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Read carefully the material on corporate medicine, then you will understand what I would do if experiencing an AMI or had CVD.

For background there are a number of articles on related topic such as hypertension, diet, cholesterol, etc. See #4 or use the internal google search engine or each page of the recommended sites, /rg, /rc, /rhi etc.   

1 long-page of illustration and photos is at

6-page, short non-technical version is at  

5 page least technical version at


1 Introduction to CVD

13 Risk factors

24 Spasms causing occlusion, bleeding, perforation with PCI

2 Bashing pharma

14 Key points for MI

25 Atherectomy

3 Causes for MI & CVD

15 The ad post hoc fallacy

26 Bypass surgery

4 JK topic articles    4a Symptoms

Ancillary materials

27 Hopes hypothesis buried

5 Recommended prompt treatment

16  Cardiac arrhythmia   16b procedures

28 Summation

6 Diagnosis of AMI

17 Thrombolysis (t-PA)

29 Non-technical summation

7 Prognosis

18 Angiogram and side effects

30 Why pharma is against aspirin

8 Treatment

19 Renal reaction to Iodine contrast

31) Merits of exercise—journal article

9 Drugs of value

20 Angioplasty procedure (PCI)

32) Restenosis 52%--journal article

10 Avoid list

21  Angioplasty for AMI & CVD

33) Description of angiogram and angioplasty procedures

11 Recovery in hospital and nursing home

22 Cholesterol embolism


12 Do list prior to MI and subsequently

23 Restenosis and increased mortality




AMI     Acute myocardial infarction


MeS    Metabolic syndrome

AS        Atherosclerosis


MI        Myocardial infarction

CABG  Coronary bypass surgery


PCI      Angioplasty

CME     Continuing medical education


PPI      Protein pump inhibitor

CVD     Cardiovascular disease


T2D     Type 2 Diabetes

KOL     Key opinion leader


t-PA    Thrombolysis, fibrolytic therapy  

Link to definition page

Two Notes:  1) following editing convention for quotes, square brackets, [ ], are insertion.  2) Footnotes are liberally used--most are details that would break the flow of discussion.

Introduction:  “Each year [2005] 1.5 million Americans experience a heart attack and 460,000 are fatal, and of those who die, almost half die suddenly, before they can get to a hospital” AHA.  630,000 die of heart disease (1 in 4 deaths) and coronary heart disease kills over 370,000, and 735,000 have a heart attack, Center for Disease Control (gov).  What will likely happen to the over 1 million American hospitalized and during recover phase?  Should they rely upon the treatment guidelines set upon by corporate medicine, which physicians adhere to for a confluence of reasons?  The following of treatment protocol (guidelines) for AMI and CVD, which are written by pharma’s KOLs (key opinion leaders) results in an average of 6 patented drugs prescribed long-term.  They cost over $100,000 per year.  There is a fundamental conflict of interest between the patient and corporate profits. This paper exposes the results of pharma’s influence.  Two themes are developed:  what should and shouldn’t be done for a heart attack (Myocardial Infarction, MI, AMI, Acute), and what should and shouldn’t be done for CVD.  Because of the mountains of tobacco science, special attention is given to expose junk treatments.[1]  The choices I would make are based upon my extensive knowledge of health science, select journal articles, and what the choruses of professors, who are critics, say.   

1)  Bashing Pharma:  To accept the analysis given below it is essential that you rise above pharma’s mantra of safe and effective: corporate medicine is shaped by maximization of profits, what I call tobacco ethics.  Sorting through pharma’s influences requires my carefully research of the journal literature free of marketing science bias[2]--what I call tobacco science.  Bad Pharma (title of a book by Prof. Ben Goldacre) has seamlessly constructed a house on distorted health science that ultimately maximizes their profits.  Through their selection of KOLs, Big bad pharma seamlessly frames the discussion:  through their KOLs they writes medical textbooks, provides the required continuing medical education (CME), and they set up clinical guidelines, all of which is supported by their tobacco science.  Physicians believe in what they have been taught, and even when skeptical about some areas, they will follow the treatment guidelines unless their patient requests otherwise.  The $800 billion gorilla (a phrase used by Prof Marcia Angell) has captured the regulatory system world-wide.  Through corporate tobacco ethics they cause much more harm than tobacco. To limit their harm, you need to understand why ‘bad’ applies to ‘pharma’, to sort out what is good from bad, and to break free of the influence of your doctors and media so that you direct your treatments and live a healthy lifestyle.  

There is a chorus of critics who have broken with pharma to uphold scientific and academic standards; they have published books and given lectures exposing the tobacco science concerning statins, cholesterol, fats, diet, fructose, psychiatric drugs, type-2 diabetes, aspirin, cardiovascular disease (CVD), etc., and bad pharma.  The pattern of pharma funding tobacco science to justify clinical guidelines applies to all major areas of treatment.  Pharma and corporate media have marginalized the critics.  Having reviewed their evidence, I stand upon their shoulders.  On the video pages you will find links to their lectures and documentaries, and a list of their books and websites.  Of the 12 topics on the video page, Section #4 is on CVD, and Section #1 on bad pharma.  Harvard Professor Marcia Angell President’s lecture will convince you of her claim:  We certainly are in a health care crisis, If we had set out to design the worst system that we could imagine, we couldn't have imagined one as bad as we have.   Once you come to recognize the business model used by bad pharma, than you have good reason to believe that tobacco ethics generates distortion based upon tobacco science to achieve marketing ethics.  It is appliesd to all areas of medicine, thus Professor Angell’s words are horrifically accurate.  As prof. Prof. Ben Goldacre states, “A perverse system produces perverse results.”  What pharma seamlessly teaches doctors as being in the best interest of their patients, very often isn’t.  Successful treatment isn’t measured by how many have survived, but rather it should be on how many would have survived if the physicians knew what the best treatment is!  Marketing is about putting lipstick on a pig, and   Pharma spends over $100 billion yearly, most of which goes to “educating” doctors—over twice what is spent on television commercials.  This message pharma’s KOLs produce is supported by clinical guidelines that are spoon-fed to the public and our doctors to create block buster drugs.  All this occurs with the support of the pharma-friendly FDA.   Safe and effective is the mantra of pharma and the FDA—not mine.    

Chorus of critics:  There is a revolt among doctors over the corruption of a once noble profession.  The AllTrials, Centre for Evidence-Based Medicine (Oxford University), and the Cochrane Collaboration which has over 37,000 volunteers, are examples of the growing opposition to corruption worked by pharma.  There is a chorus of critics who meet the highest academic standards and publish articles in the leading journals (including the JAMA, NEJM, BMJ, and Lancet (American Medical Journal, New England Journal of Medicine, and British medical Journal) and they publish nearly with every issue an article critical of pharma’s tobacco science.  My very strong academic background in science and philosophy, 40 years of studies in medicine, and 12 years of building this website has driven me to investigate the junk science and make this, as of 2009, the theme of  My investigation of the leading cause of death has led to agree with critics that pharma’s version is totally wrong and to set down what I would do if I had CVD, and/or an AMI.  The evidence I uncovered since 2004, when was found, shows that what is said about conditions, causes, and treatments for CVD is an example of pharma’s business model.  And given the frequency of their divergence from science, I must be skeptical of all claims that serve business ends.  It is as Harvard Professor Marcia Angell states:  We certainly are in a health care crisis … If we had set out to design the worst system that we could imagine, we couldn’t have imagined one as bad as we have.  If in doubt, watch her President’s Lecture, University of Montana, which proves those words, and/or click on the links above.


3)  Causes of MI and CVD:  Since I am writing on CVD and MI, it is essential to correct the misconceptions about heart attacks and atherosclerosis (AS) fed us by bad pharma about cholesterol and saturated fats being the fundamental cause of CVD.  Myocardial infarction (MI) occurs when blood flow stops to part of the heart muscle causing damage thereto which may cause heart failure, angina pain, irregular heartbeat, or cardiac arrest.  The AMI starts with young vulnerable atherosclerotic plaque leaking which when a blood clot (thrombosis) forms that blocks the flow of blood to a large portion of the heart muscles.  Atherosclerosis is therefore a syndrome affecting arterial blood vessels due to a chronic inflammatory response of WBCs in the walls of arteries” Wiki.  This inflammation (like most inflammation) is caused by pathogens, a fact known by autopsy evidences for over a hundred years.[3]  Briefly put, risk of AS very significantly increases with endothelial dysfunction[4] which permits pathogens to pass through the endothelial cells that line the artery walls and enter artery tissue below settling in the tunica intima layer.  These pathogens depending on type and numbers can cause an immune response, which will cause the white blood cells and LDL[5] to be actively transported through the endothelial cells into the tunica intima layer where the pathogens are.  This immune response creates debris which can overwhelm the debris-removal system of the macrophages (type of immune cell).  This drives the formation of young-soft plaque—think of a newly formed boil (also called a furuncle).  If not removed, this plaque will gradually harden with the growth of fibrous tissues and develop a hard cap.   Over time this process if widespread will result in condition called atherosclerosis (AS).  The harden plaque will cause the arteries to loose elasticity and thus hypertension develops.  However, it is not the hardened mature plaque that leaks, but rather the young-fresh plaque also called “vulnerable plaque (non-occlusive or soft plaque)” Wiki.  This type of plaque causes MI and ischemic strokes[6]remember this for later discussion.  This young plaque only causes under 50% occlusion which is insufficient to show up through the widely used imaging techniques of angiogram.[7]  The leaking of young plaque explains why about half of all heart attacks occur in those without the symptoms of atherosclerosis.  Those with symptomatic atherosclerosis are often (but not always) producing young, soft plaque at an accelerated rate compared to the general populace without CVD, thus their higher risk for MI.  Pharma profits greatly from treating signs such as hypertension rather than developing treatments to prevent atherogenesis.  It is like treating the fever accompanying bronchitis rather than treating the underlying bacterial lung infection.  And pharma does even better through treating LDL and its cholesterol content with a family of drugs called statins (more on that later).  Pharma’s business model doesn’t include prevention, thus the compelling evidence such as autopsy studies that prove that atherosclerosis is caused by pathogens is ignored:  not one cardiology textbook acknowledges this cause.  There are hundreds of articles on pathogens in the artery walls, yet the science is excluded by pharma’s KOL-generated account of atherogenesis and CVD.  For conformation use and enter pathogens + atherosclerosis.  There is also numerous journal articles on the immune function of LDL (enter LDL + immune).  LDL at the site of infection absorbs and neutralizes reactive chemicals and toxins, yet this too is missed by cardiology textbooks.  LDL serves two purposes one to transport for cell repair and reproduction the essential fatty acids and cholesterol and that of fighting infection.  The taught version, called lipid-cholesterol hypothesis for the development of CVD is based on metabolic syndrome (MES) and artery-clogging cholesterol and fats and it fails to mention pathogens; or that cholesterol and fatty acids constitute less than 50% of plaque.  Their flawed theory of CVD demonstrates pharma’s power to frame the discussion of medical science.[8]  Their power to generate tobacco science and to “educate” has been used to frame not just CVD, but also all areas of medicine.  Sadly research dollars and medical advice does is not significantly directed to the pathogens and endothelial dysfunction.        

The process just described with pathogens, leukocytes, and LDLs role as absorbing toxins resolves issues that the standard, pharma-generated description of the accumulation of cholesterol and fat fails.  The issues:

Why do over half of all people who have an MI, have cholesterol level below 240? 

Why do people with high cholesterol live longer (the Framingham Study)?

Why are there macrophages and other white blood cells in the atheroma?

Why is LDL actively transported to the atheroma? 

Why would humans evolve a system of vulnerable LDL that causes, rather than prevents, AMIs?

