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Understanding Atherosclerosis & its MI Link--jk

Two Changes in content coming up

  1. The cholesterol myth.  Numerous critics have pointed out that cardiovascular disease is not caused by higher levels of blood cholesterol or fats.  Pharma promotes the cholesterol myth and ignores the major causes.

  2. Major cause of cardiovascular disease is pathogens living within the middle layer of artery walls.  It initiates the immune response which involves LDL, HDL, and white blood cells.  Reactive chemicals such as simple sugars and carbon monoxide can potentiate the process resulting in the formation of plaque within the artery walls.


For confirmation from journal articles on primary role of infective agent enter into terms such as bacteria + atherosclerosis or go to and id9  for collection of articles

For confirmation of cholesterol myth enter into or cholesterol myth, or go to for collection of journal articles. 

The article written by  JK below was before he discovered the cholesterol myth, and the full extent of the corruptions worked by pharma.

Atherosclerosis how it causes over 90% of heart attacks


This article heavily relies upon Wikipedia and 40 years of reading sporadically, medical-science articles on the topics raised--jk.


There are two types of plaque formations stable and unstable. Stenosis (occlusion) over 75% accounts for about 14% of mycondria infractions, while those under 50% occlusions account for  more likely it is to be stable


Arteriosclerosis is a general term describing any hardening and thus loss of elasticity of medium or large arteries.


Arteriolosclerosis of the small arteries


Atherosclerosis is a hardening of an artery due to atheromatous plaque.  (Atherosclerosis is thus a type of arteriosclerosis.)

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  (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. 



[i]  High Prevalence of Coronary Atherosclerosis in Asymptomatic Teenagers and Young Adults, Circulation 2001; 103:2705, also at

[ii] Two clinical trials published in late 1990s, focusing on the relation between plaque structure, lumen stenosis and MI, in which each individuals coronary anatomy was tracked with both angiography and IVUS found that 75% or greater stenotic areas were responsible for only about 14% of heart attacks (at 

[iii]  There is a 1% risk of major complication (heart attack, stroke, etc.) from cardiac catheterization. 

[iv] Other expensive drugs have come out to treat high-blood pressure, however, they have been shown to be no more effective than diuretics.  See

[v]  Lowering TC (total cholesterol) through drug intervention has little effect upon risk because it is the underlying atherosclerosis that causes the cardiac events, and this condition is not reversed by lowering TC.

Development of Atherosclerosis, mechanism:

The main cause of atherosclerosis is not yet unknown,* but is hypothesized to fundamentally be initiated by inflammatory processes in the vessel wall in response to retained low-density lipoprotein (LDL) molecules.[8] Once inside the vessel wall, LDL molecules become susceptible to oxidation by free radicals,[9] and become toxic to the cells. The damage caused by the oxidized LDL molecules triggers a cascade of immune responses which over time can produce an atheroma. The LDL molecule is globular shaped with a hollow core to carry cholesterol throughout the body.

The body's immune system responds to the damage to the artery wall caused by oxidized LDL by sending specialized white blood cells (macrophages and T-lymphocytes) to absorb the oxidized-LDL forming specialized foam cells. These white blood cells are not able to process the oxidized-LDL, and ultimately grow then rupture, depositing a greater amount of oxidized cholesterol into the artery wall. This triggers more white blood cells, continuing the cycle.

Eventually, the artery becomes inflamed. The cholesterol plaque causes the muscle cells to enlarge and form a hard cover over the affected area. This hard cover is what causes a narrowing of the artery, reduces the blood flow and increases blood pressure.

Some researchers believe that atherosclerosis may be caused by an infection of the vascular smooth muscle cells; chickens, for example, develop atherosclerosis when infected with the Marek's disease herpesvirus.[10] Herpesvirus infection of arterial smooth muscle cells has been shown to cause cholesteryl ester (CE) accumulation.[11] Cholesteryl ester accumulation is associated with atherosclerosis.


*   Actually  the cause is known, but not observed.  The main elements of this process were described, for example, in an article in Scientific American in April of 1979.  It is not observed because the condition develops slowly over decades. 


