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Topic: Atherosclerotic plaque



  
 Coronary Artery Calcification: Pathophysiology, Epidemiology
Atherosclerotic calcification is an organized, regulated process similar to bone formation that occurs only when other aspects of atherosclerosis are also present.
Colocalization of cholesterol and hydroxyapatite in human atherosclerotic lesions.
Distribution of circumferential stress in ruptured and stable atherosclerotic lesions: a structural analysis with histopathological correlation.
http://www.americanheart.org/presenter.jhtml?identifier=1684

  
 Atherosclerotic plaque inflammation: The final frontier?
Recent work has provided evidence that lipid-lowering therapy prevents acute coronary complications in patients by limiting inflammation and, in turn, improving features associated with instability and thrombogenicity in atheromata (ie, ‘stabilization’) rather than merely shrinking the plaque (3,7).
Previous studies have localized MMPs in macrophages of human and experimental atheromata.
These future approaches should help to prevent acute complications of vascular inflammation more effectively and individually.
http://www.pulsus.com/CARDIOL/20_06/aika_ed.htm

  
 [No title]
The analysis in the MI and LOH positive cases was repeated at least twice and the results were highly reproducible." In their discussion, Hatzistamou et al (1996, p.187) comment: "Originally, LOH was reported in the development of human tumours and represents a manifestation of the recessive behavior of the onco-suppressor genes.
Although the incidence of LOH reported in the present investigation is not very high, this is the first report to our knowledge which demonstrates LOH in atherosclerotic lesions.
During a person's lifetime, the arterial SMCs accumulate exposure to mutagens (including ionizing radiation from natural sources and especially from medical XRAYS).
http://www.ratical.org/radiation/CNR/RMP/RAMPadd3.txt

  
 Coronary disease: Atherogenesis: current understanding of the causes of atheroma -- Weissberg 83 (2): 247 -- Heart
of atherosclerotic lesions increases as a consequence of repeated
The only logical conclusion to be drawn from the angiographic and outcome studies of statin treatment is that statin treatment stabilises atherosclerotic lesions
of drugs aimed specifically at stabilising atherosclerotic lesions.
http://heart.bmjjournals.com/cgi/content/full/83/2/247

  
 Today in Cardiology: IVUS visualizes vulnerable atherosclerotic plaque
A conundrum for cardiologists has been why therapies that lower lipids can reduce risk of events by 70% to 90% and result in no change on angiograms.
And that is why we do not see changes in angiograms when we treat with lipid lowering therapy."
Presented at the American Heart Association's 71st Scientific Sessions.
http://www.cardiologytoday.com/199812/ivus.asp?old=never

  
 Presence of Chlamydia pneumoniae in Human Symptomatic and Asymptomatic Carotid Atherosclerotic Plaque -- LaBiche et al. ...
Plaques were obtained at the time of surgery in a sterile fashion,
However, in the present study, no clear preponderance of occurrence
Plaques from 37 symptomatic and 57 asymptomatic patients
http://stroke.ahajournals.org/cgi/content/full/32/4/855

  
 Local Effects of Atherosclerotic Plaque on Arterial Distensibility -- Giannattasio et al. 38 (5): 1177 -- Hypertension
conditions or just the consequence of the atherosclerotic lesions.
and angiography, (3) no atherosclerotic lesions in the ipsilateral
of the atherosclerotic clinical or subclinical lesions is not
http://hyper.ahajournals.org/cgi/content/full/38/5/1177

  
 Expression of Interleukin-18 in Human Atherosclerotic Plaques and Relation to Plaque Instability -- Mallat et al. 104 ...
IL-18 expression was analyzed by SYBR Green real-time PCR.
To determine whether human IL-18 mRNA was expressed in human
Forty human atherosclerotic plaques removed from 35 patients
http://circ.ahajournals.org/cgi/content/full/104/14/1598

  
 Amazon.ca: Books: Assessing and Modifying the Vulnerable Atherosclerotic Plaque
Discusses examples of new methods of imaging that will lead to better modalities of prevention and treatment.
Contains the factors influencing the natural history of plaques, the correlation of vascular lesions and clinical syndromes.
Mount Sinai School of Medicine, New York, NY.
http://www.amazon.ca/exec/obidos/ASIN/0879934859

  
 Welcome to LifeScore.com! - Key Articles About Electron Beam Computed Tomography for Coronary Calcium
The relative risk for a cardiac event in patients with VCS progression was 10 fold greater than that of patients with stabilization of VCS.
The 40 treated patients who had average LDL cholesterol levels of at least 120 had a measurable increase in mean calcium volume score (mean change, +25 +/-22%, p<0.001), although it was smaller than the increase in the untreated patients.
EBCT is the only noninvasive test that can be used to assess response to therapeutic interventions aimed at shrinking coronary plaque.
http://www.lifescore.com/eb-articles.htm

  
 BFML: Research: Atherosclerotic Plaque Rupture
The objective of this project is to integrate the technologies needed to quantitatively determine an individual patient's risk for embolism due to plaque rupture.
The current criterion for predicting a patients risk for stoke is based on the percent stenosis (diameter reduction) of the carotid artery and has no physical or biochemical basis for assessing the risk for an embolic stroke.
Among the several causes are hemorrhage, embolism, thrombosis, and aneurysm rupture.
http://www.umbc.edu/bfml/apr.html

  
 Atherosclerotic Plaque Rupture
Active cathepsins appear to be associated with foam cells at the shoulders of the plaque.
· Dr Ken Rodgers found that levels of cathepsin activity are much higher in atherosclerotic plaques than in normal tissue, and that cathepsin S is of particular interest as it is active at physiological pH.
· Dr Alistair Miller is currently investigating the release of proteases by human monocyte-derived macrophages co-cultured with atherosclerotic plaque fibrous cap.
http://www.bris.ac.uk/Depts/BHI/chris/chrisres.htm

  
 Gangrene Clearing Formula: Remove Atherosclerotic Plaque
The existing research indicates that if enough antioxidant protection is available, it will prevent the oxidation of cholesterol from free radicals.
Only cholesterol in its oxidized form becomes a risk factor for atherosclerosis - taken up into the arteries, it contributes to the atheromatous plaque formation (
http://www.reversegangrene.com/E2.htm

  
 Atherosclerotic Plaque - Artery with
Macrophages (green) infiltrate plaques that eventually rupture, causing ischemia in patients with hypercholesterolemia (see 103-239 for full arterial view).
I work in layers so that any image can be modified to fit your layout or animation.
For a searchable website of all my images, please visit www.peggerrity.com
http://www.indexedvisuals.com/index2/103-208.htm

  
 Amazon.ca: Books: The Vulnerable Atherosclerotic Plaque: Understanding, Identifi- Cation and Modification
Look for books like The Vulnerable Atherosclerotic Plaque: Understanding, Identifi- Cation and Modification by subject:
Amazon.ca: Books: The Vulnerable Atherosclerotic Plaque: Understanding, Identifi- Cation and Modification
The Vulnerable Atherosclerotic Plaque: Understanding, Identifi- Cation and Modification
http://www.amazon.ca/exec/obidos/ASIN/0879934069

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