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Conclusive evidence demonstrates that the sympathetic nervous system activation is a hallmark of congestive heart failure. This has been shown via a variety of biochemical, neurophysiological, and neuroimaging approaches for studying human sympathetic neural function. The sympathetic activation appears to be an early phenomenon in the clinical course of the disease, closely related to its severity and potentiated by the concomitant presence of other comorbidities, such as obesity, diabetes mellitus, metabolic syndrome, hypertension, and renal failure. The adrenergic overdrive in heart failure is associated with other sympathetic abnormalities, such as the downregulation of beta-adrenergic adrenoreceptors at cardiac level, and exerts unfavorable consequences on the cardiovascular system. These include the endothelial dysfunction, the development of left ventricular hypertrophy, the atherosclerosis development, as well as the generation of atrial and ventricular arrhythmias, and, at very extreme levels of sympathetic activation, the occurrence of microscopic myocardial necrosis. Given the close direct independent relationships detected in heart failure between sympathetic activation and mortality, the adrenergic overdrive has become a target of neuromodulatory therapeutic interventions, which include non-pharmacological, pharmacological, and device-based interventions. For some of these approaches (specifically bilateral renal nerves ablation and carotid baroreceptor stimulation), additional studies are needed to better define their impact on the clinical course of the disease.

Subclinical abnormalities in cardiac and vascular structure reflect the adverse effects triggered by a variety of risk factors on the cardiovascular (CV) system thereby representing an intermediate step in the cardiovascular continuum; such alterations are recognized as reliable markers of increased cardiovascular risk in different clinical settings including obstructive sleep apnea (OSA). The mechanisms underlying subclinical organ damage (OD) in the OSA setting are multifactorial. Hypoxemia and hypercapnia, induced by repeated collapses of upper airways, have been suggested to trigger a cascade of events such as activation of the sympathetic tone, renin–angiotensin–aldosterone system leading to endothelial dysfunction, vasoconstriction, myocardial and vascular remodeling, and hypertension. Furthermore, coexisting non-haemodynamic alterations such as increased oxidative stress, release of inflammatory substances, enhanced lipolysis and insulin resistance have been reported to play a role in the pathogenesis of both cardiac and extra-cardiac OD. In this article we reviewed available evidence on the association between OSA and subclinical cardiac (i.e., left and right ventricular hypertrophy, left atrial dilatation) and extra-cardiac organ damage (i.e., carotid atherosclerosis, arterial stiffness, microvascular retinal changes, and microalbuminuria). This association is apparently stronger for cardiac and carotid subclinical damage than for other markers (i.e., arterial stiffness and retinal changes) and mostly evident in the setting of severe OSA.

Purpose of ReviewTo evaluate the relation between sleep alterations, with or without breathing disorders, and incidence of hypertension and other cardiovascular diseasesRecent FindingsSeveral studies have clearly shown the mechanisms linking sleep disorders and cardiovascular diseases. The sympathetic hyperactivity seems to play a fundamental role in favoring and sustaining the increase in blood pressure values. Several other mechanisms also contribute to this effect and to the increase cardiovascular risk.SummaryThe mechanisms responsible for the increase in blood pressure values in subjects with alteration in sleep quantity and quality, with or without breathing disorders, have been clearly established. The recent findings refer to the result of meta-analysis of cross-sectional studies or longitudinal studies showing a significant association between short sleep duration and hypertension. It has also been shown that sleep fragmentation could be considered the main determinant of the sympathetic activation independently of the frequency and severity of oxygen desaturation.

Purpose of ReviewTo review the results of studies of the effects of dialysis and kidney transplantation on the autonomic nervous system alterations that occur in chronic kidney disease.Recent FindingsVagal control of the heart mediated by arterial baroreceptors is altered early in the course of the renal disease. Sympathetic activation occurs, with increases in resting heart rate, venous plasma norepinephrine levels, muscle sympathetic nerve traffic, and other indirect indices of adrenergic drive. The magnitude of the changes reflects the clinical severity of the kidney disease. Both the sympathetic and parasympathetic alterations have a reflex origin, depending on the impairment in baroreflex and cardiopulmonary reflex control of the cardiovascular system. These alterations are partially reversed during acute hemodialysis, but the responses are variable depending on the specific type of dialytic treatment that is employed. Renal transplantation improves reflex cardiovascular control, resulting in sympathoinhibition following renal transplantation if the native kidneys are removed. Sympathoinhibitory effects have been also reported in renal failure patients after bilateral renal denervation.SummaryAssessment of autonomic nervous system responses to dialysis and renal transplantation provides information of clinical interest, given the evidence that autonomic alterations are involved in the development and progression of cardiovascular complications, as well as in the prognosis of chronic kidney disease.

