Hypertension and cognitive function.

Arterial hypertension, cerebrovascular disease, and dementia are related pathologies. This paper has reviewed comparatively the incidence of arterial hypertension and adult-onset dementia disorders. Hypertension is associated with cerebrovascular disease, which is in turn associated with dementia. It is the most important modifiable risk factor for stroke, which is a recognized cause of vascular dementia. In terms of pathophysiology of hypertensive brain damage, several hypotheses were developed, such as that vascular alterations induced by hypertension can induce lacunar or cortical infarcts and leucoaraiosis, that hypertension is responsible for cerebrovascular disease and acts into the contest of a pre-existing subclinic Alzheimer's disease (AD), that hypertension determines neurobiologic alterations (such as beta-amyloid accumulation) resulting in neuropathologic damage, and that aging and cerebrovascular risk factors act together to cause cerebral capillary degeneration, mitochondrial disruption, reduced glucose oxidation, and reduced ATP synthesis. The consequence of these alterations are neuronal death and dementia. Macroscopic results of these mechanisms are the so-called white matter lesions (WML), the significance of which is analyzed. Increasing clinical evidence suggests a close relationship between the reduction of elevated blood pressure and countering of both vascular dementia and AD. Antihypertensive treatment probably influences cognitive performances and prevents cognitive function alterations and the development of dementia. It is therefore important to evaluate as soon as possible cognitive functions of hypertensive patients.

Aldosterone as an independent factor in cerebrovascular damage.

Aldosterone is produced not only in the adrenal gland but also in other tissues, including the brain, where it plays an important role in the control of blood pressure and water and electrolyte homeostasis. Aldosterone has also been demonstrated to be a major factor in target organ damage independent of its effects on blood pressure. Herein we review the pathophysiology of aldosterone action in the brain and the clinical and experimental studies on the detrimental effects of aldosterone in the brain.

Baroreflex sensitivity correlates with left ventricular morphology and diastolic function in essential hypertension.

OBJECTIVES: Arterial hypertension is a common cause of cardiac organ damage, inducing morphological and functional modifications. Spontaneous baroreflex sensitivity (BRS) control of the heart rate is a key mechanism of blood pressure homeostasis, and is impaired in patients with hypertension. This study sought to assess the association between BRS and left ventricular morphology and function. METHODS: We studied 224 hypertensive patients (125 men; aged 47.8 +/- 10.8 years, mean +/- SD) compared with 51 normotensive control subjects (25 men, aged 45.7 +/- 12.5 years). Left ventricular morphology, systolic and diastolic function were evaluated by echocardiography. Spontaneous BRS was measured using the sequence method. RESULTS: BRS was inversely associated with relative wall thickness (R = 0.17; P < 0.0001) and left ventricular mass index (R = 0.03; P = 0.01); in particular, BRS was significantly impaired in patients with concentric left ventricular remodelling (median [interquartile difference] 9.4 [4.1]) and hypertrophy (9.05 [3.9]) compared with the normal left ventricle (12.3 [5]; P < 0.001). BRS showed a significant association with systolic function evaluated by midwall fractional shortening (r = 0.28; P < 0.001), stroke volume (r = 0.27; P < 0.001), stroke work (r = 0.17; P < 0.05), and fractional shortening (r = 0.17; P < 0.05). BRS was significantly decreased in patients with diastolic dysfunction; it was lower in patients with diastolic dysfunction compared with both the control group and hypertensive patients with normal diastolic function. CONCLUSION: BRS is associated with left ventricular morphology, systolic and diastolic function in hypertensive patients. In particular BRS is impaired in patients with diastolic dysfunction. These findings suggest a role for BRS as a target in arterial hypertension.

QT interval in patients with primary aldosteronism and low-renin essential hypertension.

INTRODUCTION: QT interval prolongation increases the risk of sudden death in several medical conditions. Patients with primary aldosteronism and salt-sensitive hypertension experience more cardiovascular events than those with normal-renin essential hypertension. QT interval prolongation might represent one of the risk factors for cardiovascular events in these patients. The aim of the present study was to evaluate the QT interval in patients with primary aldosteronism and low-renin essential hypertension (LREH). METHODS: Twenty-seven patients with primary aldosteronism, 17 patients with LREH, 117 patients with essential hypertension and 25 healthy individuals were studied. Plasma aldosterone, plasma renin activity, and aldosterone to plasma renin activity ratio (ARR) were determined. Corrected QT intervals (QTcs) were measured from a 12-lead electrocardiogram. RESULTS: The QTc was longer in primary aldosteronism (434 +/- 23 ms) and LREH (430 +/- 18 ms) compared with essential hypertension (419 +/- 22 ms) and healthy controls (412 +/- 19 ms) (P = 0.0004). The prevalence of QTc longer than 440 ms was higher in primary aldosteronism (48%) and LREH (23%) compared with essential hypertension (11%) and healthy controls (4%) (P < 0.0001). QTc correlated with plasma aldosterone (P = 0.01), ARR (P = 0.02), and diastolic blood pressure (P = 0.01). ARR (P = 0.01) and systolic blood pressure (P = 0.01) were identified as independent predictors of QTc. CONCLUSIONS: We postulate that the elevated aldosterone secretion contributes to the prolongation of the QT interval in patients with primary aldosteronism and LREH through both a depletion of intracellular potassium concentration and higher blood pressure values. QTc measurement might represent one simple, non-invasive and reproducible index to characterize the cardiovascular risk in patients with primary aldosteronism and LREH.

