Related Experiment Video

Updated: Jul 14, 2026

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice
05:08

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Published on: October 3, 2019

Effects of beta-blocker therapy on high sensitivity c-reactive protein, oxidative stress, and cardiac function in

Yuji Nagatomo1, Tsutomu Yoshikawa, Takashi Kohno

  • 1Cardiology Division, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.

Journal of Cardiac Failure
|July 3, 2007
PubMed

Insights

Beta-blocker therapy may reduce C-reactive protein (CRP) levels in some congestive heart failure (CHF) patients. This reduction correlates with improved cardiac function and antioxidant effects, particularly with carvedilol.

Area of Science:

  • Cardiology
  • Pharmacology
  • Biochemistry

Background:

  • Uncertainty exists regarding beta-blocker therapy's effect on C-reactive protein (CRP) in congestive heart failure (CHF).
  • Investigating beta-blockers' impact on serum CRP levels is crucial for understanding inflammation in CHF.

Purpose of the Study:

  • To determine if beta-blocker therapy decreases serum CRP production in CHF patients.
  • To correlate changes in CRP with cardiac function and other biomarkers.

Main Methods:

  • Fifty-two patients with mild to moderate CHF (left ventricular ejection fraction <40%) were randomized to metoprolol or carvedilol.
  • Serum CRP, left ventricular ejection fraction (EF), and plasma lipid peroxide (LPO) were measured before and after 16 weeks of therapy.

Main Results:

  • CRP concentration decreased significantly in patients with higher baseline CRP levels.
  • An inverse correlation was observed between changes in CRP and EF (DeltaCRP and DeltaEF) in patients with higher baseline CRP.
  • Carvedilol showed a greater reduction in CRP compared to metoprolol in patients with higher baseline CRP. Plasma lipid peroxide (LPO) also decreased significantly.

Conclusions:

  • Beta-blocker administration is linked to reduced inflammatory markers in specific CHF patients.
  • The antioxidant properties of beta-blockers, especially carvedilol, may contribute to these anti-inflammatory effects.
  • These findings suggest a potential role for beta-blockers in managing inflammation associated with CHF.
Abstract

Related Concept Videos

Heart Failure Drugs: &#946;-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
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...
Antihypertensive Drugs: Action of &#946;1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers...
Antihypertensive Drugs: Types of &#946;-Blockers01:28

Antihypertensive Drugs: Types of β-Blockers

β receptors are classified into three subclasses: β1, β2, and β3. β1 receptors are primarily located in the heart and kidneys. When they get activated, they increase heart rate, contractility, and renin release. This process enhances blood pressure and aids in stress management. In contrast, β2 receptors are situated mainly in the lungs, blood vessels, and skeletal muscles. Upon activation, they trigger smooth muscle relaxation, causing bronchodilation and vasodilation. This widens airways and...
Adrenergic Antagonists: Pharmacological Actions of &#946;-Receptor Blockers01:27

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in bronchial smooth...
Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers01:19

Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers

Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...