Why do autopsy studies find pathogens in the ruptured atheroma and plaque?

Is LDL a marker for atherogenesis?  One would expect that during the plaque forming stage of an atheroma the level of cholesterol and LDL would rise given their role in cell reproduction, growth, and repair; however, the overall demand of the infected regions of the arteries is only a very small fraction of the total body’s need based upon its constant turnover of cells.  (Remember, as stated above, both cholesterol and fats are the building blocks of cell walls and membranes, and thus the need for LDL).  Moreover the atherogenesis process is constant over long periods of time, thus there won’t be a diagnostic rise in LDL, cholesterol, C-reactive protein or other marker for inflammation.  This lack of relationship between markers for inflammation and atherogenesis entails the only an indirect association to atherogenesis.  Thus people with certain chronic infections, such as form H. pylori in the stomach and atherosclerosis, is rather an association of that bacteria and their possible migration to the artery walls where they would play a role in the development of atherosclerosis (possible a minor one), and as a consequence the association with those bacteria is both indirect and weak.  This helps to explain why though LDL and cholesterol are found in plaque they are not a significant marker for CVD.  Moreover, given the vital roles the contents of LDL plays in cell health, to lower LDL is a bad idea.  Though pharma does all it can to hide the side effects of their statins , these side effects are life-threatening, especially among for the elderly.  For more on this go to and enter in the internal Google search engine cholesterol + side effects.  The chorus of scientists and doctors who have gone public over the cholesterol myth are standing on solid grounds.  Enter Cholesterol myth in a search of books at for pages of books on this issue.  

4)  Extensive reviews of the evidence for the conditions associated with CVD  and drugs used relevant to the topic raised here are found in a number of papers:  click on links  Arrhythmia, Anticoagulants,  Atherogenesis & MI, Aspirin, aspirin inhibits atherosclerosis, Hypertension, Statins, Cholesterol Myth, Cholesterol Myth, Source History, infection in artery wall causes Cardiovascular disease, Endothelial dysfunction  and the over one dozen articles on diet related topics.  What follows builds upon those works just listed.  I will describe what I would do if I developed CVD and if I had an AMI; it is not based on pharma’s tobacco science. 

4a) Symptoms:  An MI occurs when unstable plaque leaks from a coronary artery and forms a clot downstream which often becomes larger through the formation of a blood-clot.  “In greater than 80% of MI the leaked plaque constitutes less than 40% of the obstruction.  Spontaneous thrombolysis [natural dissolving of the clot that caused the MI] occurs in about 2/3 patients within 24 hours” (Merck Manual 2006, p. 636).[9]  “The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous.  Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing.  Chest pain due to ischemia [a lack of blood and hence oxygen supply] to the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium [upper-middle abdomen], shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating), weakness, light-headedness,  nausea,  vomiting, and palpitations and sudden death (frequently due to ventricular fibrillation) can occur in myocardial infarctions.  Women also report more numerous symptoms compared with men (2.6 on average vs. 1.8 symptoms in men).[10]  The most common symptoms of MI in women include dyspnea (shortness of breath), weakness, and fatigue.  The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary embolism,  aortic dissection, pericardial effusion causing cardiac tamponade, tension pneumothorax, and esophageal rupture," Wiki.   Because of the difficulty of identifying with confidence an MI and the importance of prompt treatment, when suspecting an MI seek prompt help.  The extent of damage to the heart is can in most cases be greatly reduced if at first sign I taking sublingually several 325 mg aspirin (uncoated).  Aspirin irreversible blocks the formation of thromboxane A2 to produce an inhibitory effect on platelet aggregation (clot formation).  Since MI consists of the leaked plaque partially clogging a coronary artery and the subsequent complete or near complete blockage by the platelets that form a clot, thus aspirin is the best prompt intervention.[11]  Nitroglycerine causes dilation of the artery walls there by improving the flow of blood past the partial clot.  However, since it lowers the blood pressure, it is contraindicated for those whose systolic blood pressure is below 90.  The subsequent hospital diagnosis and clinical guideline treatment has minimal endpoint benefits—with the exception is for the few who have been resuscitated or who have required mechanical assistance to stay alive, and then survive. 

[1] To start with there hasn’t been a major breakthrough which has saved millions of lives.  Each claim is misplaced.  For example the reduction in MI and death between 1970 and 2000 is nearly entirely from the reduction in smoking, from 46% in 1976 to 16% in 201; this reduction lowers events by over 20%. Not only are their fewer smokers, but those who smoke, smokes less. At a pack a day the risk of MI doubles that of a non-smoker.  Pharma claims the reduction resulted from the use of statins and antihypertensive drugs. 

[2]  Positive bias averaged 32% (range 11 to 69%) in journal articles when compared to the raw data submitted to the FDA in drug submissions for approval, a 2008 NEJM article revealed.   The raw obtained from the FDA through the Freedom of Information Act.

[3] For a concise, convincing review of the evidence for the role of pathogens go to Ignore the Awkward! by Prof. Uffe Ravnskov chapter 15,  and these two links. 

[4] Major causal factors are carbon monoxide and other products of tobacco smoke, chronic infections such as gingivitis, and the Western high sugar and carb diet which causes fat accumulation in the liver which causes insulin resistance.  That primitive peoples have eating a traditional diet have a very low rate of MI among their elderly is strong proof.  Also those peoples who traditionally eat a healthful diet and do not smoke also have a very low rate of MI.  What is the dietary factor for endothelial dysfunction is hotly debated.  I favor as cause the transient elevated levels of fructose and glucose following a Western diet meal. 

[5] LDL has a second function that of attaching to and neutralizing toxins produced by pathogens.  LDL is a blood transport system for cholesterol and triglycerides (fat) to areas of cell growth—a healing and immune cell growth occurs during an infection. Thus there are 2 reasons for LDL to be present in the tunica intima of artery walls—where plaque accumulates.   

[6] About 85% of all strokes involve the leaking of plaque; the remaining 15% is due to a hemorrhage.  

[7] This raises the question,: Why the hell are they using imaging to find plaque which doesn’t leak and cause AMI, and the treating it with physical interventions of CABG bypass surgery and angioplasty?  These junk treatments are exposed in paragraph 20-27. 

[8] Having extensive background in health science, as I examined the contents of medical textbooks flawed.  A tragic example:  One hundred years ago many researchers considered atherosclerosis an infectious disease….  The following statement by two American pathologists, Oskar Klotz and M. F. Manning is typical for the general view at that time [1911]:  “There is every indication that the production of tissue in the intima [innermost layer of the arterial wall] is the result of a direct irritation of that tissue by the presence of infections or toxins” In Prof Uffe Ravnskov Ignore the Awkward!  How the Cholesterol Myths are Kept Alive 2010, p 134.    

[9] This is why the thrombolysis, injection of a drug that breaks up the platelet portion of the clot, proves in real-world hospital settings to be of minimal value—contrary to pharma funded studies and what their opinion leaders teach.  Moreover, because of this spontaneous resolution, must MIs go unnoticed:  “estimates of the prevalence of silent MIs vary between 22 and 64%” Wiki.  

[10] This is mainly due to size:  tall people have a bigger heart and bigger coronary blood vessels; thus complete blockage by a thrombosis is less likely.  This results in less symptoms and greater survival rate.  

[11] I have been taking an average of two 325 mg of aspirin since1992.  Aspirin (and when needed estradiol or testosterone) are the most healthful chemicals we can take.  Aspirin reduces the risk of cancer and metastatic cancer dramatically, reduces the risk of atherosclerosis, and has other health benefits.  Aspirin is a less caustic form of salicylic acid (a plant hormone) found widely in plants and made in small amounts in our body.  Mammals have evolved methods for utilizing the salicylic acid form of aspirin. 

5)  Recommended Prompt Treatment:  I would take sublingually UNCOATED 325 mg aspirin and continue with the aspirin both orally and sublingually for a total of 6 in the first hour.  I keep a small pill box in the car.  “Since 50% of all deaths from AMI occur within 2 hours of onset of the clinical syndrome, the first two hours of management are critical” Merck 1982.   Deaths in this period result primarily from ventricular fibrillation without underlying AMI or fibrillation associated with an ischemic event (AMI).  Promptly taking aspirin and getting to the hospital significantly improve my chance for survival and satisfactory recovery.   They could save my life by injecting adrenalin (epinephrine), use of CPR (cardio-pulmonary resuscitation), cardioversion (electric shock to the heart at a specific moment in the cardiac cycle of pumping) to treat abnormally fast heart beat—tachycardia--or cardiac arrhythmia, a defibrillator (random electric shock to chest), or a pacemaker to prevent arrhythmia.  Mild arrhythmia is a common effect of an AMI, and time heals, and is often without symptoms, but can be observed on an electrocardiogram.  I would absolute refuse drugs for arrhythmia; they don’t save lives and likely increase the risk of dying, but for an exception, medications for pain.  Morphine --or like opiate--and lidocaine administered through an IV to manage pain.  They can be of modest value; their usage goes back over 50 years.  The use of diagnostic equipment,  complex diagnosis with its obscure terminology, along with a concerned cardiologist and nurses is all part of the pitch to do what they think is best and what clinical guidelines and hospital administers require.  This efforts has been seamlessly orchestrated by bad pharma to gain my confidence in the cardiologist’s expertise so that I who would take an assortment of drugs approved by the FDA on the basis of surrogate  endpoints of lower blood pressure, improved heart rhythm, lower cholesterol, and improved pattern of heart beat on an electrography (ECG).   They are taken on the belief that these surrogate endpoints prove longer life; they don’t for the real-world population.  That is why surrogate endpoints and tobacco science trials are used to sully the medical literature and convince the cardiologist, nurses, and public of longer disease-free life.       

6)  Diagnosis of AMI:  Diagnosis begins with assessment of the patient’s complaints and physical status and would include an ECG (an EKG) echocardiography, a sonogram of the heart (also known as an ultrasound and echocardiography), and cardiac markers (blood work) to confirm the diagnosis.  The procedure involves reading the pattern on a sheet of graph paper or monitor.  ST elevation and depression have false positive rate of 15-20% (which is slightly higher in women than men) and a false negative rate of 20-30%,[1] Wiki.  I would refuse the angiogram and angioplasty—for reasons see Ancillary Materials #s 18-24below.  The angiogram (angiography) have risks that are grossly under rated.[2]  The ends do not justify angiogram:  I would not submit to an invasive, risky diagnosis that too often results in a treatment that is contrary (yes contrary) to my best interest, and there are other useful safe diagnostic tools.  Echocardiogram  provides helpful information including the size and shape of the heart, chamber size, pumping capacity, and the location and extent of tissue damage.  The diagnostic equipment and obscure medical jargon functions to establish the cardiologist as expert whom is committed to guiding me through my medical emergency.  Good intensions, expensive diagnostic equipment, and my medical emergency won’t frighten me into following pharma’s-KOL generated guidelines, or to convince me based on doggy- clinical trials[3] that the PCI is my best interest.  There is a longlist of abandoned procedures and drugs because they do more harm than good.  The more I submit, the more likely I will continue to submit and my prognosis will get worse.  I have seen too many people who have had the quality of their lives radically lowered and their death hastened by treatments that were to prevent an MI.     

