What Causes Heart Attacks

In this article, I lay out the case that the spectrum of heart disease that includes angina, unstable angina, and myocardial infarction (heart attack) is better understood from the perspective of events happening in the myocardium (heart) as opposed to events in the coronary arteries (the arteries that supply the heart). As we ali know, the conventional view of the cause of heart disease is that the central events occur in the arteries. In this article, I will go into more detail about why the conventional theory is largely misleading, and then I will describe the precise and welldocumented events that do lead to heart attacks. This new understanding is crucial because, as the past 50 or 50 years have shown, pursuing the coronaryartery theory has cost this nation billions of dollars in surgical costs most of which are unnecessary - and billions in medications that cause as much harm as any benefits, and has led many people to adopt a low-fat diet and which only worsens the problem. In contrast, by understanding the real pathophysiological events behind the evolution of Mls, we will be led to a proper "Nourishing Traditions"style diet, the use of the safe and inexpensive medicine g-strophanthin, and rnost important, we will be forced to look at how heart disease is a true manifestation of the cost of modern life to human health. To overcome the epidemic of heart disease, we need a new medical paradigm, a new economic system, and a new ecological consciousness; in short, a new way of life. The coronary theory misses ali of this, just as it
by Dr. Thomas Cowan
misinterprets the actual pathological events. . In writing this article, I am indebted to the work of Dr. Knut Sroka and his website www.heartattacknew. com. For ali who are interested in this important subject, it is advised to read the entire website and watch the video on the website. For health professionals and researchers, your understanding of this subject is incomplete without reading and studying two items found in the print version of the website: The Etiapathagenesis oi Caronary Heart Oisease: A Heretical Theory 8ased an Marphalagy, by G. Baroldi, and "On the Genesis of Myocardial Ischemia," by Sroka.
Rebuttal of the Conventional Theory Until recently, it was thought that most Mls were caused by progressive blackage created by plaque buildup in the major arteries leading ta the heart (there are four major coronary arteries). The plaque was thought to be cholesterol buildup in the arterial lumen (inside of the vessel), which eventually cut off blood supply to a certain area of the heart, resulting in oxygen deficiency in that area, causing first pain (angina), then progressing to ischemia (heart attack). The simple solution was to unblock the stenosis (blockage) with either an angioplasty or stent, or, if that was not possible, to bypass the area with coronary bypass grafting (CABG). Simple problem, simple solution. However, problems became apparent through a number of avenues. First, a story related by a cardiologist at a Northern California
heart symposium, at which I was a speaker, points to the first problem. He told us that during his residency he was part of a trial conducted in rural Alabama with black men. In this trial, angiograms (injections of dye into the coronary arteries to detect blockages) were done on ali the men presenting with chest pains. For the ones who had a single artery blocked, no treatment was prescribed, and the researchers predicted in their notes which part of the heart would have a subsequent heart attack if one occurred. Of course, they ali predicted that it would be in the part of the heart supplied by the blocked coronary artery. Then they waited. Eventually, many of the men did return and did have Mls, but to the researchers' surprise, less than 10% had a heart attack in the area of the heart supplied by the original blocked artery. Second, a large study conducted in 2003 by the Mayo Clinic on the efficacy of bypasses, stents, and angioplasty concluded that: a. bypass surgery relieves symptoms (chest pain); b. bypass surgery does not prevent further heart attacks; c. only high-risk patients, those whose lives are in acute danger, benefit from bypass surgery with regard to a better chance of survival.