The global rate of intensive care unit (ICU) admission during the COVID-19 pandemic varies within countries and is among the main challenges for health care systems worldwide. Conflicting results have been reported about the response to coronavirus infection and COVID-19 outcomes in men and women. Understanding predictors of intensive care unit admission might be of help for future planning and management of the disease. We designed a cross-sectional observational multicenter nationwide survey in Italy to understand gender-related clinical predictors of ICU admission in patients with COVID-19. We analyzed information from 2378 charts of Italian patients certified for COVID-19 admitted in 26 hospitals. Three hundred ninety-five patients (16.6%) required ICU admission due to COVID19 infection, more frequently men (74%), with a higher prevalence of comorbidities (1,78±0,06 vs 1,54±0,03 p<0.05). In multivariable regression model main predictors of admission to ICU are male gender (OR 1,74 95% CI 1,36-2,22 p<0.0001) and presence of obesity (OR 2,88 95% CI 2,03-4,07 p<0.0001), chronic kidney disease (OR: 1,588; 95%, 1,036-2,434 p<0,05) and hypertension (OR: 1,314; 95% 1,039-1,662; p<0,05). In gender specific analysis, obesity, chronic kidney disease and hypertension are associated with higher rate of admission to ICU among men, whereas in women, obesity (OR: 2,564; 95% CI 1,336-4.920 p<0.0001) and heart failure (OR: 1,775 95% CI: 1,030-3,057) are associated with higher rate of ICU admission. Our study demonstrates that gender is the primary determinant of the disease's severity among COVID-19. Obesity is the condition more often observed among those admitted to ICU within both genders. Clinicaltrials.gov: NCT04331574.

Obstructive sleep apnea (OSA) syndrome is the most common sleep-breathing disorder, which is associated with increase cardiovascular morbidity and mortality. OSA increases risk of resistant arterial hypertension, coronary artery disease, heart failure, pulmonary hypertension, and stroke. Studies showed the significant relationship between OSA and cardiac remodeling. The majority of investigations were focused on the left ventricle and its hypertrophy and function. Fewer studies investigated right ventricular structure and function revealing deteriorated diastolic and systolic function. Data regarding left and right ventricular mechanics in OSA patients are scarce and controversial. The results of the studies that were focused on the influence of continuous positive airway pressure and weight reduction on cardiac remodeling revealed favorable effect on left and right ventricular structure and function. Recently published analyses confirmed positive effect of treatment on cardiac mechanics. Deterioration of left and right ventricular mechanics occurs before functional and structural cardiac impairments in the cascade of cardiac remodeling and therefore the assessment of left and right ventricular strain may represent a cornerstone in detection of subtle cardiac changes that develop significantly before other, often irreversible, alterations. Considering the fact that left and right ventricular strains have important predictive value in wide range of cardiovascular diseases, one should consider the evaluation of left and right ventricular strains in the routine echocardiographic assessment at all stages of disease—from diagnosis, during follow-up and evaluation of therapeutic effects. The main aim of this review is to provide the current overview of cardiac mechanics in OSA patients before and after (during) therapy, as well as mechanisms that could be responsible for cardiac changes.

Serum uric acid (SUA) overproduction, leading to hyperuricemia, represents a metabolic dysfunction of frequent detection in a number of diseases characterized by an elevated cardiovascular risk, such as metabolic syndrome, essential hypertension, dyslipidemia, obesity, and diabetes mellitus. Similar findings have been also reported for the Atherogenic Index of Plasma (AIP), i.e., a biomarker derived from the logarithmic transformation of the ratio between plasma triglycerides and high-density plasma lipoprotein cholesterol. Both SUA and AIP have been found to be sensitive predictors of fatal and non-fatal cardiovascular events and all-cause mortality, their association representing a highly sensitive marker potentiating the predictive value of each single factor. Although a number of studies have investigated the relationships between SUA and AIP, the association between these two metabolic variables still remains in several indistinct aspects. The present paper, after briefly summarizing the main features of the Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA) study, will review the main study results related to SUA as cardiovascular risk factors. It will also report the original data collected in the PAMELA study on (1) the association between SUA and AIP and (2) the relationships between AIP and normal and elevated blood pressure, metabolic profile, and target organ damage associated with hypertension.