7)  Prognosis:  “Each year [2005] 1.5 million Americans experience a heart attack and 460,000 are fatal.  Of those who die, almost half die suddenly, before they can get to a hospital” AHA.  Crunching the numbers entails that of the 230,000 will die subsequent to arriving at the hospital: and another 230.00 0 will die because of the AMI within the couple of days-- about 1 in 6 or 16%.  This calculation is consistent with various sources of data.[4]  Mortality rate for those admitted to the hospital that is not near death, is under 5%.  Thus I presume the remaining 95% will live to go home[5].  A much different picture is given for the real-world patients.  The AHA’s Handbook of Emergency Cardiovascular Care for Healthcare Providers, 2004, p 31:  prehospital deaths 52%, 24 hours in hospital 19%, 24-48 hours in hospital 8%, and next 30 days 21%.  However, this is for all patients including the elderly and those with significant comorbidities.  What I haven’t found is numbers for those under the age of 75 and without significant comorbidities (the feeble).   Thus if I made it to the hospital with an AMI, I would probably survive the tobacco science taught by KOLs and applied by dutifully by cardiologists, it certainly isn’t in my best interest to give frick-and-frack my okay.   My father survived 4 heart attacks including two major ones.  I recall when he came home after the first one that it would take at least 10 minutes to walk one block--I was 10 years old.  He lived 23 years from the first; died from a stroke in 1976 at the age of 76.  President Dwight D. Eisenhower at the age of 65 had a major heart attack requiring 6 weeks of hospitalization.  He suffered 6 more heart attacks and died 14 years after his first one in 1969 at the age of 79.  Both men smoke over 2 packs of cigarettes a day until their first heart attack.  Their heart attacks occurred before the day of statins, hypertension drugs, thrombolysis, and bypass surgery (CABG), angioplasty, ablation, and drugs for arrhythmia.  What’s new is good for pharma.   There are much better choices, see #12 for what I would do.      

8)  Treatment:  If severe pain isn’t relieved by nitroglycerine and aspirin, then I would request lidocaine and morphine[6].  I would not take oxygen, it has been definitively shown to be of no value, and increases modestly mortality, yet is still part of the treatment protocol.[7]  I would tell my care givers that I have within the last hour taken over 1 gram of aspirin.[8]  The use of anticoagulants is “relative contraindicated(see guidelines)[9] and thus angiogram (see #s 18-24) which leads to angioplasty because of the risk of major damage to the artery.  Even If I hadn’t taken aspirin I would still refuse the angiogram and its alternative thrombolysis (see # 16-24).  I would request uncoated aspirin 325 mg aspirin, and take a total of 3.25 grams/day.  Even if I met the 90 minute window from first symptoms when modest increased survival is demonstrated in industry funded trials, I would still refuse those treatments.  Meeting that time limit is unlikely:  one study placed it at 1 per 125 patients were treated within the 90 minute window from first symptoms.[10]  Note, The industry-funded studies show that PCI for those with stable ischemia there is no benefit, and significant risk of harm (see #18-24) .  Thrombolysis,t-PA (tissue plasminogen activator) is a drug which breaks down a protein involved in the blood clot. [11] It use for reperfusion is strongly associated with strokes and major bleeding elsewhere.  Reperfusion occurs spontaneously (natural return of blood flow) in 65% of patients without interventionMerck Manual, 2006, P 636.  This is another reason while I will rely upon mother-nature.  The endothelia cells can release a protein that act like t-PA.  Moreover, reperfusion has been made much more likely by my promptly taking a large dose of aspirin.  Meta-analysis of randomized trials comparing thrombolysis to angioplasty found the later had a 2% greater comparative reduction in overall mortality-- published in the Lancet & Oxford Journal;[12] however, quality trials in real-world patients find no gain over standard medical treatment.  Synchronized electrical cardioversion can be used to manage major arrhythmia and major tachycardia (fast heart) if lidocaine and morphine are inadequate.  This is another procedure I would refuse unless there is prolonged, serious ventricular fibrillation.  Implantable Cardiovascular Defibrillator (ICD) reduces risk of sudden death which could be prudent depending on severity of AMI.   Nitric Oxide (NO) is of value short term, and thus also nitroglycerin (GNT).[13]   Glucocorticoids (GC) are a class of steroid hormones that bind to the glucocorticoid receptor (GR), and have been shown too possible reduce infarction (damage).  Given the weak evidence I would avoid them.  Other drugs such as beta blockers and ACE inhibitors for hypertension are often added.  I definitely avoid them they will impair cognitive functions, and make the heart pump slower, thus weaker a bad thing.  Their benefits have been shown only through tobacco science.  I would refuse the other drugs and treatments on the long list in the Handbook of Emergency Cardiovascular Care by the American Heart Association.  Polypharmacy entails a much higher risk that the combination of drugs will produce serious side effects, side effect that while compromised by the heart attack is much more likely to be fatal.  The body has evolved mechanism for healing, which too often pharma’s drugs interfere with. Average life span after the first AMI is 10 years; about the same as in the mid-1990s once anticoagulants became widely used as standard emergency room and recovery phase treatments.  These drugs (heparin, warfarin and dicumarol) came on the market in the late 1940s but were administered in the recovery phase to prevent “thromboembolic complications...with a major decrease in immediate morality rate following the use of dicumarol [similar to warfarin] in the first few weeks of illness,” Merck Manual, 1950, p. 1110.  Its major benefit comes from the reduced risk of a second AMI while in the hospital. Unfortunately it took 40 years before they or like drugs were used long-term prophylactically in high risk patients.  The 1961 Merck Manual 10th Ed., does not recommend the use of clot busting  inhibiting drugs as part of the emergency room treatment, but rather the subsequent use of heparin or warfarin “for the first 3 or 4 weeks (p 131).  I mention this historical bit so that you will know that the miracle claimed by pharma is more marketing.[14]  The rate of the subsequent MI was greatly reduced by the addition of an anticoagulant.  That was the last major improvement.  The advantages of aspirin over the other anticoagulants is well documented is not taught in CME classes.  Instead they hear over and over again the risk of stomach bleeds caused by aspirin, which is in fact no greater than those other anticoagulants, and only aspirin lower significantly the  risk for Alzheimer’s disease,  cancer,  MI and atherogenesis. 

9)   Drugs of value:  Morphine and lidocaine for pain; they reduce/prevent arrhythmia.  Epinephrine (adrenalin), and norepinephrine are is a strong cardiac stimulant and areis used for cardiac arrest.  The anticoagulant aspirin in high does (3.5 grams, 11 of 325 mg) is safe (once the standard dose for arthritis) and it makes unnecessary the dangerous family of anticoagulants given as standard treatment.   If subject to heartburn take an antacid also, not a PPI.

10)  Avoid list:  (in order of importance):  downers (psychotropic drug), antiarrhythmics,[15] electrical cautery for arrhythmia and like procedures, beta blockers, ACE inhibitors, and other treatments for hypertension, angiogram and angioplasty, thrombolysis (see #s 16 – 28) , all blood thinners such as heparin since high dose of aspirin prevent future blood clotshas dissolved the clot, and oxygen[16].    

11)  RECOVERY in hospital or nursing home:     I would avoid the aforementioned,  statins and other cholesterol lowering drugs.

AT HOME:  Besides the aforementioned add avoid bypass operation (CABG).  They only reduce angina pain, and there side effects are grossly under reported.  Angina with improved lifestyle will gradually diminish as the body undergoes the process of revascularization.  

12)  Do List PRIOR MI and while RECOVERING:  Limit risk factors (list below).  Low carbohydrate diet reduces reactive chemical damage by glycation[17] to the endothelia cells which starts the process of atherogenesis.  Especially limit sugar, which is 50% fructose[18] the most reactive of the monosaccharides.  I increased saturated fats and mono-unsaturated fats as replacement for carbs.  Polyunsaturated fats are subjected to rancidification in the body, a bad thing—see fats.   We have 2 major metabolic systems for the production of ATP, the energy molecule, one burns fats the other glucose from carbs.  The obesity epidemic is caused by our high carb-sugar Western diet.   Fructose is in part metabolized to fat in the liver.  High carb diet drives the storage of this fat in the liver, and as a consequence insulin resistance gradually develops.  Insulin resistance promotes fat storage principle in fat and muscle tissues.  What we are told about fats is wrong.[19]  With the low fat diet, carb are increased. The fix is to replace carbs with saturated fats and go on a cleansing diet., which takes only 2 weeks.  Regular strenuous exercise helps regulate blood glucose levels and thus lowers insulin level.  I have been on a low sugar and moderate carb diet the last 2 years. I take daily 325 mg of aspirin daily (it has many health benefits including reducing MI risk by 51%)[20] and reducinges AS risk based on its anti-inflammatory effect.  I keep in my car a small pill container with 20-325 mg aspirin uncoated.  I started taking testosterone when my level went below 350.  I got a prescription for a high dose (10% 2 gram lotion) filled at a compounding pharmacy, rather than the much lower dose branded products.[21]  It increases muscle mass and strength  (my heart is a muscle), lowers MI risk; low testosterone is associated with metabolic syndrome, MI, and aggressive prostate cancer.  My wife takes estradiol with progesterone (natural HRT)[22] from a compounding pharmacy.   It is very significantly cardiovascular protective and much more.  I take CoQ10  and vitamin C because they prevent oxidative damage to endothelial cells and long-term these antioxidants reduces angina pain, high blood pressure and risk for heart failure.   Healthful lifestyle and diet is the best way to promote revascularization.  Our body is a demand system, thus exercise is very important. 


  • Atherogenesis: forming plaque is the underlying cause of MIs.  Early stages of plaque formation cause over 80% of MIs, and half of MIs occur without diagnosed CVD.  Atherosclerosis is a marker for this process.  Plaque formation is an inflammatory response in the walls of the arteries initiated by pathogens and the subsequent immune response involving T-cells, macrophages and LDL—see MI CVD section above. 

  • High sugar high carb diet Western diet causes chemical damage to endothelia cells which line the arteries.   This damage increasing the risk of pathogen passing into the walls of the arteries.  Change to a low refined carb, low fructose diet by increasing as a source for energy fats, especially saturated & monounsaturated fats.  The unnatural rancid fats and transfats contribute to endothelial cell dysfunction.     

  • Tobacco through carbon monoxide is itsthe second  most important causal factor after which come glucose and fructose.  A pack a day long-term doubles the death rate from MI & shortens life an average of 7-12 years.  Also the reactive gasses mainly SO2 and NO2 promote atherogenesis.  

  • Diabetes mellitus type 2 doubles (T2D) risk of MI because it increases the blood sugars level, thus damaging endothelial cells that line the artery walls and are the gate keepers to the artery walls.  It also is associated with a fatty liver (NAFLD) which affects various liver regulatory systems. 

  • Low testosterone is associated with metabolic syndrome and thus increased risk of MI.

  • Low estrogen because estradiol is a regulatory hormone similar to testosterone and low levels affects many systems the net result is an increased risk of age related conditions including osteoporosis, heart attack, dementia.  It even improves blood flow.  Long-term estradiol HRT lowers the risk over 44%[23]. 

  • Obesity defined by a body mass index (BMI) greater than 30 (approximately 25% above lean body weight) increases risk 50%.  Obesity is associated with metabolic syndrome, type-2 diabetes, CVD, MI, fatty liver disease, insulin resistance, et al.

  • Polypharmacy (taking regularly 4 or more prescription drugs), some antibiotics, taking long-term NSAIDS (except aspirin), and sedative increase AMI risk .  Some such as the NSAIDs (but aspirin)[24] are atherogenic others like hypertension, arrhythmia, and psychiatric drugs weaken the muscles through their effect on neurotransmitters and thus increase risk of dying from an MI or arrhythmia.

  • Sedentary lifestyle is a major direct causal factor because of reduced vitality (weaker heart muscle) and its secondary factors, an because of its association with smoking, obesity, substance abuse, use of sedative, polypharmacy etc.  Recent study showed it to be the 3rd lead cause of death.     

