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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...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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...
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 instability].

Félix Malpartida1, Ricardo Vivancos, Cristóbal Urbano

  • 1Servicio de Cardiología, Hospital Regional Universitario Carlos Haya, Málaga, España.

Archivos De Cardiologia De Mexico
|October 22, 2008
PubMed
Summary
This summary is machine-generated.

High-sensitivity C-reactive protein (hs-CRP) levels correlate with acute coronary syndromes (ACS) severity. Elevated hs-CRP indicates unstable plaque rupture, a key factor in vulnerable plaque identification and cardiovascular event prevention.

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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
09:41

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

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

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
09:41

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

Area of Science:

  • Cardiovascular Medicine
  • Inflammation Biology
  • Biomarker Research

Context:

  • Atherosclerotic plaque instability is central to acute coronary syndromes (ACS), with plaque rupture causing up to 75% of events.
  • Identifying vulnerable plaques (VP) is crucial for predicting future cardiovascular events.
  • Inflammation is a key determinant in atherosclerosis and plaque vulnerability.

Purpose:

  • To investigate the correlation between high-sensitivity C-reactive protein (hs-CRP) levels and the severity of acute coronary syndromes (ACS).
  • To assess the role of hs-CRP as a potential biomarker for vulnerable plaque identification.

Summary:

  • This study measured hs-CRP levels in 104 patients with varying degrees of coronary artery disease.
  • Significantly elevated hs-CRP levels were observed in patients with ST-elevation ACS (50.41 mg/L) compared to non-ST-elevation ACS (19.92 mg/L) and stable angina (5.85 mg/L) (p < 0.01).
  • These findings highlight the association between inflammation, indicated by hs-CRP, and the clinical presentation of ACS, suggesting a role in vulnerable plaque assessment.

Impact:

  • The findings support the use of hs-CRP as a readily available marker to help identify patients at higher risk of ACS due to vulnerable plaques.
  • This research contributes to the evolving concept of the 'vulnerable patient,' emphasizing the need for advanced diagnostic and therapeutic strategies.
  • Improved identification and management of vulnerable plaques and patients hold the potential to reduce future coronary events and improve cardiovascular outcomes.