Abstract
The present paper will provide an update on the role of sympathetic neural factors in the development and progression of essential hypertension by reviewing data collected in the past 10 ...years. This will be done by discussing the results of the published studies in which sympathetic neural function in essential hypertension and related disease has been investigated via sophisticated and highly sensitive techniques, such as microneurographic recording of sympathetic nerve traffic and regional norepinephrine spillover. First, the relevance of the pathophysiological background of the neurogenic alterations will be discussed. It will be then examined the behavior of the sympathetic neural function in specific clinical phenotypes, such as resistant hypertension, pseudoresistant hypertension, and hypertensive states displaying elevated resting heart values. This will be followed by a discussion of the main results of the meta-analytic studies examining the behavior of sympathetic nerve traffic in essential hypertension, obesity, metabolic syndrome, and chronic renal failure. The sympathetic effects of renal denervation and carotid baroreceptor stimulation as well as the possible involvement of sympathetic neural factors in the determination of the so-called “residual risk” of the treated hypertensive patients will be finally discussed.
Physiological studies have long documented the key role played by the autonomic nervous system in modulating cardiovascular functions and in controlling blood pressure values, both at rest and in ...response to environmental stimuli. Experimental and clinical investigations have tested the hypothesis that the origin, progression, and outcome of human hypertension are related to dysfunctional autonomic cardiovascular control and especially to abnormal activation of the sympathetic division. Here, we review the recent literature on the adrenergic and vagal abnormalities that have been reported in essential hypertension, with emphasis on their role as promoters and as amplifiers of the high blood pressure state. We also discuss the possible mechanisms underlying these abnormalities and their importance in the development and progression of the structural and functional cardiovascular damage that characterizes hypertension. Finally, we examine the modifications of sympathetic and vagal cardiovascular influences induced by current nonpharmacological and pharmacological interventions aimed at correcting elevations in blood pressure and restoring the normotensive state.
Several articles have dealt with the importance and mechanisms of the sympathetic nervous system alterations in experimental animal models of hypertension. This review addresses the role of the ...sympathetic nervous system in the pathophysiology and therapy of human hypertension. We first discuss the strengths and limitations of various techniques for assessing the sympathetic nervous system in humans, with a focus on heart rate, plasma norepinephrine, microneurographic recording of sympathetic nerve traffic, and measurements of radiolabeled norepinephrine spillover. We then examine the evidence supporting the importance of neuroadrenergic factors as promoters and amplifiers of human hypertension. We expand on the role of the sympathetic nervous system in 2 increasingly common forms of secondary hypertension, namely hypertension associated with obesity and with renal disease. With this background, we examine interventions of sympathetic deactivation as a mode of antihypertensive treatment. Particular emphasis is given to the background and results of recent therapeutic approaches based on carotid baroreceptor stimulation and radiofrequency ablation of the renal nerves.
Blood pressure (BP) control in patients with hypertension is variable worldwide, and in general, it results largely unsatisfactory. Factors responsible for this phenomenon include insufficient ...national cardiovascular healthcare policies for prevention, poor patient compliance with prescribed treatment schedules, and the reluctance of physicians to modify treatment strategies when BP is still elevated, that is, the so-called therapeutic inertia. A further important factor favoring poor BP control is the limited use of combination drug treatment, despite evidence of its superior ability to control BP in patients with difficult-to-treat hypertension. In addition, combination treatment allows to achieve BP control more easily (and more quickly) as compared with monotherapy. This article, after briefly examining the main features of BP control, will review the importance in the treatment of hypertension of the drug combination strategy, based on the recommendations of the 2018 European Society of Cardiology/European Society of Hypertension guidelines. Empahsis will be given to the drug combination treatment as first step of the antihypertensive therapeutic intervention. The potential drawbacks and barriers to combination drug treatment as initial therapeutic strategy will also be briefly discussed.