  • Arrhythmia is associated with sudden cardiac arrest.  And depending on type can increase the risk of blood clotting which is causal for ischemic events.  But more significant is that it is associated with a weak heart muscle and thus lowering the chance of survival during an AMI.

  • The formation of plaque results from pathogens.  Thus there is an association with infectious conditions such as gingivitis and infectious agents including Chlamydophila pneumoniae, H. pylori, and others.  Infections leading to poor health such as colitis are causal indirectly. 

  • Poor health:  the weak, infirmed, the aged, the obese the diabetic are more likely to have an MI or sudden death due to arrhythmia.   

  • Fibrinogen, C-reactive protein, hypertension, high serum glucose and insulin resistance among others are all risks factors for MI because they are associated with underlying conditions such as infections, AS, MeS, T2D, etc.  To treat the signs and not the condition in general is fruitless, but profitable for pharma.    Cholesterol, LDL, and triglycerides are not associated with AMI and CVD.

  • Endothelial dysfunction converts young plaque into vulnerable plaque.  The integrity of the endothelial cells determines the risk of plaque leakage.  Risk factors include the Western diet, reactive chemicals such as carbon monoxide from smoking, liver disease, high blood sugars, T2D, ethanol, toxins produced by microbes, active infection at site[25], reactive chemicals released during cell and pathogen necrosis, large liquid core, and various pharmaceutical drugs.

    Three major factors working together determine risk and survival:  Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis [clotting]) and vulnerable myocardium (prone to fatal arrhythmia [weak heart]) play an important role in the outcome. Therefore, the term “vulnerable patient” may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future” AHA, 2003. 


    14)  KEY POINTS for MI:  At first sign I would take 325 mg sublingually and three 325 mg orally of not coated aspirin then .  Ccontinuing taking aspirin up to 2.5 grams in the first 2 hours and 3.5 grams per day.  I would go promptly to a hospital.  In Hospital I would tell them I am not a pill popper, thus I want minimal drugs and will continue with aspirin as my anticoagulant, no PPI for indigestion (prefer Tums), no blood pressure medications, no arrhythmia drugs, or psychotropic drugs; also no to t-PA, angiograms, and other invasive procedures.  I would tell them that I want an opiate if in significant pain such as morphine.  Lidocaine could be administered in intravenously for arrhythmia and pain.  Nitroglycerin and nitrous oxide are acceptable.  Recovery phase:  Again I would remind them that I am not you are not a pill popperand continue refusing drugs listed above, plus definitely no to statins and sedatives.   I would take with meals 2, 325 mg aspirin (see aspirin).  Standard drug arsenal consists of 3 high hypertension drugs, PPI, anticoagulant, mood elevator (actually a sedative), statins, arrhythmia, anticoagulants, and drugs, and for angina pain often a sedative sold as an analgesic such as Lyrica and acetaminophen which is an NSAID that increases the risk of an MI.  The only invasive treatment I would consider is a pacemaker.  Bypass and stent are oversold, they only manage angina pain.  But also adopting a healthy lifestyle will gradually reduce angina pain through revascularization.  I would study the article on for a heart health and start exercising and healthy diet.  The Video Library is valuable.      


    15)  The ad post hoc fallacy (after this because of that) proves naught.  My father in the pre big-Pharma era lived 23 years after his first major heart attack in 1953. He had another major one in 1955 and 2 minor ones several years later.  He died in 1976 of a stroke.   Dwight Eisenhower had a major heart attack in 1955.   Both were heavy cigarette smokers who quit after their first heart attack.   Subsequently Eisenhower had 6 more heart attacks and died of congestive heart failure in 1969, 14 years after the first one.  What pharma and the doctors (all of whom are educated by pharma) sell is hope, the reality is that for 98 out of 100 patients following the guidelines will do more harm than good, and those 2% have been resuscitated from death or near death.  Most people survive in spite of rather than because of the treatments.  The body of long living mammals is designed to heal, to believe that what has been done by your doctor made the difference is to slight the natural healing process; it is the ad post hoc fallacy of attributing causality to the treatment. 

[1] ST eleveation:   Prinzmetal's angina[4]  Acute pericarditis[5][6] ST elevation in all leads is more common with acute pericarditis.  Left ventricular aneurysm[7],  Blunt trauma to the chest resulting in a cardiac contusion[8],  Hyperkalemia[4].  Acute myocarditis[4] .  Pulmonary embolism[4].  Brugada syndrome[4].  Hypothermia[4].  J-point elevation[4].  Early repolarization ST depression may be associated with subendocardial myocardial infarctionhypokalemia, or digitalis toxicity.[2]

[2] I shudder when I visualize a hard-long object being pushed through my arteries from my leg into my heart.  I can see it bumping & rubbing against (damaging) the paper-thin single layer of endothelial cells that have essential functions as a barrier and regulator.

[3] Positive bias averaged 32% (range 11 to 69%) for clinical trials --NEJM article, 2008.  The study of neuroleptic drugs compared 74 journal articles to the raw data supplied the FDA for phase III trials.  Complete records are required of these trials when pharma applies for a patent.  This data was obtained by43 professors through the FOIA (Freedom of Information Act). See, or 

[4] I suspect that this figure is grossly inflated by relying upon death certificates (a very unreliable tally method).  If they just gave figures for sudden deaths and AMI of otherwise health people, that number would I geustimate be about 600,000 deaths—to eliminate the frail elderly & infirmed.  This is another example of disease awareness campaign done to promote the use of drugs. 

[5] One study found 0.4% of patients with a low-risk profile died after 90 days, whereas in high-risk people it was 21.1%” Wiki.

[6].  APAP (acetaminophen, Tylenol) is the most common under the not-clinically-proven assumption of enhancing the analgesic effect.  APAP is the number 1 cause of drug induced liver failure.  Tramadol and other sedatives have been given FDA approval for pain, avoid them.  Sedated you won’t be able to make informed choices concerning your treatment.     

[7] Every additional action by the care givers will be billed.  In theory oxygen should help oxygen starved heart muscles survive; however, in excess it promotes toxic oxidation of the debris from the dead heart tissue, which hinders its disposal. 

[8] Aspirin “inhibits platelet hemostasis,…  a dose of 0.65 g of aspirin approximately doubles the mean bleed time of normal person for a period of 4 to 7 days” Goodman and Gilman’s Pharmacological Basis of Therapeutics, 6th Ed, p. 692.

[9] The guide wire and balloon tip are pushed through and thus bump against the artery walls causing damage, sometimes puncturing them.  With an anticoagulant the subsequent bleed could result in a medical emergency—thus the contraindication. 

[10] Only those already in the hospital would receive PCI within 90 minutes of first symptoms.  Cholesterol embolism is very strongly associated with invasive procedures:  20 of 22 patients in a histologically post mortem proven cases.  With PCI, e.g., Cholesterol embolism issues became evident with 3 months, most within 3 weeks, at. This cause of risk is rarely mentioned, and if the adverse event occurs the physician will likely attribute it to natural causes, not their invasive treatment!  Moreover, the typical “Anticoagulant therapy appeared to exert an adverse affect” at, and also at, which found warfarin a cause.     

[11] Statements that t-PA is controversial at all timeframes and should not be considered standard of care

        American Academy of Emergency Medicine18

        Australasian College for Emergency Medicine19

        Canadian Association of Emergency Physicians (currently posted policy)20

New Zealand Faculty of the Australasian College for Emergency Medicine21

[12] There are many ways to cook the result.  One way would be to select for the trial those who have been on anticoagulants. Since pharma on the information (raw data) they don’t have to inform the journal peer article review panel of the selection of patient on blood thinners.  Given them another blood thinner in the hospital would have less affect than if a real world population was tested.

[13]  Nitrous oxide plays an important role in attenuates cardiac remodeling [enlargement] & apoptosis after MI via suppression of oxidative stress-mediated signaling pathways.  Nitroglycerin is a “ Nitrates which undergo denitration within the body to produce NO” Wiki.

[14] Pharma doesn’t mention the benefit from the reduction of smoking:  46% in the 60s to 16% in 2015.

[15]  “… Been shown to be ineffective.  Lidocaine may be used for 24 to 48 hours to treat ventricular tachycardia” (Conn’s supra 403).

[16]  Proven to be ineffective yet still routinely administered, also, higher death rate.  Oxygen increases the rate of the breakdown of the mitochondria within the muscle cells of the heart, thereby offsetting its beneficial effect.   This is also why when restoring blood flow by a PCI or angioplasty does not result in a prompt improvement in the patient’s condition.  

[17] Glycation is the random attachment of a sugar molecule—mainly glucose and fructose.  This damages tissues including the endothelial cells that line the way, and fructose which goes to the liver, in sufficient amount causes insulin resistance.  At Recommended healthful diet you will find articles on diet and cardiovascular disease.  There you can find out why saturated fats are best and polyunsaturated because of rancidification are the worst along with trans fats.  

[18] Fructose is the worse of sugar:  it is 7 times more reactive than the monosaccharide glucose, and it goes to the liver where it damages the liver 2 ways, one by glycation, the other by conversion to fat.  On a high carb diet this fat accumulates in the liver. This is because insulin is secreted by the pancreas to lower the toxic high level of blood glucose, and insulin does this by telling the body to store fat and burn glucose.  This high level of insulin gradually brings on a condition called insulin resistance, cells become resistant to insulin and more insulin is secreted.  This mucks up the weight control system for most peoplefor summary.    

[19] Polyunsaturated fats are subject to oxidation in the body and while cook, once oxidized they contribute to CVD similar to trans fats.  Polyunsaturated fats are cheap, which is why they are promoted, and saturated fats criticized, contrary to the evidence.

[20] Low dose is a pharma plow, for long term it doesn’t have an antiplatelet effect—pharma studies are all short-term.  Typical treatment following an for MI runs with insurance between 66 & 71,000 per year—but compliance is only about 31%, NEMJ (what side effects?).   

[21] Again we heave the workings of bad pharma.  They set up clinical trials designed to fail by setting up small clinical trials, using low dose testosterone,  to short a period for to produced clinically significant results.  More business as usual.   

[22]   Progesterone was not available in pill form until 1995 because of poor absorption.  The micronized in oil has not been marketed with estradiol. The combination is available only from a compounding pharmacy.  Thus there are no major endpoint studies. 

[23] Braunwald, Heart Disease …, 5th Ed, 1997supra, p. 1142.  “In a meta-analysis of case control cross-sectional, and prospective studies, the relative risk for CVD in postmenopausal subjects taking estrogen was 0.56 compared with postmenopausal subjects not taking estrogen.”The effects of the various HRT formulas other than Prempro (above) as to side effects have not been thoroughly investigated.  Prempro is the worst. Some formulas are good.  Using a progestins different than MPA, another study found 50% and the Danish study cut deaths 115%.  See The natural formula is probably best for overall healthHRT- for benefits & how bad pharma with the NIH (National Institute of Health) deliberately used the worst HRT in the WHI Trial to get women of HRT.-see footnote 14.    

[24] Aspirin is natural because the salicylic acid form of aspirin is found widely in plants. 

[25] Infection causes immune cells and they can release various digesting enzymes (MMPs 2, 3, 9 etc.) which can weaken a young cap. 

Ancillary Materials:        On Arrhythmia, tThrombolysis (t-PA), Angioplasty (PCI),       Atherectomy, & Coronary artery Bbypass graph (CABG)

While thrombolysis is reserved for an acute AMI, angiogram and angioplasty are used during an AMI as well as prior to and during recover phase.  Bypass surgery and atherectomy are done only prophylactically.


