Related Experiment Video
Updated: Aug 8, 2026
07:52
Implantation of Fibrin Gel on Mouse Lung to Study Lung-specific Angiogenesis
Published on: December 21, 2014
Fibrin(ogen) in cardiovascular disease: an update
1Dept. of Internal Medicine II - Cardiology, University of Ulm Medical Center, Robert-Koch Str. 8, D - 89081 Ulm/ Germany. wolfgang.koenig@medizin.uni-ulm.de
Thrombosis and Haemostasis
|April 2, 2003
Summary
Fibrinogen is a significant independent marker for cardiovascular disease risk, including coronary heart disease and stroke. Elevated fibrinogen levels are linked to increased risk of cardiovascular events and mortality.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Epidemiology
Background:
- Fibrinogen is widely accepted as a strong, independent risk factor for cardiovascular disease (CVD).
- Evidence stems from numerous prospective epidemiological studies and clinical observations linking fibrinogen to CVD endpoints.
- Elevated fibrinogen is associated with atherosclerosis, coronary heart disease (CHD), stroke, peripheral arterial disease, and overall mortality.
Purpose of the Study:
- To review the established association between fibrinogen and cardiovascular risk.
- To explore the pathophysiological mechanisms by which elevated fibrinogen may mediate cardiovascular risk.
- To discuss the role of fibrinogen as a cardiovascular risk marker.
Main Methods:
- Meta-analysis of prospective epidemiological studies.
- Review of clinical observations and pathophysiological mechanisms.
- Assessment of fibrinogen's association with various cardiovascular endpoints.
Main Results:
- Meta-analysis shows a 1.8 odds ratio for CHD with higher fibrinogen tertiles.
- Fibrinogen levels correlate with unstable/stable coronary artery disease and post-intervention complications.
- Similar associations found for incident stroke, peripheral arterial disease progression, and total mortality.
Conclusions:
- Fibrinogen is an important additional marker for cardiovascular risk.
- Mechanisms include its role in coagulation, platelet aggregation, endothelial function, and smooth muscle cell proliferation.
- The causal role of fibrinogen in atherothrombogenesis requires further determination.
Related Concept Videos
01:30Anticoagulant 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...
01:17Ischemic Heart Disease: Overview
Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...
01:16Clot 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.
01:26Coronary 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...
01:19Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
01:26Atherosclerosis III: Management
Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...