Plasma fibrinogen in unstable coronary artery disease

E Swahn1, H von Schenck, L Wallentin

  • 1Department of Internal Medicine, University Hospital, Linköping, Sweden.

Insights

Unstable coronary artery disease (CAD) and non-Q-wave myocardial infarction (MI) elevate fibrinogen and orosomucoid levels. These acute-phase reactants may indicate a hypercoagulable state and disease progression in CAD patients.

Area of Science:

  • Cardiology
  • Clinical Biochemistry
  • Inflammation Research

Background:

  • Unstable coronary artery disease (CAD) encompasses unstable angina pectoris and non-Q-wave myocardial infarction (MI).
  • Elevated acute-phase reactants like fibrinogen and orosomucoid are observed in inflammatory conditions, including cardiovascular disease.
  • The role of these markers in the context of unstable CAD requires further elucidation.

Purpose of the Study:

  • To investigate plasma fibrinogen and orosomucoid levels in patients with suspected unstable CAD.
  • To determine the association of unstable CAD, obesity, and smoking with these acute-phase reactants.
  • To explore the potential implications of elevated fibrinogen in unstable CAD for hypercoagulability and disease progression.

Main Methods:

  • Plasma fibrinogen and orosomucoid levels were measured in 249 patients admitted to a coronary care unit.
  • Patients were categorized into unstable CAD (including unstable angina and non-Q-wave MI) and control groups.
  • Statistical analysis was performed to identify independent contributors to elevated marker levels.

Main Results:

  • A diagnosis of unstable CAD independently contributed to elevated fibrinogen and orosomucoid levels.
  • Obesity and current smoking also independently correlated with increased levels of these acute-phase reactants.
  • In non-Q-wave MI patients, fibrinogen and orosomucoid levels were high irrespective of obesity and smoking status, suggesting myocardial necrosis as a primary driver.
  • Increased fibrinogen in unstable CAD may signify a hypercoagulable state, potentially promoting coronary lesion progression.

Conclusions:

  • Elevated fibrinogen and orosomucoid are associated with unstable CAD and non-Q-wave MI.
  • Obesity and smoking influence the basal levels and inflammatory response of fibrinogen and orosomucoid.
  • The heightened fibrinogen in unstable CAD suggests a prothrombotic state, contributing to cardiovascular event risk.

Related Concept Videos

Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
Acute Coronary Syndrome I: Introduction01:30

Acute Coronary Syndrome I: Introduction

Acute Coronary Syndrome (ACS) encompasses a spectrum of heart conditions caused by sudden obstruction of coronary arteries, typically resulting from the rupture of an atherosclerotic plaque and subsequent thrombus (blood clot) formation. This obstruction can lead to partial or complete blockage of blood flow, causing varying degrees of myocardial ischemia or infarction.ACS includes the following clinical entities:Unstable Angina (UA)Non-ST-Elevation Myocardial Infarction (NSTEMI)ST-Elevation...