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Showing posts with label Atherosclerosis. Show all posts
Showing posts with label Atherosclerosis. Show all posts

Monday, August 7, 2017

Cardiac Biomarkers and Clinical Decision Making

New video discusses the importance of cardiac biomarkers



In this video, hear from a former operating engineer at the White House who, despite an active lifestyle and basic good health, experienced sudden heart failure. In the context of his healthcare journey, the video highlights the role of cardiac biomarkers in clinical decision making and the diagnosis of a heart attack.

Diagnosed with advanced coronary artery disease, the patient underwent cardiac bypass surgery and was enrolled in a biomarker study during his postoperative course of treatment. “There’s no doubt that biomarkers have completely transformed how we care for our patients in cardiovascular medicine,” says the patient’s cardiologist.

Saturday, July 2, 2016

MCQ 6. A Male Patients with Proven Coronary Disease


MCQ 6. A very high percentage of male patients with proven coronary disease and/or raised lipid levels had an increased level of "pre-beta" lipoproteins in their blood.

What is also referred to as these lipoproteins?
a. HDL
b. VLDL
c. LDL
d. Lipo B

Wednesday, May 4, 2016

Fasting no longer necessary before cholesterol test

For the first time, a team of international experts recommends that most people do not need to fast before having their cholesterol and triglyceride levels tested.

Fasting is a problem for many patients, they explain, and note the latest research shows that cholesterol and triglyceride levels are similar whether people fast or not.

The experts represent the European Atherosclerosis Society (EAS) and the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) joint consensus initiative.

They refer to new research from Denmark, Canada, and the United States that included over 300,000 people and found it is not necessary to have an empty stomach to check cholesterol levels.

Apart from Denmark, all countries require that patients fast for at least 8 hours before checking their cholesterol and triglyceride levels - referred to as "lipid profile." In Denmark, non-fasting blood sampling has been in use since 2009.


Researchers say fasting before a cholesterol test is unnecessary.

Friday, April 8, 2016

Apolipoproteins - Novel perspectives and other challenges.

Atherosclerotic cardiovascular diseases (CVD) are the leading cause of death in the West, and dyslipidemia is considered to be one of their key risk factors. The majority of CVD cases could be prevented by effective management of dyslipidemia. The use of new biomarkers like apolipoproteins as part of extended lipid profiles may be among the most significant new tools for such a task.

Dyslipidemias
Dyslipidemias cover a broad spectrum of lipid abnormalities. Clinicians have so far paid maximum attention to elevated levels of total cholesterol (TC) and low-density lipoprotein-cholesterol (LDL-C). Many other types of dyslipidemias, however, also appear to enhance the risk of CVD. 

Lipid metabolism can become imbalanced or disturbed in several ways, resulting in changes to plasma lipoprotein function and thereafter to the development of atherosclerosis. Many patients who have high cardiovascular risk still have unfavorable lipid profiles.

Given the fast-growing interest in lipidology, clinicians have sought ways to apply evidence-based medicine daily in dyslipidemia management. There are several lipid guidelines from professional societies in different parts of the world to diagnose and make assessments of dyslipidemia. 

The role of apolipoproteins
In recent years, both Europe and the US have witnessed revisions in CVD guidelines and in the approach to lipid profiling. One major new area of attention is the role of apolipoproteins.

Read more: Apolipoproteins - Novel perspectives and other challenges.

Source: cli-online

Tuesday, April 5, 2016

Atherosclerosis, Rheumatoid Arthritis and Inflammation.

Rheumatoid arthritis (RA) has long been associated with increased cardiovascular risk, but despite substantial improvements in disease management, mortality remains high. Atherosclerosis is more prevalent in RA than in the general population, and atherosclerotic lesions progress at a faster rate and might be more prone to rupture, causing clinical events. Cells and cytokines implicated in RA pathogenesis are also involved in the development and progression of atherosclerosis, which is generally recognized as an inflammatory condition. The two diseases also share genetic and environmental risk factors, which suggests that patients who develop RA might also be predisposed to developing cardiovascular disease. In RA, inflammation and atherosclerosis are closely linked. Inflammation mediates its effects on atherosclerosis both through modulation of traditional risk factors and by directly affecting the vessel wall. Treatments such as TNF inhibitors might have a beneficial effect on cardiovascular risk. However, whether this benefit is attributable to effective control of inflammation or whether targeting specific cytokines, implicated in atherosclerosis, provides additional risk reduction is unclear. Further knowledge of the predictors of cardiovascular risk, the effects of early control of inflammation and of drug-specific effects are likely to improve the recognition and management of cardiovascular risk in patients with RA.

Rheumatoid arthritis (RA) is associated with a significantly increased risk of cardiovascular mortality, accounted for mainly by increased atherosclerotic disease.1, 2 Although the prevalence of some traditional cardiovascular risk factors is increased in RA, adjustment for these factors does not fully account for the heightened risk, suggesting that RA itself is an independent risk factor for cardiovascular disease (CVD).3 The prevalence of atherosclerosis is increased in RA, even in early disease,4 and chronic inflammation is thought to promote atherosclerosis both by modulation of traditional risk factors and also possibly by direct biological effects on the artery. In this article, we discuss the potential mechanisms that might accelerate atherosclerosis in RA, with a particular focus on inflammation.

Read more: Atherosclerosis, Rheumatoid Arthritis and Inflammation.

Figure 2: Development of an atherosclerotic plaque.
Source: NatureReviewsRheumatology
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