Risks multiply, with two factors increasing the risk of atherosclerosis fourfold.[15] Hyperlipidemia, hypertension and cigarette smoking together increases the risk seven times.[15]


  Diabetes[15] or Impaired glucose tolerance (IGT) +

  Dyslipoproteinemia[15] (unhealthy patterns of serum proteins carrying fats & cholesterol): +

  High serum concentration of low-density lipoprotein (LDL, "bad if elevated concentrations and small"), and / or very low density lipoprotein (VLDL) particles, i.e., "lipoprotein subclass analysis"

  Low serum concentration of functioning high density lipoprotein (HDL "protective if large and high enough" particles), i.e., "lipoprotein subclass analysis"

  An LDL:HDL ratio greater than 3:1

  Tobacco smoking, increases risk by 200% after several pack years[15]

  Having hypertension +, on its own increasing risk by 60%[15]

  Elevated serum C-reactive protein concentrations[15][16]

  Vitamin B6 deficiency[17][18][19]


  Advanced age[15]

  Male sex[15]

  Having close relatives who have had some complication of atherosclerosis (e.g. coronary heart disease or stroke)[15]

  Genetic abnormalities,[15] e.g. familial hypercholesterolemia

Lesser or uncertain

The following factors are of relatively lesser importance, are uncertain or unquantified:

  Obesity[15] (in particular central obesity, also referred to as abdominal or male-type obesity) +

  sedentary lifestyle[15]


  Postmenopausal estrogen deficiency[15]

  High intake of saturated fat (may raise total and LDL cholesterol)[23]

  Intake of trans fat (may raise total and LDL cholesterol while lowering HDL cholesterol)[15][24]

  High carbohydrate intake[15]

  Elevated serum levels of triglycerides +

  Elevated serum levels of homocysteine

  Elevated serum levels of uric acid (also responsible for gout)

  Elevated serum fibrinogen concentrations

  Elevated serum lipoprotein(a) concentrations[15]

  Chronic systemic inflammation as reflected by upper normal WBC concentrations, elevated hs-CRP and many other blood chemistry markers, most only research level at present, not clinically done.[25]

  Stress[15] or symptoms of clinical depression

  Hyperthyroidism (an over-active thyroid)

  Elevated serum insulin levels +[26]

  Short sleep duration[27]

  Chlamydia pneumoniae infection[15] **

**     Other chronic infections have been associated with increased risk such as gingivitis.  This ties in with c-reactive protein, which is elevated during infections.  

Visible features

Sever atherosclerosis of the aorta, autopsy specimen. 

Although arteries are not typically studied microscopically, two plaque types can be distinguished:[38]

1.    The fibro-lipid (fibro-fatty) plaque is characterized by an accumulation of lipid-laden cells underneath the intima of the arteries, typically without narrowing the lumen due to compensatory expansion of the bounding muscular layer of the artery wall. Beneath the endothelium there is a "fibrous cap" covering the atheromatous "core" of the plaque. The core consists of lipid-laden cells (macrophages and smooth muscle cells) with elevated tissue cholesterol and cholesterol ester content, fibrin, proteoglycans, collagen, elastin, and cellular debris. In advanced plaques, the central core of the plaque usually contains extracellular cholesterol deposits (released from dead cells), which form areas of cholesterol crystals with empty, needle-like clefts. At the periphery of the plaque are younger "foamy" cells and capillaries. These plaques usually produce the most damage to the individual when they rupture.

2.    The fibrous plaque is also localized under the intima, within the wall of the artery resulting in thickening and expansion of the wall and, sometimes, spotty localized narrowing of the lumen with some atrophy of the muscular layer. The fibrous plaque contains collagen fibers (eosinophilic), precipitates of calcium (hematoxylinophilic) and, rarely, lipid-laden cells.

In effect, the muscular portion of the artery wall forms small aneurysms just large enough to hold the atheroma that are present. The muscular portion of artery walls usually remain strong, even after they have remodeled to compensate for the atheromatous plaques.