In other words, the gold standard for treating arterial blockages has, at best, only minimal benefits. If you watch the video on the heartattacknew.com website and go to the FAQ called "The Riddle's >
of Mls was done in Heidelberg in the 19705.1 The conclusion was that thrornbosis sufficient to cause the MI was found in only 20% of cases. Saroldi, in the largest such study ever done, found sufficient thrombosis in 41% of cases.' He also found that the larger the area of the MI, the more often a stenosis was present, and the longer the time between MI and death, the higher the percentage of stenosis. These two facts allow some researchers to "cherry-pick" the numbers and make the stenosis rate high, as they choose to study only those with large Mls and who live the longest after the MI event. Later in this article, I will explain how the stenosis comes about as a consequence of the MI. Another observation that casts doubt on the relevance of the coronary artery theory of MI has to do with the proposed mechanism of how thrombosed arteries cause ischemia, which is by cutting off the blood supply and thereby the oxygen to the tissues. The reality isthat when careful measurements are done assessing the p02 (oxygen levei) of the myocardial cells during an MI, to the huge surprise of many, there is no oxygen deficit ever shown in an evolving MI.3 The p02 levels do not change at ali throughout the entire event. I will come back to this later when I describe what does change in every evolving MI ever studied. Again, the question must be asked, if this theory is predicated on the lowering of the p02 in the myocardial cells, and in fact the p02 doesn't change, then exactly what did happen? The conclusion is that thrombosis associated with MI is a real phenomenon, but in no pathological study has it been found in more than 50% of deaths, which raises the question, why did the other 50% even have an MI? Second, it's clear from ali pathology studies that thrombosis of significant degrees evolve after the MI occurs, again leading to the question of what caused the MI in the first place. The fact that thrombosis does occur also
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> Sol.ution," it becomes clear why this is 50. Large, stable blockages - those over 90% - are in almost 100% of the casescompletely compensated by collateral blood vessels. In fact, the view that the heart gets its blood only from the four major vessels is itself false. Starting soon after birth, the normal heart develops an extensive network of small blood vessels called collateral vessels, which eventually compensate for the interruption of flow in any one (or more) of the major vessels. As Sroka correctly points out in the video, coronary angiogram - by failing to show the collateral circulation, and by creating spasms in the coronary arteries through the injection of heavy dye under high pressure - is notoriously inaccurate at assessingthe amount of stenosis in the vessels as well as the true blood flow in the heart. To this day, most of the bypasses, stents, and angioplasties are done on minimally symptomatic patients who show a greater than 90% blockage in one or more coronary arteries. These arteries are almost always fully collateralized; the surgery does not restore blood flow because the body had aiready done its own bypass. Ask yourself: If it were true that an artery more than 90% blocked had no collateral circulation, how would that person still be alive? And does it really make sense that the eventual MI is caused when the stenosis goes from 93% to 98%? This is an insignificant difference and is completely nonsensical. Yet this is what most of the procedures are meant to accomplish, to unblock the stenosis, which, as the video shows, actually has no blood-flow repercussions. It is no wonder that in study after study these procedures faiI to provide any significant benefit to patients. For these reasons, the stableplaque model is being abandoned by conventional cardiology, in favor of a different model for the etiology of
Mls, which, as it turns out, is almost equally invalid.
Meet the Unstable Plaque 50, we ali agree that the entire focus of cardiology - the stable, progressing, calcified plaque, the thing that we bypassed and stented for years, the thing that we do CT scans of your arteries for, the thing that we told Vou is from cholesterol buildup in your arteries, the thing that "alternative cardiology," such as the Ornish program, focused on - actually is not 50 important in the etiology of heart attacks. Don't worry, though. We know that the focus of the problem must be the arteries, or 50 conventional thinking goes.Therefore, enter the unstable, or friable, plaque. This insidious fellow doesn't actually create a large blockage; rather, it's a soft, "foamy" plaque that under certain situations (we don't know which situations) rapidly evolves and abruptly closes off the involved artery, creating a downstream oxygen deficit, followed by angina, then ischemia. These soft plaques are thought to be a combination of inflammatory "buildup" and LDL, the exact two things targeted by statin drugs. Therefore, the thinking goes, because this type of plaque can build up in anyone's arteries, at any time, everyone should be on statin drugs to prevent heart attacks. (Some people even advocate putti ng therapeutic doses of statins in municipal water supplies.) Angiogram studies have been presented to show the evolution of these unstable plaques as proof that they are the true cause of the majority of Mls. As I will show in the next section, acute thrombosis does happen in patients having Mls, but it is a consequence, not the cause, of the MI. But how often does it actually happen? Let's look at pathology studies, which are the only accurate way to determine what actually happened, as opposed to angiograms, which are misleading and create many artifacts. The first major autopsy/ pathology study of people who died
ains why emergency procedures mber, the only patients who -t from bypass and stents are ost critical, acute patients) can elpful immediately post-MI to e flow in those patients who ot have adequate collateral ation to that part of their heart. 50 again, ali the existing theories asto the relevance of the coronary arteries in the evolution of the MI are fraught with inconsistencies. If this is 50, what then does cause Mls?