16)  Cardiac Arrhythmia is a broad classification, which includes too rapid heartbeat (tachycardia) above 100,  and too slow heart beat (bradycardia) below 60, and irregular heart beat. Many types of arrhythmia have no symptoms. When symptoms are present these may include palpitations or feeling a pause between heartbeats. More seriously there may be lightheadednesspassing outshortness of breath, or chest painWiki.  Arrhythmia is quite common, even among children, and it often goes unnoticed.  During an AMI, arrhythmia is quite common; and only significant for about 15% of patients.  Most episodes have no symptoms.[3]  Occasionally there may be heart palpitationsfaintingshortness of breath, or chest pain,… Atrial fibrillation [AF] is the most common serious abnormal heart rhythm… the percentage of people with AF increases with age with 0.14% under 50 years old, 4% between 60 and 70 years old, and 14% over 80 years old being affected.Wiki.  For purpose paperof this and following discussion,  I will focus up irregular heartbeat called ventricular fibrillation and use “arrhythmia” in that sense[1] and focus on its association with CVD and AMI.  While most types of arrhythmia are not serious, some predispose a person to complications such as stroke or heart failure.[1][3]  This myocardial scarring also puts the person at risk for potentially life-threatening abnormal heart rhythms (arrhythmias)…. Injured heart tissue conducts electrical impulses more slowly than normal heart tissue.  The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death,” Wiki. Ventricular fibrillation is a medical emergency that requires prompt Advanced Life Support interventions. If this arrhythmia continues for more than a few seconds, it will likely degenerate further into asystole ("flatline"). This condition results in cardiogenic shock and cessation of effective blood circulation. As a consequence, sudden cardiac death (SCD) will result in a matter of minutes… death often occurs if sinus rhythm is not restored within 90 seconds of the onset of VF, especially if it has degenerated further into asystole” Wiki.  Drugs are ineffective, thus standard treatment consists of discharge of direct current form a defibrillator, and for high risk patients the use of an implantable cardioverter defibrillator.    

16b) Procedures:  I would not submit to taking a drug for arrhythmia for three major reasons:  they are not a magic bullet that goes only to the nerves that regulate the heart beat and restore its normal pattern of muscular contraction;[2] second they have numerous side effects made all the more likely as the number of drugs given increases,; and third their usage has been strongly associated with cardiac deaths because of drug induced arrhythmia—this is called  proarrhythmia.[3]  In the Cardiac Arrhythmia Suppression Trial (CRAST, 1989-1999) two anti-arrhythmia drugs were tested against a placebo[4] to see if they could prevent “sudden death in patients who were at higher risk because they had certain kind of abnormal heart rhythm.  The drugs prevented these abnormal rhythms, so everyone thought they must be great:  they were approved onto the market to prevent sudden death in patients with abnormal rhythms, and doctors felt pretty good about prescribing them.  When a proper trial measuring death was conducted, everyone felt a bit embarrassed:  the drugs increased the risk of death to such a huge extent that the trial had to be stopped early…. (it’s been estimated that well over a hundred thousand people had died as a result).”  Bad Pharma, by Prof. Ben Goldacre, 2013, p. 133-34.   After 10 months on the drugs, there were 43 deaths for the drug cohort and just 16 for the placebo group, a nearly 3 fold increase risk of death, and for non-arrhythmia causes of deaths there were 17 among those receiving the drug and 5 in the placebo cohort, an over 3 fold increase risk of death.  These drugs were standard treatment for AMI given to patients without arrhythmia, not just the select group tested in the CRAST clinical trial.  These older drugs have been replaced by a new generation of drugs that supposedly manage arrhythmia differently and therefor save lives in industry funded studies.[5]   In a much more pharma- friendly world, trials such as the CRAST (1991, 1989) aren’t run today.  These drugs “are widely prescribed for patients after they had a heart attack when they had only mild abnormal heart rhythms…. They actively increased their risks of dying” Goldacre supra 176-7.  Knowing this, I would refuse all drugs for arrhythmia.  Secondly, pharma has emphasized irregular heart-beat, while the major player AMI is down played, thus causing the cardiologist to believe that these events often occur spontaneously in the diseased heart.  Wrong:  The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction, or "heart attack"[15] Wiki.  And knowing that the expansion of the market is one way that pharma maximizes profits, I would be very, very conservative about what I would allow in my body.  Similarly I would refuse all physical interventions such as electric cautery and cardioversion except under the most-dire circumstances.   Doing more does not entail doing good.   


17)  Thrombolysis (t-PA):  The theory of restoring blood flow by administering a drug which dissolves the platelet blood portion of the clot (but does not dissolve plaque) is attractive, but how effective???   There are for thrombolysis numerous contraindicated,[6] which would eliminate most patients; however in clinical situation over-treatment is the norm, and the doctor will go forward with t-PA though the net sums for risks and benefits is negative.  Guidelines extend the time frame for t-PA beyond the period of modest benefit (90 minutes since first symptoms).[7]  As stated repeatedly, trials results are seriously flawed by design since they are funded by pharma for marketing purposes ., and doctors cherry pick asand  pharma’s  and their KOLs use those of lowest quality and --thus most favorable—to educate cardiologists in CME classes.  The cardiologists then repeat what they have learnt to their patients.  The real-world outcomes for thrombolysis are quite different.  Even with the most prompt thrombolysis (under 1 hour) in ideal patients, survival increased by 3.5% compared to control patients (Braunwald 5th ED 1217).[8]  That the use of placebo control patients is permitted by oversight committees is indicative that the benefit from t-PA is minimal.   Thrombolysis causes 5 types of reperfusion injuries (thus the benefits are much less than reported); “(1) lethal reperfusion injury—a term referring to reperfusion-induced death of cells that were still viable at the time of restoration of coronary blood flow.  (2) Vascular reperfusion injury—progressive damage to the microvasculature such that there is an expanding area of no reflow and loss of coronary vasodilatory reserve.   (3) Stunned myocardium—salvaged myocytes display a prolonged period of contractile dysfunction following restoration of blood flow owing to abnormalities of intracellular biochemistry leading to reduced energy production.  (4) Reperfusion arrhythmias—burst of ventricular tachycardia and on occasion ventricular fibrillation that occur within seconds of reperfusion…. (5) The loss of magnesium with ischemia, followed during reperfusion by sudden exposure of severely ischemic cells to both calcium and oxygen upon restoration of flow, has been observed to affect severity of ischemic damage in several animal species” (Braunwald supra 1213-14).  (6) In real-world situation (versus select ideal patient in a trail with highly trained physicians) for 29 hospitals in Cleveland, there was a 3 fold increase of intra-cerebral hemorrhage compared with a matched number who did not receive t-PA in the 3-hour window from admission (15.7% vs 5.1%) JAMA.  In one analysis monitoring of performance of what is termed “real world patients, it was determined that just 1 patient in 125 was helped, which happens to be the number given such treatment within the 90 minute window of first symptoms, at.  This hemorrhages caused more than offsets the 3.5% improved survival for those treated in the first 1.5 hours from symptoms. The risk of hemorrhage is not just limited to the brain (stroke), but applies to all tissues.  Another study used Danish patient to measure the number likely to benefit with alteplase, a t-PA: “we estimated that 0.4% of unselected stroke patients would benefit from alteplase treatment—at 1999.   Often instead of “survival” pharma uses “benefit”.  The same study found that 4% benefited, but if a treatment hasn’t the ability to increase survival, than how can meaningfully improve the quality of life?  “Benefit” is a vague term subject to inflation.  These dismal results for drugs that effectively breakup clots applies not just to strokes, but aslo to heart attacks.  The reason is that by the time treatment has begun, the tissue that is not receiving oxygen has already died.   Within about 20 minutes for tissues that are have a high rate of metabolism most of the cells have died, including neuron and myocytes (muscle cells).  Thus whatever type of method is used to restore oxygen, the result are essentially the same.  What benefit these treatments have for peripheral tissue that is being oxygenated by diffusion from other not affected capillaries, this is offset by the damage of the invasive procedure (angioplasty) or the inability to form clots due to t-PA. Moreover, thrombolysis opens the door for long-term treatment with anticoagulants and polypharmacy. 


18)  Angiogram, also called angiography, arteriography, coronary catheterization, also called and coronary angiogram:  a widely overused diagnostic tool which can lead into a PCI (angioplasty #19).  Depending on the type of angiogram, access to the blood vessels is gained most commonly through the femoral artery,[9] to look at the left side of the heart and at the arterial system; or the jugular or femoral vein, to look at the right side of the heart and at the venous system. Using a system of guide wires and catheters, a type of contrast agent (which shows up by absorbing the x-rays), is added to the blood to make it visible on the x-ray images.  The X-ray images taken may either be still images, displayed on an image intensifier or film, or motion images. The heart images are taken at 15–30 frames per second, not using a subtraction technique, Wiki.   (For a longer description at #31).  As for the risks:  “After an angiogram, a sudden shock can cause a little pain at the surgery area, but heart attacks and heart strokes usually don't occur, as they may in bypass surgery (CABG). The contrast medium that is used usually produces a sensation of warmth lasting only a few seconds, but may be felt in a greater degree in the area of injection. Additionally, damage to blood vessels can occur at the site of puncture/injection, and anywhere along the vessel during passage of the catheter.” Wiki. Thus the procedure seems safe, but a critical review of the literature comes to the opposite conclusion. 

Cardiac Catheterization (heart cath) is the insertion of a catheter into a chamber or vessel of theheart. This is done both for diagnostic and interventional purposes. Subsets of this technique are mainly coronary catheterization, involving the catheterization of the coronary arteries, and catheterization of cardiac chambers and valves of the cardiac system.  In 2009 there were 600,000 of these procedures.  "Cardiac catheterization" is a general term for a group of procedures that are performed using this method, such as coronary angiographyand left ventricle angiography. Once the catheter is in place, it can be used to perform a number of procedures including angioplasty, percutaneous coronary intervention (PCI), balloon septostomyelectrophysiology study or catheter ablation. …  Other common diagnostic procedures include measuring pressures throughout the four chambers of the heart and evaluating pressure differences across the major heart valves. Interventional cardiologists can also use cardiac catheterization to estimate the cardiac output, the amount of blood pumped by the heart per minute,[1]Wiki.  By the end of this section, the evidence as to why I would not allow this procedure and its sister the angiogram will allow you to understand why I would submit to it.  Simply put, angiogram and cardiac catheterization do not lead to beneficial treatment (with a few rare exceptions, thus why go the risks?

Risks from angiogram (description of procedure in last section) and angioplasty:

1)   Gateway to treatments not worth their risks:  The subsequent treatments for the finding of over 50% occlusion.  nearly all patients once submitting to an angiogram now follow their cardiologist’s recommendations.  But  hHigh -quality scientific studies reveal that the prescription of anticoagulants (but for aspirin), angioplasty (balloon or use of a stent), CABGbypass surgery, and the assortment of drugs increased likelihood that the patient will tatakesn for high cholesterol and blood, all these  pressure lowering medications are allare, counting side effects and dollar costs, on an average worse than nothing at all.  Testing for a condition where the interventions do more harm than good is not in my the patient’s best interest.[10]  Angiogram opens the door to the sales pitches by the cardiologist using pharma’s tobacco science.  My father would not have lived 23 years since his major heart attack if the current standard guidelines and  confirmed treatments were available in 1953 and he followed them.  The loss of trust in guidelines is earned. 

2) Risks angiogram:  (at, From the NIH (National Institute of Heath) government site

Cardiac catheterization carries a slightly increased risk when compared with other heart tests. However, the test is very safe when performed by an experienced team.[What follows on the NIH site proves the opposite!]

