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Related Concept Videos

Coronary Artery Disease I: Introduction01:30

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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...
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Calcium-Scoring CT ScanA calcium-scoring CT scan, also known as coronary artery calcium (CAC) scan, detects calcium deposits in the coronary arteries. This test assesses the risk of coronary artery disease (CAD), which can lead to cardiovascular events such as angina, heart failure, and sudden cardiac arrest.A calcium-scoring CT scan is generally recommended for individuals at intermediate risk of CAD without symptoms. It includes:Men aged 40-75 and women aged 50-75: Especially those with a...
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Atherosclerosis I: Introduction01:30

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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...
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Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

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Atherosclerosis is a progressive disorder that leads to the thickening and narrowing of arterial walls due to plaque buildup. This condition can cause various symptoms depending on the arteries affected:Coronary Artery Disease (CAD): This condition affects the coronary arteries and may lead to chest pain (angina), shortness of breath (dyspnea), heart attacks, and other heart disease symptoms.Cerebrovascular Disease: This affects blood flow to the brain, causing transient ischemic attacks (TIAs)...
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Coronary Artery Disease II: Pathophysiology01:26

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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...
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Aortic Regurgitation II: Clinical Features and Diagnostic Tests01:22

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Aortic valve regurgitation (AR) occurs when the aortic valve fails to close properly, allowing blood to flow backward from the aorta into the left ventricle. This backflow can result in two distinct clinical presentations: acute and chronic AR, each characterized by its own set of symptoms and physical findings.Acute Aortic RegurgitationAcute AR presents with a sudden onset of severe symptoms. Patients typically experience profound dyspnea (shortness of breath), chest pain, and signs of left...
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Related Experiment Video

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Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
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Increased Aortic Valve Calcification in Familial Hypercholesterolemia: Prevalence, Extent, and Associated Risk

Gert-Jan R Ten Kate1, Sven Bos2, Admir Dedic1

  • 1Department of Radiology, Erasmus Medical Centre, Rotterdam, the Netherlands; Interuniversitair Cardiologisch Instituut Nederland, Utrecht, the Netherlands; Department of Cardiology, Thorax Centre Rotterdam, Rotterdam, the Netherlands.

Journal of the American College of Cardiology
|December 25, 2015
PubMed
Summary

Heterozygous familial hypercholesterolemia (he-FH) is linked to increased aortic valve calcification (AoVC). LDLR-negative mutations are the strongest predictor of AoVC extent, emphasizing LDL-C metabolism

Keywords:
LDLR-negative mutationaortic valve calcificationcalcific aortic stenosiscoronary artery calcificationfamilial hypercholesterolemialow-density lipoprotein receptor

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Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
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Area of Science:

  • Cardiovascular Medicine
  • Genetics
  • Radiology

Background:

  • Familial hypercholesterolemia (FH) is characterized by elevated LDL cholesterol (LDL-C) due to LDL receptor (LDLR) mutations.
  • Homozygous FH exhibits 100% prevalence of symptomatic aortic valve calcification (AoVC).
  • The prevalence and risk factors for AoVC in heterozygous FH (he-FH) are not well understood.

Purpose of the Study:

  • To determine the prevalence and extent of subclinical AoVC in asymptomatic he-FH patients.
  • To identify risk modifiers associated with AoVC in he-FH.
  • To compare AoVC in he-FH patients versus non-FH controls.

Main Methods:

  • 145 asymptomatic he-FH patients and 131 controls underwent CT calcium scoring.
  • AoVC was defined by calcium in aortic valve leaflets; extent was measured by AoVC-score (Agatston units).
  • Risk modifiers investigated included LDLR mutation status (LDLR-negative), maximum untreated LDL-C (maxLDL), LDL-C, blood pressure, and coronary artery calcification (CAC).

Main Results:

  • AoVC prevalence (41% vs 21%) and AoVC-score (51 vs 21) were significantly higher in he-FH patients compared to controls (p < 0.001 and p = 0.007, respectively).
  • Independent predictors of AoVC included age, untreated maxLDL, CAC, and diastolic blood pressure.
  • LDLR-negative mutations were the strongest predictor of AoVC-score (OR: 4.81; p < 0.001).

Conclusions:

  • Asymptomatic he-FH is associated with a high prevalence and significant extent of subclinical AoVC.
  • LDLR-negative mutations represent a critical risk factor for AoVC in he-FH.
  • These findings underscore the crucial role of LDL-C metabolism in the etiology of AoVC.