Several studies reported an association between nonalcoholic fatty liver disease (NAFLD) and the risk of incident hypertension. The objective of this systematic review and meta-analysis was to obtain ...a precise and reliable estimate of the nature and magnitude of this association. We systematically searched Ovid-MEDLINE up to March 2021 for observational studies in which NAFLD was diagnosed in adults using blood-based panels, imaging techniques or liver biopsy and with a follow-up ≥1 year. Measures of association from individual studies were meta-analyzed using random-effects models. Of the 1108 titles initially scrutinized, we included 11 cohort studies with data on 390 348 participants (52% male) and a mean follow-up of 5.7 years. In the overall analysis, NAFLD was associated with a moderately increased risk of incident hypertension (hazard ratio 1.66; 95% confidence interval (CI), 1.38-2.01; test for overall effect z = 5.266; P < 0.001). There was significant heterogeneity among the studies (P < 0.001). Sensitivity analyses showed that estimates were not affected by geographical location, duration of follow-up and adjustment for baseline blood pressure values. On the other hand, the magnitude of the association was lower in studies that adjusted for baseline adiposity compared with those that did not, explaining part of the observed heterogeneity. No significant publication bias was detected by funnel plot analysis and Egger's and Begg's tests. This large meta-analysis indicates that NAFLD is associated with a ~1.6-fold increased risk of developing hypertension. Further studies are needed to investigate the role of NAFLD severity in terms of inflammation and fibrosis on incident hypertension.
Autonomic cardiovascular control is impaired in hypertension, leading to a reduction in the parasympathetic tone and to an increase in the sympathetic influences to the heart and peripheral vessels. ...The sympathetic dysfunction depends on a variety of reflex and nonreflex mechanisms and participates at development and progression of the essential hypertensive state. This has been shown to be the case for borderline hypertension, for moderate and severe high blood pressure, and for resistant hypertension as well. In addition, the adrenergic overdrive participates at the pathophysiology of the complex cardiometabolic alterations, known as "end-organ damage," detectable in the clinical course of hypertensive disease. In the present article, we will review the main features of the adrenergic abnormalities characterizing essential hypertension, the mechanisms potentially involved in this neural abnormality, and its consequences as well. We will also discuss the most recent information achieved in the field and the areas worthy of future investigations.
The coronavirus disease 2019 (COVID-19) may cause not only an acute respiratory distress syndrome (ARDS) but also multiple organ damage and failure requiring intensive care and leading to death. Male ...sex, advanced age, chronic lung disease, chronic kidney disease and cardiovascular disease, such as hypertension, diabetes and obesity have been identified as risk factors for the COVID-19 severity. Presumably, as these three cardiovascular risk factors are associated with a high prevalence of multiorgan damage. In the present focused clinical review, we will discuss the cardiovascular complications of COVID-19 including acute cardiovascular syndrome (acute cardiac injury/COVID cardiomyopathy, thromboembolic complications and arrhythmias) and post-COVID-19 sequelae. Preliminary data shows that the cause of acute cardiovascular syndrome may be multifactorial and involve direct viral invasion of the heart and vascular system, as well as through the immune and inflammation-mediated systemic cytokine storm. COVID-19 survivors may also show persistently elevated blood pressure and sinus tachycardia at rest. Furthermore, poor diabetic control, persistent renal damage and cerebral sequelae, such as persistent cognitive and neuropsychiatric alterations are also frequently reported. A particular attention should be paid towards cardiovascular protection in COVID-19 patients who develop acute cardiovascular syndromes during hospitalization, and/or permanent/semipermanent sequelae after recovery from COVID-19. These conditions may require careful clinical assessment, treatment and close follow-up to avoid short-term and long-term complications.
Sympathetic neural factors are involved in energy balance as well as in blood pressure control. This represents the background for the hypothesis that an adrenergic overdrive may be implicated in the ...development and/or progression of the metabolic syndrome. Indirect and direct markers of sympathetic drive have confirmed this hypothesis, by showing the occurrence of an adrenergic activation both at the cardiac and peripheral vascular level. It is likely that this sympathetic dysfunction is triggered by reflex mechanisms (arterial baroreceptor impairment), metabolic factors (insulin resistance), and humoral agents (angiotensin II, leptin). The adrenergic overdrive exerts a number of adverse effects on the cardiovascular system, by favoring the genesis of cardiac hypertrophy, vascular hypertrophy, arterial remodeling and endothelial dysfunction and thereby aggravating the already elevated cardiovascular risk profile of the patient. This carries obvious clinical and therapeutic implications, including the suggestion that sympathetic inhibition should be included among the goals of both pharmacological and non-pharmacological interventions employed in the treatment of the metabolic syndrome.
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