Cardiac Risk Factor: High Cholesterol

The ravaging effects of hypercholesterolemia starts very early in life. We now know that even children aged 10-14, with multiple cardiac risk factors including hypercholesterolemia, have already developed coronary plaques of 40-50%. The screening for hypercholesterolemia should start at the pediatric age group.

We don’t screen all of our patents for high cholesterol, let alone the young adults. Once high cholesterol is detected, adequate interventions or treatment with statins are not initiated in everyone. Once treatment is started some of the medications are not titrated to optimal levels; no wonder only a very small fraction of our patients are properly managed in this context.

High cholesterol is another major cardiac risk factor in the genesis of atherosclerosis. Low-density cholesterol is often the nidus to develop a cholesterol plaque, and will eventually clog up the coronary arteries leading to angina, myocardial infarction, or death. It is estimated that we have over 90 million adults whose cholesterol level is above 200 - a situation that will warrant reevaluation and dietary modifications. However, we have over 36 million people with a cholesterol level of 240 or above - a situation that needs close attention, dietary restriction, and possibly pharmacological intervention. We clearly have about 20 million Americans who need pharmacological intervention for reducing their chances of coronary death, heart attack, and peripheral vascular disease.

Modest reduction of severe cholesterol can be achieved by strict dietary discipline. Red meat, egg, liver, bacon, cheese, lobster, and other sources of saturated fatty acids are the major offenders that should be curtailed or avoided.

There is a large array of cholesterol-lowering medications on the market. However, a group of drugs commonly called statins, (simvastatin, lovastatin, pravastatin, and atorvastatin), have shown remarkable benefits not only in lowering cholesterol, but also in reducing the process of atherosclerosis, whose effects are later translated into lesser clinical events.

It is also encouraging and exhilarating to see that simvastatin was capable of reducing future coronary events in as much as 38% of the hypercholestrolemic population who never had clinical evidence of CAD to begin with. (Primary prevention)

In a landmark study published in 1994, popularly known as the 4S study (The Scandinavian Simvastatin Survival Study), when people with known CAD (marked by angina or previous MI) were treated with 20-40 mg of simvastatin, a 30-35% reduction was noted in future episodes of MI, death, or coronary bypass graft surgery. In addition, episodes of cerebral stroke were reduced by 28%. Similar results have been reported with pravastatin and atorvastatin too. It is also encouraging and exhilarating to see that simvastatin and pravastatin were capable of reducing future coronary events in as much as 38% of the hypercholestrolemic population who never had clinical evidence of CAD to begin with (primary prevention). It must be clearly understood that the most important effect of a statin-type of cholesterol-lowering agent is to passivate an angry cholesterol plaque, thereby reducing the chance of erosion, rupture, and the subsequent chain of events.

Of the many modalities of treatment for coronary artery disease, optimal reduction of blood cholesterol level with the help of clinically proven medications is the sole intervention that is known to arrest the progression of atherosclerosis, passivate the plaque, and even a chance to reverse this process by resorption of the plaque.

In light of unchallengeable evidence like this, it is a crime if eligible patients are not treated with clinically proven statin agents for primary and secondary prevention of CAD. However, it is a travesty to see that only a meager two million people are now receiving cholesterol-lowering drugs for a disease, which is grossly under-treated.

Make it a point to take your cholesterol-lowering medications with the evening meals, as hepatic cholesterol and triglyceride synthesis occurs mostly during nighttime hours.