Heart failure is a complex condition driven by an imbalance between vasodilator and vasoconstrictor mechanisms, where neurohormonal activation precipitates structural changes and disease progression.
Heart failure pathophysiology is driven by a deleterious imbalance in neurohormonal systems, leading to disease progression.
Congestive heart failure is a major health problem associated with high morbidity and mortality. Insights into the pathophysiology of this syndrome have changed considerably during the past decade. Heart failure is no longer considered to be a purely haemodynamic disorder but is regarded as a complex condition, characterised by a shift in the balance between opposite forces: the vasodilator-natriuretic mechanisms (natriuretic peptides, prostaglandins, vagal tone, nitric oxide pathway, and possibly adrenomedullin) and the vasoconstrictor-antinatriuretic mechanisms (catecholamines, angiotensin II, aldosterone, arginine-vasopressin, and endothelin) (fig Moreover, activation of the neurohormonal systems in response to cardiac injury has a deleterious effect on the heart mediated via complex systemic and local mechanisms. These events precipitate functional and structural changes in the heart and peripheral vasculature, which ultimately cause the disease to progress.
Komajda et al. (Mon,) conducted a review in Congestive heart failure. Heart failure is a complex condition driven by an imbalance between vasodilator and vasoconstrictor mechanisms, where neurohormonal activation precipitates structural changes and disease progression.
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