However, atheromas within the vessel wall are soft and fragile with little elasticity. Arteries constantly expand and contract with each heartbeat, i.e., the pulse. In addition, the calcification deposits between the outer portion of the atheroma and the muscular wall, as they progress, lead to a loss of elasticity and stiffening of the artery as a whole.

The calcification deposits, after they have become sufficiently advanced, are partially visible on coronary artery computed tomographyor electron beam tomography (EBT) as rings of increased radiographic density, forming halos around the outer edges of the atheromatous plaques, within the artery wall. On CT, >130 units on the Hounsfield scale (some argue for 90 units) has been the radiographic density usually accepted as clearly representing tissue calcification within arteries. These deposits demonstrate unequivocal evidence of the disease, relatively advanced, even though the lumen of the artery is often still normal by angiographic orintravascular ultrasound.

Rupture and stenosis

Although the disease process tends to be slowly progressive over decades, it usually remains asymptomatic until an atheromaulcerates, which leads to immediate blood clotting at the site of atheroma ulcer. This triggers a cascade of events that leads to clot enlargement, which may quickly obstruct the flow of blood. A complete blockage leads to ischemia of the myocardial (heart) muscle and damage. This process is the myocardial infarction or "heart attack".

If the heart attack is not fatal, fibrous organization of the clot within the lumen ensues, covering the rupture but also producingstenosis or closure of the lumen, or over time and after repeated ruptures, resulting in a persistent, usually localized stenosis or blockage of the artery lumen. Stenoses can be slowly progressive, whereas plaque ulceration is a sudden event that occurs specifically in atheromas with thinner/weaker fibrous caps that have become "unstable".

Repeated plaque ruptures, ones not resulting in total lumen closure, combined with the clot patch over the rupture and healing response to stabilize the clot, is the process that produces most stenoses over time. The stenotic areas tend to become more stable, despite increased flow velocities at these narrowings. Most major blood-flow-stopping events occur at large plaques, which, prior to their rupture, produced very little if any stenosis.

From clinical trials, 20% is the average stenosis at plaques that subsequently rupture with resulting complete artery closure. Most severe clinical events do not occur at plaques that produce high-grade stenosis. From clinical trials, only 14% of heart attacks occur from artery closure at plaques producing a 75% or greater stenosis prior to the vessel closing.[citation needed]

If the fibrous cap separating a soft atheroma from the bloodstream within the artery ruptures, tissue fragments are exposed and released. These tissue fragments are very clot-promoting, containing collagen and tissue factor; they activate platelets and activate the system of coagulation. The result is the formation of a thrombus (blood clot) overlying the atheroma, which obstructs blood flow acutely. With the obstruction of blood flow, downstream tissues are starved of oxygen and nutrients. If this is the myocardium (heart muscle), angina (cardiac chest pain) or myocardial infarction (heart attack) develops.


The failure of numerous studies to show positive endpoint results (notwithstanding the positive bias and lack of peer review) call in to question the use of the improved cholesterol profile as proof of health benefits.  Endpoint results would be a reduction in death and a reduction in stenosis are rarely reported, though undoubtedly desired by the pharmaceutical industry.  Skepticism about these drugs merits given their side effects and cost is the prudent course—JK.


In general, the group of medications referred to as statins has been the most popular and are widely prescribed for treating atherosclerosis. They have relatively few short-term or longer-term undesirable side-effects, and several clinical trials comparing statin treatment with placebo have fairly consistently shown strong effects in reducing atherosclerotic disease 'events' and generally ~25% comparative mortality reduction, although one study design, ALLHAT,[40] was less strongly favorable.

The newest statin, rosuvastatin, has been the first to demonstrate regression of atherosclerotic plaque within the coronary arteries byIVUS (intravascular ultrasound evaluation).[7] * The study was set up to demonstrate effect primarily on atherosclerosis volume within a 2 year time-frame in people with active/symptomatic disease (angina frequency also declined markedly) but not global clinical outcomes, which was expected to require longer trial time periods; these longer trials remain in progress.

