CHD Risk Factors

  • Age : Males 45 years or more. Females 55 years or more or premature menopause.
  • Family history of premature CHD
  • Smoking
  • Hypertension
  • Diabetes
  • HDL-Cholesterol < 35 mg / dl.

Being overweight is the second leading cause of preventable death in the United States


Dietary Sources of Vitamin E


Lipid Profile  


Hyperlipidaemia has emerged as one of the most important preventable and modifiable risk factors for coronary heart disease (CHD). Clinical signs of this condition are an increase in the fasting serum cholesterol level (hypercholesterolaemia) or the fasting serum triglyceride level (hypertriglyceridaemia) or both. A meta- analysis of 16 randomised trials involving cholesterol-lowering interventions reported a 2.5% reduction in CHD incidence for every 1% cholesterol reduction. Lipid levels may be affected by diet, exercise, smoking, certain medications (e.g : beta blockers, thiazide diuretics, glueocorticoids) and concurrent disease states (e.g . kidney and liver diseases).


The major plasma lipids include cholesterol, triglycerides and phospholipids. Lipoproteins are macromolecular complexes that play an important role in the transport and metabolism of lipids. Lipoproteins have been classified on the basis of their densities into five major classes, chylomicrons, very low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), low-density lipoproteins (LDL) and high-density lipoprotelm (HDLP).


Total cholesterol (TC) is a sum of HDL cholesterol, LDL cholesterol and 20% of the triglyceride value. TC level is an excellent predictor of CHD. Since atheroselerosis begins early in life cholesterol levels in young adults predict CHD risk 30 to 40 years later. Cholesterol measurement will thus reduce the long-term risk for CHD.

•Although the role of high triglycerides as an independent factor in the development of CHD remains controversial, data from several prospective studies suggest that triglycerides are probably an important risk factor. Hypertriglyceridaemia is often associated with increased plasminogen activator inhibitor levels and impaired fibrinolysis. This is especially of importance in the Indian context since triglyceride levels are considered to be significantly elevated in Indians. However, recent data show that cholesterol levels are also significantly elevated in the Indian population.

The relation between VLDL and CHD is unclear at present. However, elevated VLDL levels occur quite commonly in persons afflicted by premature CHD. Moreover, VLDL gives rise to LDL, which has been undoubtedly proven to be atherogenic.

•LDL cholesterol is highly atherogenic, hence high levels of LDL increase the risk of CHD.
LDL = TC - (HDL + triglyceride/5)

•HDL cholesterol has been found to be inversely related to subsequent development of CHD, i.e. as HDL cholesterol increases, CHD risk decreases.

•Cardiac risk ratio i.e. Total cholesterol/ HDL, is an extremely potent predictor of CHD

•Lp (a), an LDL particle to which a large plasminogen-like protein, termed apo(a) has been linked via a disulfide bond is an atherogenic lipoprotein. There has been speculation that apo(a) could competitively inhibit the binding of plasminogen to its reeeptor and thus decrease plasmin formation and thrombolysis.


The NCEP recommends that aduIts above 20 years shouid have total cholesterol and HDL measured at least once every five years.If these levels are abnormal, a lipoproteinanalysis which measures 12 hours fasting total cholesterol, HDL and triglyceride is recommended. TC and LDL levels may be reduced by illness, inflammation, surgery and trauma. Hence, the measurements should be repeated after the illness has subsided. Patients at higher risk should be tested more often.


Effective control of the blood lipid levels reduced cardiovascular morbidity and mortality both in patients with established CHD and in those at risk of developing CHD. Hence knowledge of the various aspects of the lipid profile and the significance of each of the parameters is vital and is essential part of management of CHD and people at risk of CHD.

Drugs that reduce blood cholesterol levels also cut heart patients' long-term risk of dying. Researchers now report that aggressive treatment to reduce blood fats (lipids) in patients with chest pain or those who have just had a heart attack can reduce their risk of dying by as much as 60%.


Most of the dietary fat is absorbed into the blood in chylomicrons. Triglyceride is removed from the chylomicrons by lipoprotein lipase in the blood, fatty acids released are taken up by the adipose tissue (Fat storage tissue) and the chylomicron ramnants are removed by the liver.Triglyceride taken up by the liver is broken down to 2-carbon fragments which are used in many metabolic processes. Free fatty acids liberated by the adipose tissue is also taken up by the liver and used in simillar way.
In these processes lipid aggregates are formed containing triglycerides, phospholipids and cholesterol. These are combined with apoproteins to form Lipoproteins which are released into the blood.
These Lipoproteins are:
1. VLDL - Very Low Density Lipoproteins
2. IDL - Intermediate density Lipoproteins
3. LDL - Low Density Lipoproteins
4. HDL - High Density Lipoproteins
The density of the lipoproteins is determined by the relative protein and lipid content with high density lipoproteins containing high protein and less lipids.
The liver synthesises more cholesterol than any other organ. The cholesterol is incorporated into lipoproteins or converted to bile acids or excreted into bile. In biliary obstruction of any kind serum lipid concentration increases mainly due to formation of abnormal lipoprotein known as Lipoprotein X.

Lipid Profile Values

ADULT VALUE Desirable Borderline High Risk
Cholesterol <200 mg /dl 200-240mg /dl >240 mg /dl
Triglycerides <200 mg /dl 200-400 mg /dl 400-1000 mg /dl
HDL-Cholesterol >60 mg /dl 35-45 mg /dl <35 mg /dl
LDL-Cholesterol <130 mg /dl
( <100 mg /dl if the patient has CHD )
130-160 mg /dl >160 mg /dl
Cholesterol to HDL Ratio < 4.0 5.0 > 6.0