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PostPosted: 18 Aug 2014 01:46 
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Mohammed,

Thank you for your kind words, which will encourage all of us to share,learn and gain from each other. Do tell us more about the Squirrel please , wont you.

The 3 points you make are key for practical clinical approach to Atherosclerosis .

Allow me to conclude , by replying to Badri's question on Statins and Plaque stabilisation.

LIPIDS AND PLAQUE STABILISATION.


Besides inhibition of HMG-CoA reductase, statins show pleiotropic effects and considerably reduce the plaque burden by:

(1) diminution of the plaque lipid-rich core;

(2) reduction in the inflammation with decreased macrophage and foam cell formation;

(3) promotion of fibrous cap thickening; and

(4) decreasing platelet reactivity, and aggregation.

All these effects translate to an overall improvement in endothelial function, which can play a crucial role in preventing plaque formation altogether.

G Mohan.


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PostPosted: 18 Aug 2014 02:00 
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Hello dear Mohammed,

Thank you for your kind words, which encourages us all to share,learn and gain from each other. By the way , tell us more about the Squirrel , wont you!

The three points you mention are key to the practical ,clinical management of Lipids.

To conclude the chapter, allow me to reply to Badri's question on Lipids and Plaque.

STATINS AND PLAQUE STABILISATION.

Mechanisms of plaque stabilization with statins.

The traditional view of cardiovascular disease held that the degree of stenosis defined high-risk lesions and that removal of cholesterol shrank these lesions and thereby enlarged the lumen.

Advances in understanding of the pathophysiology of the acute coronary syndromes refute this view.

We now appreciate that vascular biology determines plaque stability and that statins stabilize plaque by favorably altering this biology. They do so chiefly (but probably not exclusively) by cholesterol lowering.

In addition to reducing the cholesterol content of plaque, lipid lowering inhibits inflammation, and decreases collagenolytic activity and thrombotic potential.

The role of lipid-independent effects remains unclear because many studies used statin concentrations too high to have any clinical relevance.


However, data suggest that statin-induced alterations in the function of small G proteins may contribute to the anti-inflammatory and antithrombotic actions of statins in clinical practice.



Besides inhibition of HMG-CoA reductase, statins show pleiotropic effects and considerably reduce the plaque burden by:
(1) diminution of the plaque lipid-rich core;

(2) reduction in the inflammation with decreased macrophage and foam cell formation;

(3) promotion of fibrous cap thickening; and

(4) decreasing platelet reactivity, and aggregation.

All these effects translate to an overall improvement in endothelial function, which can play a crucial role in preventing plaque formation altogether.

G Mohan.


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PostPosted: 18 Aug 2014 12:44 
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Hi Mohan
I see your name under the last post column dated 18th August, I don't see your posting. Please check this and repost it.

UA Mohammed


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PostPosted: 18 Aug 2014 17:39 
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sorry Mohan,
I failed to go to the second page; now every thing ok;
about the squirrel, don't kindle me. What do you want, me to teach you about Ramayana? Oh my god!!
Best wishes
UA


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PostPosted: 21 Aug 2014 22:52 
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Mohan and Mohammed,

You have both covered the topic very well. I am not sure if there is anything more to add. However like the squirrel I would like to add this to your discussion. I have had elevated Triglycerides and LDL for very many years and have been on statin for a long time. Although the levels were reasonably well controlled in spite of increasing the dosage of statin, the triglyceride and LDL levels could never be brought to healthy levels and remained at the upper limit of normal or just above normal. One of our class mates last year suggested that I add Fenofibrate to the statin. What a difference that has made. The levels are now well controlled and I have even been able to reduce the dosage of statin by half.


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PostPosted: 24 Aug 2014 10:07 
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Excellent comprehensive review by Mohan
HDL levels are controlled by genetic mechanism. Red wine , grape extract and exercise may play a mild to moderate effect in elevating HDL level. Antioxidants may help in reducing the work of HDL in cleaning the endothelium of deposits caused by LDL. A very low HDL is a predictor of early heart disease. Meticulous cleansing of the oral cavity helps in reducing inflammation which has been incriminated in the production of plaque formation.( Coxackie virus? )

_________________
Raghuthaman


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PostPosted: 24 Aug 2014 13:39 
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Hi friends
There is always another side for every coin.
While we were busy with this topic, I stumbled upon an article in the net under the caption:Growing Doubt on Statin Drugs: The Problem of Drug-Lifestyle Interaction . A few points from it are given below:
* I'm growing increasingly worried about the irrational exuberance over these drugs, especially when used for prevention of heart disease that is yet to happen.
*The problem is that statins have not been well-studied in elderly women. The medical establishment have extrapolated findings of clinical trials on younger, mostly male, patients to all patients with high cholesterol levels. This is a striking jump to make, given that low cholesterol levels in the elderly are associated with higher death rates.
*When statins are used for primary prevention, there is a small lowering of future vascular events (stroke/heart attack) over five to 10 years. The absolute risk reduction is in the range of seven per 1000. That means you have to treat 140 patients with a statin (for five years) to prevent one event. Or this: for 99.3% of statin-treated patients, there is no benefit.
*There is also general agreement that statins increase the risk of developing diabetes, especially in women, and that risk is about the same as preventing a stroke or heart attack, approximately 1%
*Another fact is that patient-level (raw) data from the industry-sponsored cholesterol trials have not been independently analyzed. Systematic reviews from the Cochrane group have analyzed only published data rather than the raw data. There is likely a difference
*There is great debate about the incidence of statin side effects, such as muscle pain, cognitive issues, decreased energy, sexual problems, and kidney and liver injury, among others.
*A study presented in April 2014 at the Society of General Internal Medicine meeting in San Diego showed that individuals prescribed statin therapy for high cholesterol consumed more calories and more fat than non-statin users. And, not surprisingly, this increase in calories paralleled an increase in BMI in statin users.
*An analysis of a prospective cohort study of men (published in JAMA Internal Medicine) revealed that physical-activity levels were "modestly" lower among statin users compared with nonusers independent of other cardiac medications and of medical history.
* If statin users consume more calories, gain weight, and exercise less, it becomes easy to see why cardiovascular benefits are so small.
*It's been really hard to explain why the striking reductions in LDL cholesterol—up to 30% to 50%—from statins haven't translated into significant future benefit.

*One possibility is that cholesterol levels are a lousy surrogate for outcomes. That surely seems true in the elderly, but what about in younger patients and those with familial high cholesterol? These patients are definitely at increased cardiovascular risk. So cholesterol levels are surely not unimportant. There are convincing data, for instance, that higher HDL levels are associated with lower CV risk.
*When you step back and look at medications as chemical modifiers of cellular processes in complex biologic systems like our body, it's easy to understand that health comes not from pills. Not even statins.

The link: http://www.medscape.com/viewarticle/827 ... uac=8586DG

UA Mohammed


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PostPosted: 31 Aug 2014 14:22 
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Hello friends
I think the topic on atherosclerosis cannot be closed without mentioning about the testing of serum lipid levels. Only one point I would like to touch upon is the timing of the testing. I deliberately open this topic to have a discussion on this so that our young friends will also benefit. It is a widely held notion that the lipids should be tested on fasting state only. Is it so?
But as I understand the only component that is affected by food is the triglycerides level. Recently there is an emphasis that postprandial hypertriglyceridemia is a cardiovascular risk factor. If you do it on fasting state you may miss it. I think if we do away with the insistence that this should be done only on a fasting state, we can reduce the inconvenience to the patients and the blood for testing be taken then and there and another visit for the sake of the testing may be dispensed with.
I want your considered opinion on this.

UA Mohammed


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