English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

uch information has been collected over the past few years on the main features of neuroadrenergic abnor- malities that characterize cardiovascular disease. We learned, eg, that in a number of pathological states adrenergic influ- ences lose their homeostatic regulatory function and become "less sympathetic," not only favoring the development of the disease itself but also contributing to its clinical progression. We also learned that elevated circulating plasma norepineph- rine levels do not invariably reflect sympathetic activation and that complex but accurate methodologic approaches to quantify neuroadrenergic drive should be of help in dissecting the peripheral (reduced clearance and or reuptake of norepi- nephrine) versus the central (increased in central sympathetic outflow) origin of the sympathetic activation characterizing a given physiological or pathophysiological condition. Other key findings of recent investigations in the field of neural cardiovascular control should not be forgotten. They include, eg, the evidence that sympathetic influences on cardiac, renal, thermoregulatory, and metabolic function are not independent entities but rather complex phenomena integrating each other in a "neurally exchanging network." They also include the evidence that, in several cardiovascular and noncardiovascu- lar diseases, therapeutic counterbalance of adrenergic over- drive may be clinically relevant for reducing cardiovascular risk, improving cardiovascular function, and possibly retard- ing the progression and favoring the regression of the end-organ damage. This therapeutic goal is based on a well-documented rationale, namely the evidence that in a number of diseases (heart failure, acute myocardial infarc- tion, stroke, and renal failure) sympathetic activation has proven clinical and prognostic relevance.1

Qualitative Assessment of Sympathetic Neural Drive in Cardiometabolic Disease