ASIANET: Increasing HDL-C With Fibrate the Real Key to Reducing CHD Risk in Many High Risk Patients

the Real Key to Reducing CHD Risk in Many High Risk Patients

BOSTON, Mass., March 27 /PRNewswire-AsiaNet/ -- The following press release was issued today by the Boston University School of Medicine:

Only increases in high density lipoprotein cholesterol (HDL-C) but not reductions in low density lipoprotein cholesterol (LDL-C) may reduce the risk of heart attacks (myocardial infarctions) and cardiac deaths in many men with established heart disease.

This is the conclusion of a new analysis of the landmark Veterans Affairs High-Density Lipoprotein Intervention Trial (VA-HIT) published in The Journal of the American Medical Association (JAMA 2001; 285: 1585-91).

VA-HIT was undertaken in 2,531 men with known heart disease and low HDL-C as well as low LDL-C. It tested the hypothesis that raising a low HDL-C with a fibrate would significantly reduce coronary heart disease (CHD) events.

Patients were randomised to either a gemfibrozil or placebo group for a five year period. The study showed that fibrate treatment significantly increased HDL-C and reduced major CHD events by 22% compared to placebo.

Now, multivariate analysis of the lipid values in VA-HIT demonstrates that:

-- Only the absolute level of HDL-C achieved with therapy predicted a reduction in non-fatal heart attacks and CHD death.

-- A 5 mg/dl (0.13 mmol/l) increase in HDL-C with fibrate reduced CHD events by 11%.

-- The beneficial effect of increasing HDL-C was independent of other CHD risk factors, including age, hypertension, diabetes, smoking and body mass.

-- Neither baseline nor treatment levels of LDL-C or triglycerides significantly altered the risk of a CHD event.

Commenting on the results, Dr Sander Robins of Boston University School of Medicine, Boston, USA, said: "This analysis has important clinical implications. A low HDL-C is present in about 40% of US men with known heart disease and in about 25% of men a low HDL-C is the most prevalent lipid abnormality. VA-HIT shows us that by raising HDL-C with a fibrate we can significantly reduce non-fatal myocardial infarctions and CHD deaths.

Therefore, the primary goal of treatment for thousands of men must be to increase HDL-C."

The analysis is also important for selecting appropriate drug therapy.

Numerous studies show that statins effectively reduce CHD risk in those patients with elevated LDL-C. However, such benefits have never been demonstrated by statins in a large population with a truly low HDL-C (of less than 35 mg/dl) represented in VA-HIT. Such patients have a significantly greater CHD risk than that seen in any major statin study, except for The Scandinavian Simvastatin Survival Study (4S) where LDL-C levels were in a distinctly high range.

Dr Robins said: "Fibrates produce a great variety of favourable metabolic changes (mediated in large part by peroxisome proliferator-activated alpha receptors [PPAR]). Therefore, it is not possible to assume that the benefits associated with fibrate-induced increases in HDL-C in VA-HIT may necessarily be achieved by other therapeutic interventions which increase HDL-C by other mechanisms."

Many patients recruited for VA-HIT had diabetes. In these patients, gemfibrozil produced a larger absolute reduction in CHD events than the non-diabetic. Among patients with diabetes, where low HDL-C is a common abnormality, the rate of cardiovascular morbidity and mortality is exceptionally high.

Another study undertaken at the request of the World Health Organization, the Diabetes Atherosclerosis Intervention Study (DAIS), was published in The Lancet last week. It shows that another fibrate, fenofibrate, reduced the progression of coronary artery disease by 40%.

Before the end of the year, international experts will publish recommendations based on VA-HIT and DAIS. Their goal will be to reduce heart attacks and CHD in patients with low HDL-C.

SOURCE: Boston University School of Medicine

CONTACT: Dr Sander Robins,

Section of Endocrinology,

Nutrition and Diabetes of Boston University School of Medicine,

617-414-3790, or

fax, 617-414-1339, or

[email protected]

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