Risks of the procedure include the following:

  • Cardiac tamponade  a medical emergency [accumulation of blood or fluid inside the membrane sack that surrounds the heart.  It can lead to heart failure, pulmonary edema, shock, and death, see]


  • Irregular heartbeats [arrhythmia]

  • Injury to a heart artery [perforation of artery is significant risk at, less or injuries much more common]

  • Low blood pressure

  • Allergic reaction to contrast dye or a medicine administered during the exam

  • Stroke


  • Heart attack [See heading kidney damage below, for a 15 fold association with MI.[11]]


  • [Cather caused infections that can lead to death—missed by article.][12]


Considerations associated with any type of catheterization [thus also for balloon and PCI] include the following:

  • Bleeding, infection, and pain at the IV or catheter site. [which is an artery, not vein.  frequent complications from arterial puncture wounds as well as major systemic haemorrhage, at]. 

  • Damage the blood vessels or surrounding structures by soft plastic catheters [the wire with surrounding mesh tube is not soft, thus causes bruising to the single cell layer protective endothelia cells and underlying layerballoon expansion and stent] .

  • Blood clots could form on the catheters and later block blood vessels elsewhere in the body [risk of clinically significant strokes, MI, renal damage, etc. and of course subclinical events, mini strokes and MIs].

  • Kidneys damaged by contrast dye (particularly in people with diabetes or prior kidney problems).  [Is symptomatic in 30% of angiograms.[13]  Below this major issue is developed.]

    [Missed:  1) cholesterol embolism” which causes events in other areas than stroke (listed above), and which in fact is under 20% cholesterol; it should be termed “plaque embolism.” 2) coronary- artery spasm which causes occlusion leading in worse cases to AMI and death; 3) perforation of coronary artery; 4) restenosis which occurs in over 30% to 50% of angioplasties by month 6; 4) cancer from high exposure to x-rays during the 1 hour procedure; 5) “Thrombosis within a stent causing myocardial infarction and death” at ] 

    Summary angiogram:  a very invasive procedure involving using a system of guide wires and catheters that to enter the coronary blood vessels and then inject a contrasting agent.  The procedure depending on finds can take up to 2 hours and involves multiple blood vessels for entry.  See description of procedure above at beginning of this section.   Given the assorted risks (all grossly underestimated)  multiplied by the fact the subsequent treatments based upon finding , my with rare exceptions are a net negative, the prudent response is would be to refuse the procedure.  What follows are the evaluations of angioplasty and bypass surgery.  At the links you may read about the drug prophylactics which are good only for pharma; see hypertension, statins, arrhythmia, and anticoagulants.  It is easiest to say no at the start.


    19)  Renal reaction to the iodine contrasting fluid:  On Renal damage from the conservative Medscape site:

    Modern intravenous contrast agents are typically based on iodine.  Iodine contrast agents are used for the following:  angiography, Venography, ….  Iodine-based contrast media are usually classified as ionic or non-ionic. Both types are used most commonly in radiology due to their relatively harmless interaction with the body and its solubility,” Wiki.   On Renal damage from the conservative Medscape site “Severe symptoms include the following: life-threatening arrhythmiaarrhythmias ,  (ie, ventricular tachycardia), hypotension, overt bronchospasm, laryngeal edema, pulmonary edema, seizures, syncope, and death.  Moderate symptoms include the following: persistent vomiting; diffuse urticaria; headache; facial edema; laryngeal edema; mild bronchospasm or dyspnea; palpitations, tachycardia, or bradycardia; hypertension; and abdominal cramps… Nephropathy:  Contrast agent–related nephropathy is an elevation of the serum creatinine level that is more than 0.5 mg or more than 50% of the baseline level at 1-3 days after the ICM injection.  The elevation peaks by 3-7 days, and the creatinine level usually returns to baseline in 10-14 days.[14]  The incidence of contrast agent–related nephropathy in the general population is estimated to be 2-7%. As many as 25% of patients with this nephropathy have a sustained reduction in renal function; most commonly when the nephropathy is oliguric.[15]  A second article exposing the assorted risks:  ICM [iodine contrast medium] can cause hypotension and bradycardia. Vasovagal reactions, a direct negative inotropic effect on the myocardium, and peripheral vasodilatation probably contribute to these effects. The latter 2 effects may represent the actions of cardio-active and vasoactive substances that are released after the anaphylactic reaction to the ICM. This effect is generally self-limiting, but it can also be an indicator of a more severe, evolving reaction.  ICM can lower the ventricular arrhythmia threshold and precipitate cardiac arrhythmias and cardiac arrest. Fluid shifts due to an infusion of hyperosmolar intravascular fluid can produce an intravascular hypervolemic state, systemic hypertension, and pulmonary edema. Also, ICM can precipitate angina.  Other non-idiosyncratic reactions include syncope; seizures; and the aggravation of underlying diseases, including  pheochromocytomas,  sickle cell anemia, hyperthyroidism, and myasthenia gravis.  Delayed reactions:  Delayed reactions become apparent at least 30 minutes after but within 7 days of the ICM injection. These reactions are identified in as many as 14-30% of patients after the injection of ionic monomers and in 8-10% of patients after the injection of nonionic monomers.[25]   Common delayed reactions include the development of flulike symptoms, such as the following: fatigue, weakness, upper respiratory tract congestion, fevers, chills, nausea, vomiting, diarrhea, abdominal pain, pain in the injected extremity, rash, dizziness, and headache.  Conclusion DARS (delayed adverse reactions to contrast media are not rare but are often are not recognized as being linked to contrast administration and may be falsely ascribed to other drugs.  These side effects are problematic because the patient is usually without medical supervision” American Journal of Roentgenology, 2014.  Another study of the 2,308 patients used N-acetylcysteine to lower the risk of contrast-induced nephropathy found that “the incidence of contrast induced acute kidney injury (primary endpoint) was 12.7%”.[16]   The is is another research based article that diverges with the KOL-generated literature found such as in Wikipedia, WebMD, and textbooks, which paint a rosy picture for the sake of business.  The risks described are just for the contrasting agent.  This is the pattern of corporate medicine to hide the issues and sell the fluff.  For a similar situation of risks buried read 2003 for Scientific American on what is referred to by cardiologist as “pumpheadthe normal result following bypass surgery (CABG), at.  Reduced cognitive function “42% at five years (NEJM) based on a decline of 1 standard deviation,[17] 15 IQ points!   I doubt that today’s editors of Scientific American, given their current pharma-friendly editorial policy, would publish this at article on pump head, or an article on chemohead from chemotherapy, or on the decline in cognitive functions from taking psychiatric drugs.  How can the doctors inform us if these and other side effects are deliberately hidden and/or minimalized by pharma?           

    Look at the illustration page firsts

20)  Angioplasty (PCI) procedure:  in most cases it is a continuation of the angiogram procedure.  Thus all of the angiogram’s the negative effects listed apply and then those for angioplasty (below):  A sheath is a vascular tube placed into the access artery, such as the femoral artery in the groin that allows catheter exchanges easily during these complex procedures.  A balloon catheter is a long, thin plastic tube with a tiny balloon at its tip.  A stent is a small, wire mesh tube. Balloons and stents come in varying sizes to match the size of the diseased arteryat.   “Angioplasty is an endovascular procedure to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.  An empty, collapsed balloon, known as a balloon catheter, is passed over a wire into the narrowed locations and then inflated to a fixed size. The balloon forces expansion of the stenosis (narrowing) within the vessel and the surrounding muscular wall, opening up the blood vessel for improved flow, and the balloon is then deflated and withdrawn.  stent may or may not be inserted at the time of ballooning to ensure the vessel remains open. Percutaneous coronary intervention (PCI), commonly known as coronary angioplasty is a therapeutic procedure to treat the stenotic (narrowed)the stenotic (narrowed)   coronary arteries of the heart found in coronary heart diseaseWiki.  It has been increasingly recognized, since the late 1980s, that coronary catheterization does not allow the recognition of the presence or absence of coronary atherosclerosis itself  [namely the immature soft plaque that causes under 20% occlusion and 80% of AMIs], only significant luminal changes [over 50%] which have occurred as a result of end-stage complications of the atherosclerotic process. See IVUS and atheroma for a better understanding of this issueWiki, 2016.  This procedure of placing a sent or expanding the catheter to open a clogged coronary artery will dislodge debris from the atheroma that will travel throughout the body to cause ischemic events and thus tissue destruction.   There are issues with placing the stent:  Stent-dislodge (migration), wrong location, and loss:  Mishaps happen; this includes loss of stent during incursion process which requires an attempt to retrieve the stent.  In one case of the 38 lost, 35 were retrieved and 3 were crush by balloon procedure and left there—see.  Fortunately this mishap is rare according to industry; but sufficient for a patent (6,027,509) to be issued for a retrieval device—at, and another patented 5913871 device at.   Upon looking at the imaging (see example at illustration page), I can only wonder how many stents and balloon procedures are performed at locations that are not a cause of the MI or cause of the angina pain.  And it gets worse when we consider the sum total of negative effects associated with angiogram (prior summary) and PCI (developed below).   

Benefits:  A red flag as to its merit is the scarcity of clinical trials that compare preventative  long-term drug treatment to angioplasty with drugs.  The short-term 2004 MASS II found at 12 months the standard treatment group (203 patients) had an insignificant greater survival rate than the angioplasty group (98.5 vs 95.6%), a 1.9% difference.   Moreover for PCI with drugs cohort there were 5 more patients who undergone either an additional PCI or a CABG than the standard medical treatment cohort.  These results for additional procedures  and death falls well below the standard for significance (95% confidence interval) in a trial for 408 patients.   This means that the positive result for medical treatment only has about a 40% of being negative if the trial was ran again.   Since it is an industry funded trial, where the mischief lies is not known since pharma owns the raw data and doesn’t share it with the reviewers.  The MASS II trial is supported by other better trials:  According to some clinical trials, bypass surgery and angioplasty procedures have had at best a minimal effect, if any, on improving overall survival. Typically mortality of bypass operations is between 1 and 4%, of angioplasty between 1 and 1.5%, Wiki. The failure of PCI[18] lies with the fact that it fails to treat the actual cause of AMI, young plaque causing less than 50% occlusion.  Neither of these physical interventions come close to the benefits of exercise—see next to last journal article reproduced at bottom.  The prestigious Cochrane found similar benefits in their metastudy comparison.[19] The side effects and restenosis explains why I would not undergo a PCI. 


21)  Angioplasty as primary treatment for AMI or for preventive therapy for patients with with CVD:  Given the risks associated with thrombolysis, my a use of high dose of aspirin an angioplasty would appear to be preferred.[20]   The artery-opening procedure alleviates chest pain far more quickly than medical therapy, but has not been shown to prolong life. The "vast majority of heart attacks do not originate with obstructions that narrow arteries" Wiki 2014.  However, other studies show there is no advantage to having both procedures (Braunwald 1375-76).  This statement by Braunwald means that since I have taken high dose of aspirin, there is no advantage to undergoing an angioplasty.  The bias of market studiesing entails that these benefits are overstated.  Adverse events associated with PCI include those listed for angiogram since the procedure involves an angiogram followed by adding a shunt.  Adverse cardiovascular events associated with thrombotic occlusion occur in 4% to 12.8% of patients after coronary angioplasty”, AHA  1997.  More telling is a study of real-world patients who at one month had major adverse events[21] of 16.5%, 65 of 406 undergoing stent placementAHA.  Among the major issues following an angioplasty are cholesterol embolism, dislodging of stent, restenosis, and the damage to the endothelia cells.

