographic LVH were characterized by higher daytime ambulatory blood pressure, LVMI (particularly the posterior wall), and 24-h urinary cortisol, while office blood pressure, septal: posterior wall ratio and 24-h urinary cortisone were comparable in all patients. In control individuals, LVMI averaged 91 ± 18 g/m2and 24-h urinary free cortisol and cortisone, respectively, were 34.7 ± 6.6 μg per 24 h and 64.3 ± 10.8 μg per 24 h (P< 0.05 versus patients). Neither LVMI nor the contributing ventricular dimensions showed significant correlation with 24-h urinary free cortisol or cortisone in the control group.ConclusionsOur data provide evidence for a significant relationship between LVMI and cortisol production independently of arterial blood pressure in untreated mild to moderate hypertension.