Atheromatous plaqye is divided into three compenents:

            1.  The atheroma (from greek athera meaning porridge), which is the nodular accumulation of a soft, flaky, yellowish material at the center of a large plaque.

            2.  Underlying areas ofr cholesterol crystals.

            3.  Calcification at the outer base of older more advanced lesions. 

THE PROCESS:  Atherosclerosis develops from low-density lipoprotein cholesterol (LDL), colloquially called "bad cholesterol". Most researchers believe that, when this lipoprotein gets through the wall of an artery, oxygen free radicals  react with it to form oxidized –LDL.  The body’s immune system responds by sending specialized white blood cells (marcophages and T-lymphocytes) to absorb the oxidized-LDL.  These white blood cells are not able to process the oxidized-LDL, and ultimately grow, then rupture and in so doing deposit the oxidized LDL within the artery wall.  This trigtgers more white blood cells thereby continuing the cycle. 

Eventually the artery become inflamed.  The cholesterol plaque causes the muscle cells in the artery wall to enlarge and from a hard cover over the affected area.  This hard cover is what causes a narrowing of the artery, which results in a reduced blood flow and increased blood pressure. 

Another mechanism (less well understood) results from chronic infection which affect the vascular smooth muscle cells.  Chickens, for example, develop atherosclerosis when infected with Maek’s disease herpesvirus.  Herpesvirus infetion of arterial smooth muscle cells has been shown to casue cholesteryl ester (CE) accumulation. Cholesteryl ester accumulation is associated with atherosclerosis. 

Atherosclerosis is a life long process.  For example, autopsies of soldiers killed in the Korean and Vietnam Wars revealed that they showed evidence of the disease.  Another necropsy study revealed that 1 in 6 teenagers demonstrated coronary atherosclerosis, and 85% of the subjects older than 50.[i]  In the U.S. (data for 2004), about 65% of men and 47% of women, the first symptom of atherosclerotic cardiovascular disease is a heart attack.  Most artery flow disrupting events occur at locations with less than 50% lumen narrowing (~20% stenosis is average).  [Reader should note that most illustrations and photographs are of extreme narrowing and without compensatory external diameter enlargement.]    

There are three problems from plaque formation:  enlargement, restriction of blood flow, and rupture with clogging.  The atheromatous plaques, though long compensated for by artery enlargement, will eventually lead to plaque ruptures and stenosis (narrowing) of the artery, and therefore, an insufficient blood supply to the organ it feeds.  If the compensating artery enlargement process is excessive, then an aneurysm results.  These complications are chronic, slowly progressing and cumulative.  The third problem comes from the sudden ruptures, which cause the formation of thrombus that will rapidly slow or stop blood flow.  This leads to death of the tissues fed by the artery in approximately 5 minutes.  This catastrophic event is called an infraction.   When it occurs in a coronary artery is causes a myocardial infraction (MI, a heart attack).  Since atherosclerosis is a body-wide process, similar events occur also in the arteries of the brain (the second most common type of dementia is vascular dementia) intestines, kidneys, legs, etc.  

DIAGNOSIS:  Diagnosis of asymptomatic atherosclorsis is traditionally done through a stress test which evaluates the arterial blood flow during physical exercise, compared to blood flow while at rest.  The patient walks on a treadmill while his hart functions are check with an electrocardiogram (ECG). Unfortunately the test only reveals occlusions greater than 75% and most MIs result from those less than 50%.  Individuals with 75% or greater stenosis were found to be responsible for only about 14% of heart attacks.[ii]  Severe stenosis (75% or greater) usually are stable and the less severe stenosis are automatically compensated for by vasodilation (widening or relaxing) of the ventricular arterioles during exercise, and do not usually produce enough of an imbalance of relative blood flow to be detectable by a stress test.   

Angiogram or intracoronary ultrasound can provide even greater information, but at the risk of complications associated with cardiac catheterization.  Treadmill tests have a sensitivity of 67%, specificity of 70%.  Nuclear test have a sensitivity of 81%, specificity of 85-95%.  However, for reasons stated above, stenosis is not a good predictor of MI, and thus the correlation of test results to MI is low. 

Over the last couple of decades other methods have  been developed for detecting atherosclerotic disease.  These include coronary calcium scoring by CT; (2) carotid IMT (intimal medial thickness) measure by ultrasound; and IVUS (intravascular ultrasound which uses a specially designed catheter with a miniaturized ultrasound probe attached to the distal end of the catheter.[iii]  This latter test allows for an image from inside the blood vessel out through the surrounding blood column, visualizing the endothelium (inner wall) of the blood vessel. 

ACCELERATING PLAQUE FORMATION:  (1) Exposure to reactive oxygen is the most common way to accelerate atherosclerosis, and the most common source is carbon monoxide a product of tobacco smoke (including second-hand smoke).  (2) Shut down the shut-off mechanism.  The body’s immune system responds by sending specialized white blood cells (marcophages and T-lymphocytes) to absorb the oxidized-LDL. (This is an active area of research, see _____)  There is also a polypetide which stops this process.  Unfortuantely all COX-2 inhibitors but for aspirin shut off this stop signal.  Taking an NSAID--but for aspirin—thus accelates atherioclorsis (see http://healthfully.org/aspirin/id17.html).  (3) Diabetes and obesity (obesityh is found in 55% of those diagnosed with type 2 diabetes)  High level of blood glucose damage small blood vessels and accelerate plaque formation.  In time the MI risk becomes double that of the general population—about the same as one who smokes a pack a day for 20 years.  Because of the present rate of obesity it is estimated that 1 in 3 Americans born after 2000 will develop diabetes in their lifetime.   

TREATMENTS:  The problem with medications insertion of a stent or a bypass operation prior to an MI is that statistically they result in only minor risk reduction.  Because of this imaging and stress testing have little to do with risk reduction.  The best of all interventions are the lifestyle changes of exercise, weight loss, and avoiding tobacco smoke. (Exercise and weight loss reduce blood pressure, a major risk factor.)  Ironically, testing and medical interventions are most efficacious not in themselves but by promoting lifestyle changes.  

Medical interventions do far less than is commonly believed.  The best of medical interventions is aspirin which reduce risk of MI by 23% by its effect upon thrombus.  The second best is the taking of a diuretic[iv] to reduce blood pressure—if such be an issue.  For example the bypass operation statically adds about one year to life, however, it does often ameliorate the pain of angina.  As stated before statins help, but mainly, if not entirely, through an aspirin like mechanism that reduce the risk of thrombus.  These conclusions are confirmed by the Framingham Risk Table.[v] 

CONCLUSION:  Ad post hoc proctor hoc reasoning and financial considerations have made intervention the norm.   Go to a doctor and ask him for treatment, and it is treatment you’ll get, for that is his source of revenue.  Selling drugs is the source of revenue for big PhARMA.  Performance is measured by the productions of profits.  As for your heart, the best thing is free:  a healthy lifestyle.