Lung Ultrasound-Implemented Diagnosis of Acute Decompensated Heart Failure in the ED: A SIMEU Multicenter Study.

BACKGROUND: Lung ultrasonography (LUS) has emerged as a noninvasive tool for the differential diagnosis of pulmonary diseases. However, its use for the diagnosis of acute decompensated heart failure (ADHF) still raises some concerns. We tested the hypothesis that an integrated approach implementing LUS with clinical assessment would have higher diagnostic accuracy than a standard workup in differentiating ADHF from noncardiogenic dyspnea in the ED. METHODS: We conducted a multicenter, prospective cohort study in seven Italian EDs. For patients presenting with acute dyspnea, the emergency physician was asked to categorize the diagnosis as ADHF or noncardiogenic dyspnea after (1) the initial clinical assessment and (2) after performing LUS ("LUS-implemented" diagnosis). All patients also underwent chest radiography. After discharge, the cause of each patient's dyspnea was determined by independent review of the entire medical record. The diagnostic accuracy of the different approaches was then compared. RESULTS: The study enrolled 1,005 patients. The LUS-implemented approach had a significantly higher accuracy (sensitivity, 97% [95% CI, 95%-98.3%]; specificity, 97.4% [95% CI, 95.7%-98.6%]) in differentiating ADHF from noncardiac causes of acute dyspnea than the initial clinical workup (sensitivity, 85.3% [95% CI, 81.8%-88.4%]; specificity, 90% [95% CI, 87.2%-92.4%]), chest radiography alone (sensitivity, 69.5% [95% CI, 65.1%-73.7%]; specificity, 82.1% [95% CI, 78.6%-85.2%]), and natriuretic peptides (sensitivity, 85% [95% CI, 80.3%-89%]; specificity, 61.7% [95% CI, 54.6%-68.3%]; n = 486). Net reclassification index of the LUS-implemented approach compared with standard workup was 19.1%. CONCLUSIONS: The implementation of LUS with the clinical evaluation may improve accuracy of ADHF diagnosis in patients presenting to the ED. TRIAL REGISTRY: Clinicaltrials.gov; No.: NCT01287429; URL: www.clinicaltrials.gov.

Aortic size index enlargement is associated with central hemodynamics in essential hypertension.

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)>2 cm/m(2)). Central hemodynamic variables were significantly associated with ASi. Patients with increased ASi were significantly older (60 ± 10 vs. 50 ± 11 years, P < 0.0001) and had higher levels of the augmentation index (AIx; 28 ± 10 vs. 21 ± 10 P < 0.0001), augmentation pressure (AP; 13 ± 6 vs. 8 ± 5 mm Hg, P < 0.0001), and central pulse pressure (cPP; 44 ± 10 vs. 39 ± 8 mm Hg, P<0.0001) 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.

Anti-hypertensive drugs and left ventricular hypertrophy: a clinical update.

Structural remodelling of the heart, known as left ventricular hypertrophy (LVH), is a consequence of systemic hypertension, and is associated with an increased risk of cardiovascular morbidity and mortality. Therefore, particular attention should be paid to the identification, prevention and treatment of this condition in hypertensive patients. LVH seems to benefit from all classes of anti-hypertensive drugs; however, antagonists of the renin-angiotensin-aldosterone system (RAAS) have demonstrated an additional benefit in the inhibition and reversal of myocardial interstitial fibrosis. Nevertheless, in evaluating the degree of arterial hypertension and organ damage, many neuro-hormonal systems are involved, primarily the sympathetic nervous system, thereby explaining the use of different classes of anti-hypertensive drugs to prevent or reduce LVH. The RAAS antagonists are actually the recommended anti-hypertensive agents to prevent organ damage in hypertensive subjects or in hypertensives with evidence of LVH to reduce cardiovascular mortality and morbidity.

[Left ventricular diastolic function and dysfunction: a single cardiac target for various systemic diseases]. / Funzione e disfunzione diastolica ventricolare sinistra: un target cardiaco unico per malattie sistemiche diverse.

Several systemic and cardiac diseases cause an impairment of left ventricular filling or of the ability to maintain cardiac output, without an increase in end-diastolic pressure. Prevalence of diastolic dysfunction has been found to be higher than systolic dysfunction in most studies. Many physiological conditions (age, sex and body weight), and pathological processes, such as cardiac or systemic diseases, can increase the incidence of diastolic dysfunction. Early diagnosis of left ventricular diastolic impairment has been demonstrated to have important therapeutic implications. Several invasive or non-invasive methods to investigate diastolic properties of the left ventricle have been described; a large number of studies compared different parameters of diastolic function in order to find the most accurate: this is of particular prognostic relevance since diastolic dysfunction may remain asymptomatic for a long period before resulting in overt heart failure. The purpose of this article is to provide an extensive review of the contemporary literature regarding diastolic function assessment and its role in daily practice.