lhe Etiologyof Myocardial Ischemia Any accurate theory of the cause of myocardial ischemia must account for the risk factors most associated _ with heart disease. These are: being male, having diabetes, smoking cigarettes, and experiencing chronic psychological/emotional stress. 'Interestingly, none of these risk factors directly link to pathology of the coronary arteries. Diabetes and cigarette use cause disease in the capillaries, not the large vessels, and stress has no direct effect on coronary arteries that we know of. In addition, during the past five decades or 50, the four main medicines of modern cardiology B-blockers, nitrates, aspirin, and statin drugs - ali have some benefits for heart patients (albeit ali with serious drawbacks as well), which must be addressed in any comprehensive theory of myocardial ischemia, which I will attempt to do here. The real revolution to come in the prevention and treatment of heart disease has been inaugurated through our understanding of the role of the autonomic nervous system in the genesis of ischemia and its measurement through the tool of heart-rate variability. First, some brief background. We have two distinct nervous systems. The first, the central nervous system, controls conscious functions such as rnuscle and nerve function. The second nervous system is called the autonomic (or unconscious) nervous system (AN5), which controls the function of our internal organs. The autonomic
nervous system is divided into two branches, which in health are always in a balanced but ready state. The sympathetic, or fight-or-flight, system is centered in our adrenal medulla and uses the chemical adrenaline to tell our bodies that danger is afoot, it's time to run. It does so by activating a series of biochemical responses, the center of which are the glycolytic pathways that accelerate the breakdown of glucose to be used as quick energy 50 that we can make our escape. In contrast, the parasympathetic branch, centered in the adrenal cortex, 15 the rest-and-digest arm of the autonomic nervous system. The particular nerve of the parasympathetic chain that innervates the heart is called the vagus nerve. It slows and relaxes the heart whereas the sympathetic branch accelerates and constricts the heart. It is the imbalance of these two branches that is responsible for the vast majority of heart disease. Using heart-rate variability monitoring, which gives a realtime, accurate depiction of the status of these two branches of the AN5, it has been shown in four studies that patients with ischemic heart disease have, on average, a reduction of parasympathetic activity of more than a third. Typically, the worse the ischemia, the lower the parasympathetic activity (5/134). Furthermore, about 80% of ischemic events have been shown to be preceded by significant, often drastic, reductions in parasympathetic activity related to physical activity, emotional upset, or other causes." This finding contrasts with others that show that people who have normal parasympathetic activity, then have an abrupt increase in sympathetic activity (physical activity, or often an emotional shock), never suffer from ischemia. In other words, without a preceding decrease in parasympathetic activity, activation of the sympathetic nervous system does not lead to MI.7 Presumably, we are meant to have times of excess sympathetic activity: that is normal
Heart Attacks
life. What's dangerous to our health is the ongoing, persistent decrease in our parasympathetic, or liferestoring, activity. This decrease in parasympathetic activity is mediated by the three chemical transmitters of the parasympathetic nervous system: acetylcholine, NO, and cGMP. This is where it becomes fascinating, for it has been shown that women have stronger vagaI activity than men, probably accounting for the sex difference in the incidence of MI.8 Hypertension causes a decrease in vagal activity, smoking causes a decrease in vagal activity, diabetes causes a decrease in vagaI activity, and physical and emotional stressalso causes a decrease in parasympathetic activitv.":" 50 ali the significant risk factors have been shown to downregulate the activity of the regenerative nervous system in the heart. On the other hand, the main drugs used in cardiology - nitrates stimulate NO (nitrous oxide) production, which upregulates the parasympathetic nervous system. Aspirin and statin drugs also stimulate the production of ACH and O, two of the principal mediators of the parasympathetic nervous system (until they cause a rebound decrease in these substances, which then makes the parasympathetic activity even worse). Finally, B blockers are called B-blockers because they block the activity of the sympathetic nervous system. To summarize, the risk factors and interventions that have actually been borne out through time ali help balance the AN5. Whatever their effect on plaque and stenosis development is of minor relevance. 50, what is the sequence of events that leads to an MI? First, and in the vast majority of cases the pathology wi II not proceed unless this condition is met, there is a decreased tonic activity of the parasympathetic nervous system. Then comes an increase in the sympathetic >
