P1007Aortic root diameters and aortic regurgitation in hypertensive patients and normal subjects.

PURPOSE: : The association between aortic root diameters and aortic regurgitation in hypertension (HT) is disputed with lack of understanding of the underline mehanisms lT. We investigate the relationship between aortic root diameters and aortic regurgitation in newly diagnosed and never treated hypertensive patients and in a group healthy subjects. METHOD: Participants were 175 hypertensives (42 F and 133 M) and 305 normotensives (134 F, 168 M) age matched (mean age 52.4±13 vs 52.6 ±15.2 years). Antropometric, office blood pressure (BP) measurements, a comprehensive echocardiography and local carotid stiffness study were performed. Aortic measures for annulus, sinuses of Valsalva, sinotubular junction and ascending aorta were taken in late diastole according to the leading edge method. The sinotubular junction/annulus ratio was calculated. RESULTS: Hypertensive patients had significantly higher body surface area (BSA), systolic (SBP) and diastolic pressure (DBP), mean arterial pressure (MAP) and pulse?pressure (PP) (p<0.0001) than normotensives. Annulus and sinotubular junction diameters, indexed by BSA and after adjustment for gender, MAP, heart rate?(HR), were significantly higher in normotensives than hypertensives. Considering subjects with aortic regurgitation (trivial or mild) we found a higher prevalence in?hypertensives (25.7 % vs 10.2%, p<0.0001). Moreover in hypertensives we found no difference in aortic diameters between patients with or without aortic regurgitation?but ascending aorta /BSA (p=0.002) whereas in healthy subjects aortic regurgitation was associated with larger aortic root diameters included sinotubular junction/annulus ratio (table 1). In the logistic regression analysis, aortic regurgitation was associated with age, gender, BP parameters, one point carotid stiffness parameters. CONCLUSIONS: Hypertensive patients had smaller indexed aortic root dimensions than normal subjects but they had heigher prevalence of trivial-mild aortic regurgitation in contrast to normotensives who had aortic regurgitation combined with larger aortic diameters.

Aldosterone and Left Ventricular Remodeling.

Experimental and clinical evidence obtained in the last 2 decades clearly indicates that protracted exposure to inappropriately elevated aldosterone levels causes significant changes in left ventricular structure and function. Animal studies have demonstrated that aldosterone induces myocardial inflammatory changes and fibrosis in the presence of a high salt diet. Moreover, the effects of aldosterone on the heart have been investigated in different clinical conditions. These conditions include systolic and diastolic heart failure, essential hypertension, and primary aldosteronism that offers a unique clinical model to study the cardiac effects of excess aldosterone because these effects are isolated from those of the renin-angiotensin axis. A relatively clear picture is emerging from these studies with regard to aldosterone-related changes in left ventricular mass and geometry. Conversely, no direct effect of aldosterone on left ventricular diastolic function can be demonstrated and improvement of diastolic function obtained in some studies that have employed mineralocorticoid receptor blockers could result from left ventricular mass reduction. Animal experiments demonstrate that effects of aldosterone on the left ventricle require high salt intake to occur, but the evidence of this contribution of salt to aldosterone-induced cardiac changes in humans remains weaker and needs further research. The article reviews the results of clinical studies addressing the role of aldosterone in regulation of LV remodeling and diastolic function, and focuses on the possible relevance of salt intake.