Fluid retention and heart failure11/29/2023 ![]() Systemic RAAS activation occurs with increased plasma renin activity, which initiates the activation of the primary targets for clinical intervention: angiotensin II (Ang II) and aldosterone. Activation of RAAS is associated with left ventricular dysfunction, cardiac dilation, sodium and extracellular fluid retention (edema), and cachexia/sarcopenia. However, the effects of the NP system are attenuated in advanced HF Stages C and D. ![]() The NP system acts to counter the SNS-RAAS by promoting diuresis, natriuresis, and vasodilation. An elevation in plasma norepinephrine signifies SNS activation, which occurs at Stage B in clinical and experimental HF and is strongly associated with progression of systolic dysfunction, congestion, and RAAS activation. Neurohormonal activation may initially compensate for impaired cardiac function however, prolonged activation has deleterious effects on cardiac structure and performance, leading to symptomatic HF associated with edema. Regardless of the cause of DCM, the progression from asymptomatic to symptomatic HF is associated with interdependent, neurohormonal alterations of the sympathetic nervous system (SNS), the renin–angiotensin–aldosterone system (RAAS), and the natriuretic peptide (NP) system. Transition from presymptomatic HF to symptomatic HF is critically important for patients as it leads to a marked decline in the quality of life and is associated with significant morbidity and mortality. Subsequently patients develop symptomatic HF (Stages C and D), which is associated with fluid retention (edema), breathlessness, fatigue, exercise intolerance, and death. Patients at risk for DCM have Stage A HF and usually progress to Stage B, where there is a decline in systolic function both Stages A and B are without symptoms or are presymptomatic. ![]() The American College of Cardiology/American Heart Association (ACC/AHA) staging system suggests that HFrEF predictably progresses though four stages, from A to D. Dilated cardiomyopathy (DCM) due to nonischemic or ischemic causes is characterized by progressive heart enlargement with rEF, which is a major risk factor for the development of symptomatic heart failure with reduced ejection fraction (HFrEF). The prevalence of symptomatic HF will increase 46% from 2012 to 2030. Symptomatic heart failure (HF) with reduced ejection fraction (rEF) affects millions and is the most common reason for heart transplantation. Thus, specific assessment and targeting of elevated renin activity may enhance diagnostic and therapeutic precision to improve outcomes in appropriate patients with HFrEF. Modulation of renin activity in experimental HF significantly reduces edema formation and the progression of systolic dysfunction and improves survival. Plasma renin activity levels are also reported to be elevated in patients and animals with rEF before the development of symptomatic HF. Clinical and experimental studies indicate that plasma renin activity is elevated with symptomatic HFrEF with edema in patients, as well as in companion animals and experimental models of HF. Here, we review the role of active renin, a crucial, upstream enzymatic regulator of the RAAS, as a prognostic and diagnostic plasma biomarker of heart failure with reduced ejection fraction (HFrEF) progression we also discuss its potential as a pharmacological bio-target in HF therapy. Regardless of the cause, symptomatic heart failure (HF) with reduced ejection fraction (rEF) is characterized by pathological activation of the renin–angiotensin–aldosterone system (RAAS) with sodium retention and extracellular fluid expansion (edema). ![]()
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