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Related Concept Videos

Coronary Artery Disease IV: Preventive Measures01:26

Coronary Artery Disease IV: Preventive Measures

Effective preventive measures for coronary artery disease (CAD) focus on controlling modifiable risk factors, including cholesterol abnormalities and lifestyle changes.Cholesterol ManagementFirst, the Mediterranean diet and the American Heart Association advocate for maintaining low-density lipoprotein (LDL) cholesterol levels below 100 mg/dL, with a more stringent recommendation of below 70 mg/dL for individuals at high risk. LDL cholesterol, often termed "bad cholesterol," can lead to the...
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...
Atherosclerosis III: Management01:26

Atherosclerosis 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...
Coronary Artery Disease I: Introduction01:30

Coronary Artery Disease I: Introduction

Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...
Coronary Artery Disease III: Clinical Manifestations01:30

Coronary Artery Disease III: Clinical Manifestations

Coronary Artery Disease (CAD) is a primary health risk worldwide, leading to significant morbidity and mortality. The condition arises from the buildup of atherosclerotic plaques within the coronary arteries, resulting in diminished blood supply to the heart muscle.The clinical manifestations of CAD vary widely, from asymptomatic stages to severe, life-threatening conditions. Understanding these manifestations is crucial for early diagnosis and effective management.Angina Pectoris: The Warning...
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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.
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Natriuretic Peptides (BNP)
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Related Experiment Video

Updated: May 31, 2026

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
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Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein

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PON-dering differences in HDL function in coronary artery disease.

Chieko Mineo1, Philip W Shaul

  • 1Division of Pulmonary and Vascular Biology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9063, USA.

The Journal of Clinical Investigation
|June 25, 2011
PubMed
Summary

High-density lipoprotein (HDL) from patients with coronary artery disease (CAD) impairs endothelial function, unlike healthy HDL. This dysfunction may stem from reduced paraoxonase 1 (PON1) activity, impacting nitric oxide production and repair.

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Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles
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Last Updated: May 31, 2026

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
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Published on: October 12, 2017

Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles
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Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles

Published on: November 10, 2017

Area of Science:

  • Cardiovascular Biology
  • Endothelial Function
  • Lipid Metabolism

Background:

  • High-density lipoprotein (HDL) cholesterol typically promotes endothelial health by stimulating nitric oxide (NO) production and repair.
  • The protective role of HDL may be compromised in cardiovascular disease states.

Purpose of the Study:

  • To investigate the effect of HDL from patients with stable coronary artery disease (CAD) or acute coronary syndrome (ACS) on endothelial function.
  • To explore the potential mechanisms underlying HDL dysfunction in CAD and ACS.

Main Methods:

  • Assessing endothelial cell nitric oxide (NO) synthesis.
  • Evaluating endothelial repair capacity.
  • Measuring HDL-associated paraoxonase 1 (PON1) activity in patient samples.

Main Results:

  • HDL from stable CAD or ACS patients inhibited endothelial NO synthesis, contrasting with HDL from healthy individuals.
  • HDL from these patients also impaired endothelial repair.
  • Reduced HDL-associated paraoxonase 1 (PON1) activity was observed in HDL from CAD and ACS patients.

Conclusions:

  • HDL's cardiovascular impact is dependent on its quality and associated enzyme activity, not just quantity.
  • Dysfunctional HDL, potentially due to decreased PON1 activity, may contribute to atherogenesis in CAD and ACS.
  • These findings warrant further investigation in prospective studies and for the development of HDL-targeted therapies.