However, for most people, changing their physiologic behaviors[clarification needed], from the usual high risk to greatly reduced risk, requires a combination of several compounds, taken on a daily basis and indefinitely. More and more human treatment trials have been done and are ongoing that demonstrate improved outcome for those people using more-complex and effective treatment regimens that change physiologic behaviour patterns to more closely resemble those that humans exhibit in childhood at a time before fatty streaks begin forming.

The statins, and some other medications, have been shown to have antioxidant effects, possibly part of their basis for some of their therapeutic success[citation needed] in reducing cardiac 'events'.

The success of statin drugs in clinical trials is based on some reductions in mortality rates, however by trial design biased toward men and middle-age, the data is as, as yet, less strongly clear for women and people over the age of 70.[41] For example, in theScandinavian Simvastatin Survival Study (4S), the first large placebo-controlled, randomized clinical trial of a statin in people with advanced disease who had already suffered a heart attack, the overall mortality rate reduction for those taking the statin, vs. placebo, was 30%. For the subgroup of people in the trial who had Diabetes Mellitus, the mortality rate reduction between statin and placebo was 54%. 4S was a 5.4-year trial that started in 1989 and was published in 1995 after completion. There were three more dead women at trial's end on statin than in the group on placebo; whether this was due to chance or some relation to the statin remains unclear. The ASTEROID trial has been the first to show actual disease volume regression[7] (see page 8 of the paper, which shows cross-sectional areas of the total heart artery wall at start and 2 years of rosuvastatin 40 mg/day treatment); however, its design was not able to "prove" the mortality reduction issue since it did not include a placebo group: the individuals offered treatment within the trial had advanced disease, and treatment with placebo was judged to be unethical.


*  I can only wonder why given the improvement of cholesterol profile, why this isn’t consistently reported.

Enter supporting content here

Those who have a financial interest in the outcome manipulate the results, Major study finds that all 37 journal articles positive effects over stated; the average was 32%. Statins cause erectile dysfunction, cognitive imparement, and cancer.  

Lipitor (2011) lifetime sales $131 billion, tops all drugs.  Plavix at $60 billion is second.



52% short term


LA Times, Health section, July 21, 2008  --  excerpts

Vytorin, the combination drug (simvastatin (better known by its commercial name Zocor) and ezetimibe--known as Zetia) prescribed to lower cholesterol, sustained another blow today, when the author of a major clinical trial announced that the medication had failed to drive down hospitalization and death due to heart failure in patients with narrowing of the aortic valve. In the process, researchers in Norway detected a significant blip in cancers in the 1,800 subjects they followed

Today's findings suggested something more ominous: the incidence of cancer -- and of dying of cancer -- was significantly higher in the patients taking Vytorin. Altogether, 67 patients on placebo developed cancer during the trial. Among subjects on Vytorin, 102 developed cancers of various kinds.*  This is the second adverse press—the first being in March 08, when the ENHANCE trial found that Vytorin fared no better than a placebo at reducing plaque buildup on the walls of patients' arteries.* *

Comments by jk

Simvastatin (Zocor) is off patent.  Thus in a scramble for profits a combination drug (on patent) was introduced.  Direct to consumer market cost $155 in 07—mainly TV ads. 

*  The pressing issue is that since the development  of Statins, the very first animal studies in the 60s it has been known that Statins increase the incidents of cancer.  However, nearly all studies done thereafter have not included cancer. 

*  Several studies have failed to find a reduction in the build of plaque, even thought the statins including Zocor, reduce LDL and cholesterol.  Few studies include the principle reason for taking a statin, namely a reduction in the death rate.  Claims for such reduction probably entail a failure to control the contravening variable, aspirin usage.  Given a pile of evidence, including the very mechanism of plaque formation, which involves inflammation process, I must conclude that the use of statins is highly suspect.  Given the harm done including cognitive impairment, weakness, and cancer, if my skepticism is born out, the harm done by statins as a course of treatment will far surpass that of VIOXX which killed over 200,000 people world wide by accelerating atherosclerosis.