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Orthostatic hypotension (OH) may be dependent upon various neurogenic and non-neurogenic disorders and conditions. Neurogenic causes include the main autonomic failure syndromes, primary (multiple system atrophy, pure autonomic failure, and autonomic failure associated with Parkinson's disease) and secondary (central nervous system diseases, peripheral neuropathies and systemic diseases). Non-neurogenic causes of OH include cardiac impairment, fluid and electrolyte loss, vasodilatation, and old age. A number of drugs may also cause OH, through their vasoactive action or by interfering with the autonomic nervous system. Symptoms of OH are debilitating, often confining patients to bed, and longitudinal studies have shown that OH increases the risk of stroke, myocardial ischemia and mortality. The therapeutic goal is to decrease the incidence and severity of postural symptoms, rather than restore normotension. In non-neurogenic OH, treatment of the underlying cause may be curative. In neurogenic OH a combination of non-pharmacological and pharmacological measures is often needed. Patient education and non-pharmacological measures represent the first step; among these interventions, fluid repletion and physical countermanoeuvres have been proven very effective. Pharmacological treatment comprises a number of agents acting on blood vessels, on blood volume or with other pressor mechanisms. The drugs most currently used are fludrocortisone and midodrine. Fludrocortisone expands the extravascular body fluid volume and improves alpha-adrenergic sensitivity. Midodrine is a peripheral, selective alpha1-adrenergic agonist that causes arterial and venous vasoconstriction. Despite the wide use of these drugs, multicentre, randomised and controlled studies for the treatment of OH are still scarce and limited to few agents and groups of patients. Pharmacological management of OH substantially improves the quality of life of patients, although it may be problematic. The development of supine hypertension and subsequent congestive heart failure should be avoided, especially in those patients with a pre-existing cardiovascular risk, such as in diabetes or ischemic heart disease.

This study shows a high prevalence (17%) of ascending aortic dilatation in patients affected by essential hypertension, without further complications. Dilatation of the ascending aorta is associated both to an increased left ventricular mass and arterial stiffness.

The aim of this study was to evaluate the association between brachial and central blood pressure (bBP and cBP) levels and aortic root dilatation (ARD) in essential hypertensive patients. A total of 190 untreated and treated essential hypertensive patients (mean age, 55±11 years) were considered for this analysis. We measured pulsatile hemodynamics and the proximal aortic diameter directly using tonometry, ultrasound imaging (echocardiography) and Doppler. Ninety-one hypertensive patients had an ARD (defined as aortic size index (ASi)42 cm/m 2 ). Central hemodynamic variables were significantly associated with ASi. Patients with increased ASi were significantly older (60 ± 10 vs. 50 ± 11 years, Po0.0001) and had higher levels of the augmentation index (AIx; 28±10 vs. 21±10 Po0.0001), augmentation pressure (AP; 13±6 vs. 8±5 mm Hg, Po0.0001), and central pulse pressure (cPP; 44 ± 10 vs. 39 ± 8 mm Hg, Po0.0001) compared with patients with normal ASi. In a logistic regression analysis, the AIx was the only significant predictor of ASi. In hypertensive patients, the AIx and cBP were associated with ARD, whereas the bBP was not. Patients with an increased ASi may lose part of the elastic properties of the aorta, demonstrating a strict correlation between ASi and central hemodynamic indexes, in particular, the cPP and AIx.

Arterial hypertension is associated with an increased risk of atrial fibrillation (AF), and leads to a pronounced increase in morbidity and mortality. Left atrial volume (LAV) is an important prognostic marker in the older populations. The aim of our study was to identify the clinical and echocardiographic determinants of LAV in middle-aged (o70 years old) essential hypertensive patients.We evaluated cardiac structure and function in 458 patients, 394 treated and untreated mild to moderate essential hypertensives patients (mean±s.d. age 48.4±11.1 years) with no associated clinical condition and 64 normotensive control participants (age 45.7 ± 12.8 years; P ¼ 0.12). A multivariate analysis was performed to calculate the relative weight of each of the variables considered able to predict LAV. The LAV index (LAVi) was significantly increased in the essential hypertensive group vs the control group and was significantly dependent on blood pressure levels (SBP and DBP, Po0.05 for both) and body mass index (BMI) (Po0.0001). Considering the left ventricular (LV) variables, the LV mass index (LVMI) (R 2 ¼ 0.19, Po0.001) and LAV were increased in essential hypertensive patients with left ventricular hypertrophy (LVH), and patients with enlarged LAV showed lower systolic and diastolic function and an increased LVMI. The LAVi is dependent on blood pressure levels and anthropometric variables (age and BMI). Further structural (LVMI) and functional (systolic and diastolic) variables are related to the LAVi; LVMI is the most important variable associated with LAV in mild to moderate essential hypertensive adult patients. These findings highlight the importance of left atrium evaluation in adult, relatively young, essential hypertensive patients.

LAV evaluation in hypertensive population can contribute to the identification of subjects affected by hypertensive heart disease other than the conventionally evaluated terms (LVH and CR).

Primary aldosteronism is the most frequent cause of secondary hypertension, accounting for up to 11% of cases in selected populations. Patients affected by primary aldosteronism have shown higher prevalence of cardiovascular and cerebrovascular events compared with patients with essential hypertension, despite similar blood pressure levels. Several studies have been performed over past years aiming to explain these data; many of these evaluated echocardiographic differences in hypertension-related cardiac organ damage between primary aldosteronism and essential hypertension. This article summarizes the present knowledge about structural and functional alteration of the human left heart in primary aldosteronism.