22)  Cholesterol embolism: (often cholesterol crystal embolism or athero-embolism, sometimes blue toe or purple toe syndrome or trash foot or warfarin blue toe syndrome[1]:338) occurs when cholesterol is released, usually from an atherosclerotic plaque, and travels as an embolus in the bloodstream to lodge (as an embolism) causing an obstruction in blood vessels further away. Most commonly this causes skin symptoms (usually livedo reticularis), gangrene of the extremities and sometimes renal failure; problems with other organs may arise, depending on the site at which the cholesterol crystals enter the bloodstream.[2] When the kidneys are involved, the disease is referred to as athero-embolic renal disease (AERD).[3] The diagnosis usually involves biopsy (removing a tissue sample) from an affected organ. Cholesterol embolism is treated by removing the cause and giving supportive therapy; statin drugs have been found to improve the prognosis.[2]  is the leaking of plaque, and thus the labeling it as “cholesterol” is deliberately misleading.[22]  The rate is embolism major adverse events at 20%:  but their placement carries a 20% incidence of procedure-related complications, which potentially are related to the distal embolization of atherosclerotic debris—AHA.  And it gets worse because the plaque can lodge in the brain resulting in cognitive decline or a stroke, and it can cause a MI. 


23) Restenosis and increased mortality:  Restenosis occurring in the first six months after angioplasty is caused largely by smooth muscle cell proliferation and fibrointimal hyperplasia (often called neointimal proliferation), as well as elastic recoil.  It is usually defined as a greater than 50% reduction in luminal diameter” at BMJ 2003.[23]  In cardiac procedures, balloon angioplasty has been associated with a high incidence of restenosis, with rates ranging from 25% to 50%, and the majority of these patients need further angioplasty within 6 months[4]Wiki.  In the real world patient population that figure is closer to 50%.  Moreover, the risk of dying from PCI procedure in the next 30 days due to PCI was over 50% higher than those who died from cardiac event not related to PCI.[24] In other words in the first month, PCI doubles the rate of deaths from cardiac events.   Furthermore those who get standard medical treatment (drugs) had lower rate of deaths than those who received drugs and had a PCI or bypass operation, MASS-II trial, see Capo supra 325.  In the supplemental section is hope’s hypothesis buried, it explains why doing something doesn’t increase your chance of survival, though it does lower angina pain. 


24)  Spasms causing occlusion, bleeding at sight of angioplasty, and perforation of coronary artery:  These are all major risks mentioned in some journal articles (for example), for which clinics are highly motivated to ignore or attribute to natural progression of coronary artery disease.  The BMJ 2015 points out that of those who suffer in the US from bleeding event following a PCI, 12.1% of them die from it in the hospital.   The list of  issues with an oversold invasive procedure is long.  The true risk shall never know, and for whom patients in the clinical setting will not make an informed choice.  Only a nerd such as me has the ability, time, and inclination to sort it out as best I can from a very biased journal literature and medical textbooks can make a reasonable informed choice.   I am not faulting the cardiologist, but rather it is a bad system which causes the bad results; one that is very good at marketing.     Thus I am not aware of quality figures for these types of events, and if there are they are surely under estimated.   


25) Atherectomy:   The advantages of atherectomy when compared to balloons (angioplasty) and stenting are less vessel  barotrauma, no foreign object (stent metal) left in the body and leaving all future options open for the patient at the treated site There are four types of atherectomy devices: orbital, rotational, laser, and directional.  The decision to use which type of device is made by the interventionist, based on a number of factors. They include the type of lesion being treated, the physician's experience with each device, and interpretation of the devices' risks and effectiveness, based on a review of the medical literatureWiki.  In Cochrane Review, the benefit for elective rotational atherectomy of coronary artery disease was comparable to that of angioplasty for major adverse coronary events, but had increased risk of vascular spasm, perforation, and transient vessel occlusion. Thus like PCI, it should not be used for prevention. However in theory the procedure should cause less down-stream MIs (listed as about 20%, see above). A 1998 trial achieved modest benefits over balloon angiography, AHA,  Braunwald hold results similar, though procedure takes longer.   Given the minimal advantage and the under reported cholesterol embolism (see above), it is recommended that this procedure like PCI should be limited to the first 2 hours from symptoms.


26) Bypass surgery (CABG):  While not performed during an AMI for an obvious reason; the surgery is common:  in 2001 there were over 500,000 bypass surgerieCABGss performed in the US (making it the most common major surgery) with the average cost of $61,000 for a total of $32 billion”, Colpo, The Great Cholesterol Con, 5 Ed 2012 p. 323.  The two major trials comparing surgery to standard treatment came out with reduced angina pain, but no lives saved, and there is at least a 5% increased chance of dying in the first month from surgery.[25]  And there is a very real major decline in cognitive function, which occurs in all CABGS, so common that it merits a Wikipedia article entitled pumpheadalso called postperfusion syndrome.  In 2003 for Scientific American’s article on what is referred to by cardiologist as “pumphead warned of major cognitive decline the normal result following CABG, at.  The main cause is mini-strokes caused by micro-embolisms (tiny air bubbles).[26]  Reduced cognitive function “42% at five years” (NEJM) based on very CABG friendly decline of 1 standard deviation.[27]  And there is the fact that those undergoing a CABG, die sooner than those who adopt a healthful lifestyle, and those who receive standard drug management (see Colpo supra 324-25).  The fundamental reason why angioplasty fails to extend lives applies to CABG (mature plaque is does not leak to cause AMIs).  Read carefully the summary below, it explains why invasive treatments do not address the underlying cause.   One more cautionary note, the comparison of implant devices is a crap shoot.  Industry published journal articles again and again show that the regulatory system doesn’t function.  Facing an eminent end of life choice, I would probably opt for a device such as a left ventricular assist device.  If not eminent  the evidence would have to demonstrate very significant benefit. I would like my father deal with major angina pain rather that shorten my life, rather than experience a very traumatic operation in which my heart is stopped, a vein is taken from my leg, and my sternum is split.  The long term results fail to show in quality studies a significant increase in survival.  Exercise and diet is the best path to health.    


27) Hope’s hypotheses buried:  doing a risky procedure where the sum total of events is negative is not doing the right thing.  In the paper on cancer (#23) I labeled this hope’s hypothesis.  This faith that some will be saved occurs because with a body of data there are some which do much better than the average (and others that do much worse).  To assume that a person who lives 23 years following a PCI or CABG would have died sooner without that treatment doesn’t stand up unless that treatment has been shown in quality studies to add years to the lives of the entire population.  Quality PCI studies in real world populations fail to show this benefit.  Fortunately regular aerobic exercise does extend lives—see supplement below for the journal article.   In Part 5, I present a list of other proven ways to lower the risk of developing CVD and to promote healing.

There are 2 excellent ways to determine the merits of a treatment:  1) is to run a clinical trial designed to rigorously assess long term the benefits and  designed to uncover all risks in a real-world population (not a select ideal population favoring a positive outcome).  The second way is to open up the General Practice Research Database (GPRD, UK) or similar databases for analysis, because this will reveal outcomes in real world patients with various co-morbidities and taking an assortment of medications.  The data bank will reveal if for example patients on the diabetes drug sulfonylurea who undergo a PCI are at great risk for MI following a PCI due to the procedure than the general population of diabetics on different medicationsnot taking that drug.  We need the governments require wide university access to the data banks opened up.  See Ben Goldacre’s Bad Pharma, p. 156, 227.  There are computer programs to tease out the risks from the data.  Pharma with the support of government regulators has kept the evidence sealed. If GPRD and other computer databanks became available for computer analysis, then marketing of drugs would be greatly diminished.  Pharma spends twice that of research on marketing.  Remove market and the costs of drugs would drop.  Marketing is about sales.; it exaggerates the benefits and buries the down sides.  The mantra of pharma is safe and effective.  Marketing would not be cost effective if physicians knew the merits of treatments and clinical guidelines were rewritten to uphold the highest scientific standards for patients.

28)  SUMMARY (Invasive therapies bad idea):  Undergoing an angioplasty is not the end of invasive treatment.  Because of restenosis occurs in about 60% of who undergo insertion of a stent by 3 year6 monthss, and  it is the norm for angiograms to be repeatedly performed, frequency is influenced by angina pain and other signs of CVD.  And with each new angiogram a significant percentage will undergo angioplasty or bypass surgeryCABG to fix further occlusions.   Thus the risk of adverse consequence is multiplied by subsequent procedures.  Since the treatment of clogged coronary arteries doesn’t treat the cause of over 80% of MIs, the claimed significant risk reduction for AMIbenefits can only be based upon junk science.  

Allow me to explain why a logical idea is shot down with ugly facts:  As stated before and strongly supported by evidence, pharma has sold the public and doctors on a grossly flawed explanation for CVD and MI—see above causes of CVD item 3 or the link.  Pharma knows that those who undergo these procedures will very likely take all the (useless) drugs his cardiologist proscribes, which if followed and patented run over $70,000 a year--list.  Fact one, over 80% of thrombosis caused AMI result from leaking young fresh plaque.  Fact 2, the young plaques in major coronary arteries causes only about 20% occlusion.[28]  Fact 3, an angiogram only reveals an occlusion greater than 50%.  Fact 4, both bypass surgery CABG and angioplasty treat what shows up in angiogram; thus they are not treating the future cause of AMI, the coronary vessels with young-immature plaque.  To understand the process just below the endothelial cells of your arteries, think of having a young fresh inflamed boil that could leak.  When the young plaque leak it could causes an AMI depending on the amount that leaks and where.  It will block down-stream a narrower coronary artery.  It is the amount of plaque that leaks, where it lodges, and the degree of subsequent clotting caused by platelets that determines if you will have a major heart attack.  The prophylactic bypass or stent will not likely affect the events that follow caused by the leaked young-fresh plaque.[29]  A person with advanced CVD will have many occluded coronary vessels and very probably is still forming young fresh plaque.  This is why the best studies state that within 6 months approximately half experience restenosis (see #23).  The result is the same with or without the physical intervention:  A prophylactic bypass operation or angioplasty does not treat the cause of AMI, the young immature plaque.   While a single ruptured plaque can be identified during autopsy as the cause of a coronary event, there is currently no way to identify a culprit lesion before it rupturesWiki, see image of heart vessels.  This inability to identify where the event will occur makes replacing a small section of a coronary artery through bypass surgeryCABG, or by expansion through angioplasty, entails that the treatment will not alter the risk of an AMI; the small benefit is more than canceled by the increased risks from these procedures.  In the real world patient population (not the carefully selected subset of patients) the results are worse.  It is why most trials are comparing one invasive treatment to another and not to those who undergo just drug treatment. 

