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Related Concept Videos

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
Inflammation01:38

Inflammation

Overview
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...
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...
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...

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Related Experiment Video

Updated: Jun 28, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

Inflammation and plaque vulnerability.

Prediman K Shah1

  • 1Division of Cardiology and Atherosclerosis Research Center, Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Suite 5531 8700 Beverly Blvd, Los Angeles, CA 90048, USA. shahp@cshs.org

Cardiovascular Drugs and Therapy
|October 25, 2008
PubMed
Summary
This summary is machine-generated.

Atherosclerotic plaque rupture, not just size, triggers acute ischemic events. Plaque composition, inflammation, and lipid core size are key drivers of rupture and thrombosis.

More Related Videos

In vivo Near Infrared Fluorescence (NIRF) Intravascular Molecular Imaging of Inflammatory Plaque, a Multimodal Approach to Imaging of Atherosclerosis
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In vivo Near Infrared Fluorescence (NIRF) Intravascular Molecular Imaging of Inflammatory Plaque, a Multimodal Approach to Imaging of Atherosclerosis

Published on: August 4, 2011

Related Experiment Videos

Last Updated: Jun 28, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

In vivo Near Infrared Fluorescence (NIRF) Intravascular Molecular Imaging of Inflammatory Plaque, a Multimodal Approach to Imaging of Atherosclerosis
09:43

In vivo Near Infrared Fluorescence (NIRF) Intravascular Molecular Imaging of Inflammatory Plaque, a Multimodal Approach to Imaging of Atherosclerosis

Published on: August 4, 2011

Area of Science:

  • Cardiovascular Medicine
  • Pathophysiology
  • Immunology

Background:

  • Acute ischemic syndromes result from arterial occlusion, often caused by thrombus formation at atherosclerotic plaques.
  • Plaque rupture or erosion underlies thrombus development, with composition now recognized as critical over size or stenosis.
  • Vulnerable plaques exhibit specific features like large necrotic lipid cores and inflammation.

Purpose of the Study:

  • To elucidate the role of plaque composition and inflammation in athero-thrombosis.
  • To understand the mechanisms driving plaque rupture and subsequent thrombus formation.
  • To identify key factors influencing plaque instability and cardiovascular events.

Main Methods:

  • Review of current understanding of atherosclerotic plaque pathophysiology.
  • Analysis of factors contributing to plaque rupture and thrombosis.
  • Exploration of the role of inflammation and immune cells.

Main Results:

  • Plaque composition, particularly necrotic lipid core size and inflammation, is more critical than stenosis severity for rupture.
  • Inflammation drives fibrous cap degradation by releasing collagen-degrading enzymes and causing smooth muscle cell death.
  • Inflammation also promotes thrombosis via tissue factor elaboration.

Conclusions:

  • Understanding plaque vulnerability and athero-thrombosis pathophysiology offers new avenues for preventing cardiovascular events.
  • Targeting inflammation and plaque instability may be crucial for therapeutic interventions.
  • Focusing on plaque characteristics beyond stenosis is essential for risk assessment.