Related Experiment Videos

Relationship between RANKL and neuroendocrine activation in elderly males with heart failure

Goran Loncar1, Biljana Bozic, Vojkan Cvorovic

  • 1Cardiology Department, Clinical Medical Center Zvezdara, Belgrade, Serbia. loncar_goran@yahoo.com

Endocrine
|October 22, 2010
PubMed

Insights

Elevated serum receptor activator of nuclear factor-κB ligand (sRANKL) is linked to neuroendocrine activation in elderly males with systolic heart failure. This finding suggests sRANKL may play a role in heart failure pathogenesis.

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Bone Biology

Background:

  • Receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG) are key regulators of bone remodeling.
  • Emerging evidence suggests a link between RANKL/OPG and cardiovascular disease, including heart failure.
  • Neuroendocrine activation, indicated by biomarkers like NT-pro-BNP and adiponectin, is implicated in heart failure pathophysiology.

Purpose of the Study:

  • To investigate the association between serum RANKL (sRANKL) and markers of neuroendocrine activation in elderly males with congestive heart failure (CHF).
  • To assess the relationship between sRANKL levels and clinical/echocardiographic parameters in this patient cohort.

Main Methods:

  • A case-control study involving 75 elderly males with mild to moderate CHF (left ventricular ejection fraction <40%) and 20 age/BMI-matched healthy male volunteers.
  • Serum levels of sRANKL, OPG, NT-pro-BNP, adiponectin, and leptin were measured.
  • Clinical and echocardiography data were collected; statistical analyses included comparative analysis, risk assessment, correlation, and multivariate regression.

Main Results:

  • CHF patients exhibited significantly higher sRANKL levels compared to controls (126.8 vs. 47.8 pg/ml, P < 0.0001).
  • Increased sRANKL was associated with a significantly higher risk of systolic CHF (OR = 10.286, P < 0.0001).
  • In CHF patients, sRANKL positively correlated with NT-pro-BNP and adiponectin, and inversely with BMI and creatinine clearance. sRANKL was an independent determinant of NT-pro-BNP.

Conclusions:

  • Serum RANKL is significantly associated with markers of neuroendocrine activation, specifically NT-pro-BNP and adiponectin, in elderly males with systolic heart failure.
  • These findings suggest a potential role for sRANKL in the complex pathogenesis of heart failure.
  • Further research is warranted to elucidate the precise mechanisms underlying the association between sRANKL and heart failure.

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
Heart Failure III: Clinical Manifestations01:26

Heart Failure III: Clinical Manifestations

Heart failure (HF) manifests primarily as dyspnea, fatigue, and fluid retention, resulting in peripheral and pulmonary edema. Symptoms may vary depending on which ventricle is more affected, left or right.Left-Sided Heart FailureAlso known as left ventricular failure, this condition results from the left ventricle's inability to fill or eject sufficient blood into the systemic circulation. It leads to pulmonary congestion, which occurs when the left ventricle fails to eject blood effectively...
Heart Failure VII: Nursing Interventions01:30

Heart Failure VII: Nursing Interventions

The first step in nursing management of a patient with heart failure involves thoroughly assessing the patient's medical history.Subjective Data: Obtain the patient's medical history of coronary artery disease, hypertension, myocardial infarction, and symptoms like dyspnea, orthopnea, and paroxysmal nocturnal dyspnea.Objective Data: Conduct a physical examination to identify findings such as jugular vein distention, pulmonary crackles, tachycardia, murmurs, peripheral edema, and vital signs,...
Heart Failure VI: Adjunct Therapies01:22

Heart Failure VI: Adjunct Therapies

Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.