There is a large industry pushing angiogram, angioplasty, and bypass surgery  (CABG).  There are well over one million five hundred thousand procedures performed in the US annually.  Pharma promotes these procedures because over 90% of those patients will take some or all the drugs their cardiologist prescribes and their insurance covers.  Clinics promote those procedures because of the cash cow; for example in 2001 there were over 500,000 bypass surgeries CABGs performed in the US (making it the most common major surgery) with the average cost of $61,000 for a total of $32 billion (Colpo supra 323).  The health insurance companies profit because their rates reflect costs, and higher cost yield higher net profits.[30]  

This leaves on the table one last benefit from angioplasty and bypass surgery CABG, namely that for those with extreme angina pain, it can be a quick fix; however, for about half of patients it fails to be a fix.[31]  There is a better solution:   follow the recommendations below to stop atherogenesis and are willing to allow your body through revascularization to heal, then o

As for those experiencing an AMI, by time of intervention, if more than 90 minutes from first symptoms, after which there is no benefit to restoration of blood flow, since the damage has already occurred to the heart muscle.  Even for those who fall within the 90 minute window, the benefit is under 5% increase in survival.  Moreover On the basis of the NINDS study, thrombolysis could only help, at most, 1 of every 125 stroke patients8at 1999 .  This number given the similarity of the 2 events (stroke and AMI) also applies to both thrombolysis and PCI.  Thus nearly every patient with AMI is undergoing invasive, risky procedures which do not increase the rate of survival.   Thus I am advising that for all cases at point zero, arriving at a clinic with an AMI, the decision to undergo an angiogram will lead to significantly more harm than good.  Assuming that there is a subgroup which truly does shows a net benefits, there is no way at point zero for the patient or doctor to know if you are part of that subgroup; moreover given the norm of biased by design in clinical trials (average of 32%) and side effects grossly underestimated, the claimed benefits are merely a sales pitch.  Even if near death, a significant number of patients survive without angioplasty.  I would put my trust in my body to weather the storm and submit to only the minor interventions listed rather than relying on a very misinformed medical profession to perform procedures which on the average do more harms than good.  I think of my father who survived 2 major and 2 minor heart attacks (1953 through 1960) and who regained his health; he died from a stroke in 1976.  His extreme angina pain[32] gradually went diminished until he was pain free by 1964.   President Eisenhower survived 6 heart attacks.  Finally, if you follow my recommendations for healthful heart, you will be in the group who does very significantly better that pharma’s approach for treating CVD.  I have at the end of this paper attached a journal article that confirms the superiority of 20 minutes of daily exercise.   Its benefits include lower risk for AMI, reduction in angina, and overall feeling much healthier compared to conventional treatments.     At Part 5 is the collection of healthful choices, ways that have been shown to reduce risks.  Remember that these papers are periodically updated.   Also each sections home page has an internal Google search engine as does each page in the recommended section.     



Treatment decisions today for CVD and MI are predicated upon tobacco ethics.  I strongly recommend that you watch what university professor’s say about bad pharma.  At are posted over 110 links to YouTube lectures and documentaries.  With each link I provide from 2 to 5 lines of description.  The collection of links is divided into 12 sections.  Section 4 is on cardiovascular disease.  There is a list of worthy books I have read--at.

[1] With an AMI, if the heart is beating unusually fast it is probably based upon need, and if slow because of damage to the myocardium (heart muscle).  Both can be easily remedied if there is such need.  Epinephrine (adrenalin) or an analogy is the preferred method for increase cardiac output.  I would avoid drugs to slow my heart; they relax muscles and cloud the brain.  If it is prolong and life threatening, there are several electrical ways to corrects a weak, fluttering heartbeat, I would choose them.    

[2] Most popular are those which block neurotransmitters and therefor affect both cognitive functions and mobility by causing muscles to relax.  For more on these and other drugs used which are widely used to treat hypertension, link. 

[3]  This side effect is so common that it merited a Wikipedia article.  Proarrhythmia is a new or more frequent occurrence of pre-existing arrhythmias, paradoxically precipitated by antiarrhythmic therapy’ Wiki, 

[4] They received encainide, or flecainide, or placebo, see NEJM 1991, complete. 

[5] This is the normal pattern of bad pharma in their drive to expand the market based upon tobacco trials.

[6] Absolute Contraindications: Previous intracranial bleeding at any time, stroke in less than 6 months, closed head or facial trauma within 3 months, suspected aortic dissection, ischemic stroke within 3 months, active bleeding diathesis, uncontrolled high blood pressure (>180 systolic or >100 diastolic), known structural cerebral vascular lesion, arterio-venous malformations, thrombocytopenia, known coagulation disorders, aneurysm,  brain tumors, pericardial effusion.  Relative contraindications:  Current anticoagulant use, invasive or surgical procedure in the last 2 weeks, prolonged cardiopulmonary resuscitation (CPR) defined as more than 10 minutes, known bleeding diathesis, pregnancy, hemorrhagic or diabetic retinopathies, active peptic ulcer, and controlled severe hypertension.  The For AMI guidelinesthe re is a window ofis 4-6 hours from onset of symptoms.

[7] Studies vary greatly on death rates, but it averages about 16%.  That is 16 per hundred who arrive in the hospital die there.  A 5% reduction in deaths for those who are treated with t-PA in the first 90 minutes entails that the treatment saves less than 1.  These numbers are very close to those for angioplasty.  Thus if 100 patients are treated with either procedure in the real-world clinical practice, less than 1 life would be saved. For one thing only about 1 in 125 is treated in the 90-minute window.  Clinics use a 6-hour window, not the 90 minute one.  .  It is very hard to sort out the deaths caused by the treatments because in the industry funded studies they are attributed to the AMI.  Industry funded studies favor the industry.  Read Prof. Ben Goldacre’s Bad Pharma, the books is about how trials are ran and written up.  Industry is actively protecting their investment.   

[8] The number eligible for thrombolysis using the 90 minute from first symptoms entails “On the basis of the NINDS study, thrombolysis could only help, at most, 1 of every 125 stroke patients8at 2000.  This number given the similarity of the 2 events probably also applies AMI for both thrombolysis and PCI.  See footnote 37 for a discussion of the difference between % save and lived saved.  If 5/100 die without the treatment, and 4/100 treated, there is a 20% increased survival; however, 100 had to be treated to save 1 life, and the side effects including other causes of death and dollars are not figured in.    

[9] To use a major artery with its high blood pressure entails a significant risk for major bleeding.  

[10] A number of tests have been shelved because of the negative net results in the real-world patient population, these include PSA for prostate cancer, X-ray lung cancer screening are two examples; and critics have questioned the Pap smear and mammogram.

[11] Patients who develop CIN after PCI have a 15-fold higher rate of major adverse cardiac events during hospitalization than patients without this complication.13  They also have a 6-fold increase in myocardial infarction and an 11-fold increase in coronary vessel reocclusion.12  At.  

[12] “Infections, especially of the bloodstream, are common in patients with CVCs; sometimes these infections are fatal,” Cochrane Review.

[13] The reason why clinical trials often give a much lower figure is that they don’t look for the issue by doing the blood work which shows elevated creatinine, but only include those who have a medical emergency.  Moreover the assorted symptom are often called idiopathic (cause unknown) assuming that the patient reports them and their doctor records them. 

[14] I found a study in which 30% of those undergoing a angiogram had subsequent elevated creatinine.  Creatinine elevation is a marker for kidney damage.  I certainly don’t want to stress my kidneys.   

[15] Oliguria is defined as a urine output that is less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL daily in adults.  It is one of the clinical hallmarks of renal failure and has been used as a criterion for diagnosing and staging acute kidney injury, previously referred to as acute renal failure. At onset, oliguria is frequently acute. It is often the earliest sign of impaired renal function and poses a diagnostic and management challenge to the clinician. 

[16]  This figure of 12.7% and all that has been uncovered above demonstrates the bias of pharma’s KOLsS in Wikipedia:  If the patient is allergic to the contrast medium, much more serious side effects are inevitable; however, with new contrast agents the risk of a severe reaction are less than one in 80,000 examinations” Wiki.  What counts as severe reaction???

[17]Decline in postoperative function was defined as a drop of 1 SD or more in the scores on tests of any one of four domains of cognitive function. This would entail, e.g. going from 100 IQ to 85 IQ, only 15.8% of the population would score lower—see Wiki.

[18] Similar results were for the CABG cohort of the trial.  Both groups had very significant reduction in angina compared to the MT group 88%, 79%, and 46% were angina free at 1 year.  These results have been known for decades, that these procedures reduce short-term angina superior to that of just drugs. 

[19] The findings of this update are consistent with the previous (2011) version of this Cochrane review and show important benefits of exercise-based cardiac rehabilitation that include a reduction in the risk of death due to a cardiovascular cause and hospital admission and improvements in health-related quality of life, compared with not undertaking exercise.

[20] As stated above typical angioplasty (PCI) involves the use of an anticoagulant.  Given that heparin is inferior to aspirin (see above), aspirin should be requested over heparin or other adjunction to PCI treatment.   

[21] Major events (primary endpoints) are all deaths, MI, emergency bypass, and revascularization by 30 daysAHA.

[22] Plaque described:  An atheroma is an accumulation of degenerative material in the tunica intima (inner layer) of artery walls. The material consists of (mostly)macrophage cells,[1][2] or debris, containing lipids (cholesterol and fatty acids), calcium and a variable amount of fibrous connective tissue. The accumulated material forms a swelling in the artery wall, which may intrude into the channel of the artery, narrowing it and restricting blood flow” Wiki.

[23] This article reads like a sales pitch for PCI with everything new diminishing older issues.  The lack of spine in medical journals as to review and correction of industry spin is a main theme of Prof. Ben Goldacre’s book Bad Pharma—highly recommended.

[24] In the study 17% of deaths among the 4078 consecutive patient who underwent elective or emergency PCI, 17% of death were attribute  to cardiac deaths not related to PCI and 38% were related to PCI. at AHA 2012. 

[25] Again I must remind you that industry and government funded studies favor industry.  The best study found average bias at 32%.

[26] One problem “in addition to bubbles, clotted shards of blood cells, particles of corroded tubing and arterial plaque—all collectively called emboli—can make their way through the pump and canulae and back into the body… and they can block blood flow in a manner akin to a mini stroke, starving or even killing nearby tissue.” (p. 80-81).  “Micro-emboli—one tenth the size of the detectable ones and numbering 200 to 300 an hour—may still escape discovery and potentially damage body or brain tissue.  Newman and others believe that these types of anomalies during surgery, could cause cognitive problems in patients” at. CPB [CABG] may contribute to immediate cognitive decline. The heart-lung blood circulation system and the connection surgery itself release a variety of debris into the bloodstream, including bits of blood cells, tubing, and plaque. For example, when surgeons clamp and connect the aorta to tubing, resulting emboli may block blood flow and cause mini strokes. Other heart surgery factors related to mental damage may be events of hypoxia, high or low body temperature, abnormal blood pressure, irregular heart rhythms, and fever after surgery  Wiki.

[27]Decline in postoperative function was defined as a drop of 1 SD or more in the scores on tests of any one of four domains of cognitive function.” This would entail, e.g. going from 100 IQ to 85 IQ, only 15.8% of the population would score lower—see Wiki.

[28]lder plaque is stable and unlikely to cause a medical emergency, though, for example, it can cause stable angina.  Most MIs occur with less than 50% and typically at locations with about 20% stenosis (narrowing), prior to sudden lumen closure resulting in an MI”Wiki—Note, this quote has been removed.  Most medical articles in Wikipedia have been  edited by pharma’s KOLs to create consistency with what is taught physicians.  I have found numerous changes in the last 3 years. 

[29] According to some clinical trials, bypass surgery and angioplasty procedures have had at best a minimal effect, if any, on improving overall survival” wiki.

[30] All me to explain, assume health insurance companies average 15% profits, and suppose the average family of 4 pays $2,000 directly or indirectly (as through taxes) for coverage.  Making 15% of $2,000 is more than making 15% of $1,500.  Competing with other companies, they save costs by beating down payments to clinics, drug companies, doctors, etc.; and by increasing co-pays, pocketing the spread being Medicare payment and cost of drug, they fatten their profits.      

[31] Though not relevant to discussion of those with angina pain, those without pain run about 15% of developing angina from the procedure for some will undergo spasm and/or blockage from a cholesterol embolism

[32] A month after release from the hospital, It took him a month al 15 minutes to walk one block; the same after the 2nd 2 years later.   

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"I firmly believe that if the whole materia medica [medical drugs], as now used, could be sunk to the bottom of the sea, it would be all the better for mankind,—and all the worse for the fishes.."  Oliver Wendell Holmes Sr.

He also wrote:  "Drugs are what you take while you wait for the body to heal." 

Disclaimer:  The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for medical advice, diagnosis, and treatment.