The heart's other enemy

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There has been some criticism in certain quarters on cholesterol being the main culprit in the development of coronary artery disease.

Many articles have popped up online, talking about "the cholesterol lie" and how inflammation is, instead, the chief cause of heart disease.

It is getting more common for an inflammation test to be included in general health screening, and patients often ask me how to interpret the results.

Is inflammation the new and only culprit?

My stand is that cholesterol is the traditional culprit and inflammation may play an equally important role.

 

INJURY TO BLOOD VESSELS

Inflammation is traditionally defined as a localised reaction that produces redness, warmth and pain.

It is the result of injury to the wall of the blood vessels from factors such as smoking, cholesterol-containing particles and high blood sugar levels.

This will then attract an invasion of white blood cells into the affected area.

These white blood cells also take in cholesterol and ultimately form the lipid core of the cholesterol plaque.

Inflammation in the cholesterol plaque itself also makes it more prone to rupture, which then leads to a heart attack.

It was observed that patients with inflammatory disorders, such as rheumatoid arthritis, have a higher probability of developing coronary artery disease.

When inflammation occurs, the levels of inflammatory markers in the blood will be elevated.

The most extensively studied marker of inflammation is the C-reactive protein (CRP).

Elevated CRP levels indicate there is inflammation in the body.

But a traditional measurement kit cannot detect inflammation in the blood vessels of the heart.

However, with a more sensitive test called high-sensitivity C-reactive protein (hs-CRP), doctors are now able to measure low levels of inflammation in the walls of heart arteries.

In the late 1990s, a study of 28,000 healthy women showed that the risk of suffering a first heart event was two or three times higher in people with a high level of hs-CRP, compared with those who had low readings.

This was independent of their cholesterol levels.

But that was not all. The study also found that those with high levels of both low-density lipoprotein (LDL), or bad cholesterol, and hs-CRP had the highest number of heart events.

Hence, there is no firm evidence to show that inflammation is an independent cause.

Currently, clinical guidelines advise that the hs-CRP screening test should be carried out only in those who are not at a high risk of developing coronary heart disease.

If a patient is already at high risk, there is no need for any further tests.

This risk is calculated by entering the person's variables into a specially created equation.

If his 10-year coronary heart risk is less than 7.5 per cent, then he is not considered at high risk of developing heart disease.

The American Heart Association has also proposed that three hs-CRP cut-off points be used.

A hs-CRP level that is less than 1mg/dL indicates a low risk of developing a coronary heart event, 1mg/dL to 3mg/dL indicates an average risk, and more than 3mg/dL signifies high risk.

If hs-CRP levels are more than 10mg/dL, then the person may be suffering from some kind of infection and this would make the prediction of risk inaccurate.

It is then advisable for the hs-CRP test be repeated in two weeks to allow any infection to settle down.

If the hs-CRP result is above 3mg/dL, the best way to lower it is through diet, exercise, smoking cessation and good control of one's blood pressure.

REDUCING INFLAMMATION

Studies have shown that obesity, diabetes and smoking contribute to an inflammatory reaction in the body. While lifestyle modifications can help to lower hs-CRP levels, so can drugs.

The most exciting and only study to date on this topic is the Jupiter trial published in 2008.

It studied 18,000 healthy men and women who had normal LDL cholesterol levels and hs-CRP of 2mg/dL or higher. Researchers gave half of them a cholesterol-lowering medication called rosuvastatin.

The drug lowered their hs-CRP levels by 37 per cent and, in an unexpected surprise, significantly reduced their risk of stroke, heart attack, hospitalisation and even death.

This was an amazing result and to this day, many professionals are still debating the validity of the findings.

My opinion is that in a healthy person who has an elevated hs-CRP level, lifestyle modifications would be the preferred mode of reducing his hs-CRP levels. This means losing weight, exercising more and giving up unhealthy habits such as smoking.

If these changes elicit a good response, then maintaining a healthy lifestyle would be the main mode of treatment.

If one's hs-CRP levels fail to improve, I would advise a detailed discussion about the available scientific data and let the person decide if he wants to go on medication.

 
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