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Related Concept Videos

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

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

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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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...
Coronary Artery Disease IV: Preventive Measures01:26

Coronary Artery Disease IV: Preventive Measures

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The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...

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Related Experiment Video

Updated: Jun 5, 2026

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
09:06

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

Lupus Atherosclerosis Prevention Study (LAPS).

M A Petri1, A N Kiani, W Post

  • 1Professor of Medicine, Johns Hopkins University, 1830 East Monument Street Suite 7500, Baltimore, MD 21205, USA. mpetri@jhmi.edu

Annals of the Rheumatic Diseases
|December 24, 2010
PubMed
Summary
This summary is machine-generated.

Atorvastatin did not reduce subclinical atherosclerosis in patients with systemic lupus erythematosus (SLE). This 2-year study found no significant differences in coronary artery calcium or carotid artery measures between the atorvastatin and placebo groups.

Related Experiment Videos

Last Updated: Jun 5, 2026

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
09:06

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

Area of Science:

  • Rheumatology
  • Cardiology
  • Clinical Pharmacology

Background:

  • Cardiovascular disease (CVD) is a leading cause of mortality in patients with systemic lupus erythematosus (SLE).
  • Subclinical atherosclerosis is a significant concern in SLE patients.
  • Investigating interventions to mitigate CVD risk in SLE is crucial.

Purpose of the Study:

  • To evaluate the efficacy of atorvastatin in reducing subclinical atherosclerosis in SLE patients.
  • To assess the impact of atorvastatin on atherosclerosis progression over a 2-year period.

Main Methods:

  • A randomized, placebo-controlled trial involving 200 SLE patients without clinical CVD.
  • Participants received either atorvastatin 40 mg daily or placebo.
  • Subclinical atherosclerosis was assessed using coronary artery calcium (CAC) and carotid duplex ultrasound (intima-media thickness/plaque) at baseline and 2-year follow-up.

Main Results:

  • No significant difference was observed in the progression of coronary artery calcium between the atorvastatin and placebo groups.
  • Carotid intima-media thickness and plaque progression also showed no significant differences.
  • Disease activity, inflammation markers, and endothelial cell activation remained comparable between groups.

Conclusions:

  • Atorvastatin treatment did not demonstrate a reduction in subclinical atherosclerosis measures over 2 years in SLE patients.
  • The study found no significant impact on disease activity or biochemical markers of inflammation.
  • The anti-inflammatory effects of statins seen in the general population were not replicated in this SLE cohort.