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> nervous system actrvity, usually a physical or emotional stressor, which raises adrenaline production, which directs the myocardial cells to break down glucose using aerobic glycolysis (remember, no change in blood flow as measured by the p02 in the cells has occurred). This development redirects the metabolism of the .heart away from its preferred and most efficient fuel source, which is ketones and fatty acids. This explains why heart patients often feel tired before their events. This also explains why a high-fat, low-glucose diet is crucial for heart health. As a result of the sympathetic increase and resulting glycolysis, a dramatic increase in lactic acid production occurs in the myocardial cells. This happens in virtually 100% of Mls, with no coronary artery mechanism required.P-" As a result of the increase in lactic acid in the myocardial cells, a localized acidosis occurs. This acidosis causes the calcium to be unable to enter the cells, making the cells less able to contract." This inability to contract causes localized edema, dysfunction of the walls of the heart (called hypokinesis, the hallmark of ischemic disease as seen on stressechoes and nuclear thallium stress tests), and eventually necrosis of the tissue, which we call an MI. The localized tissue edema also alters
the hemodynamics of the arteries embedded in that section of the heart, causing the sheer pressure that ruptures the unstable plaques, which further blocks the artery and worsens the hemodynamics in that area of the heart. Only this explanation tells us why plaques rupture, whattheir role in the MI process is, and when and how they should be addressed; that is, only in the most critical, acute situations. Only this explanation accounts for ali the observable phenomena associated with heart disease. The true origin of heart disease could not be more clear. The final question is, why is this understanding of heart disease relevant, besides being of academic interest? The first and obvious answer isthat if you don't know the cause, you can't find the solution. The solution is to protect our parasympathetic activity, use medicines that support it, and nourish the heart with what it needs. Nourishing our parasympathetic nervous system is basically the same as dismantling a way of life for which humans are ill suited. This way of life, in my view, is otherwise known as industrial civilization. The known things that nourish the parasympathetic nervous system are contact with nature, loving relations, trust, economic security (a hallmark of indigenous peoples the world over), and sex - in a sense, a whole new world. The medicine aspects of the that supports ali parasympathetic
Dr. Tom Cowan discovered lhe work of lhe two men who would have lhe rnost influence on his career while leaching gardening as a Peace Corps volunleer in Swaziland, South Africa. He read Nulrition and Physical Degeneration, by Weslon Price, and a fellow volunteer explained lhe arcane principies 01 Rudolf Steiner's biodynamic agriculture, These events inspired him 10 pursue a medical degree. Tom graduated from Michigan State University College of Human Medicine in 1984. After his residency in family practice at Johnson City Hospital in Johnson City, New York, he seI up an anthroposophical medical practice in Pelerborough, New Hampshire. Dr. . Cowan relocated 10 San Francisco in 2003.
Dr. Cowan has served as vice presidenl of lhe Physicians Associalion for Anthroposophical Medicine and is a lounding board member of lhe Weslon A. Price Foundation. During his career he has studied and written about many subjects in medicine. These include nutrition, horneopathv, anthroposophical medicine, and herbal medicine. He is lhe principal author of lhe book The Fourfold Palh 10 Hea/ing, which was published in 2004 by New Trends . .. Publishing, and is lhe coauthor of The Nourishing Traditions Book of Baby and Cbttd Care, publtshed m 2013. He writes lhe' Ask lhe Doctor" column in Wise Traditions in Food Farming and the Hea/ing Arts, lhe foundation's quarterly magazine, and has lectured throughout lhe US and Carrada. He has three grown children and currently practices medicine in San Francisco, where he resides with his wife, Lynda Smith Cowan. Dr. Cowan sees patients aI his office in San Francisco, does long-distance consults by telephone, and IS acceptmg new patrents, He also gives lectures and presentations,
nervous system is a medicine from the strophanthus plant called ouabain, or g-strophanthin. G-strophanthin is an endogenous hormone made in the adrenal cortex from cholesterol, whose production is inhibited by statin drugs, that does two things that are crucial for heart health and are done by no other medicine. First, it stimulates the production and liberation of ACH, the main neurotransmitter of the parasympathetic nervous system. Second, and crucially, it converts lactic acid - the main metabolic poison in this process - into pyruvate, one of the main and preferred fuels of the myocardial cells. In other words, it converts a "poison" into a nutrient. Perhaps this "magic" is why Chinese medicine practitioners say that the kidneys (i.e., adrenals, where ouabain is made) nourish the heart. In my years of using ouabain in my practice, I have not had a single patient who had an MI while taking it. It is truly the gift to the heart. Finally, this understanding of heart disease leads us to the correct diet, one that is loaded with healthful fats and fat-soluble nutrients, and is low in the processed carbohydrates and sugars that are the hallmark of industrial, civi Iized Iife.
Notes 1. Doerr W et al, Berlin-Heidelberg- ew York: Springer; 1974 2. Baroldi G, Silver M. The Etiopathogenesis of Coronary Hesn. Disease: A Heretica/ Theory Based on Morph%gy. Eurekah.com; 2004. 3. Helfant, RH, Forre51er JS, Hampton JR, Haft JI, Kemp HG, Gorlin R. Coronary heart disease. Differential hemodynamic, metabolic and electrocardiographic effects in subjects with and without angina during atrial pacing. Circu/ation. 1970;42:601-610. 4. Sroka K. On the genesis of myocardial ischemia. Z Csrdiol. 2004;93:768-783. doi:10.1oo7/soo392-0040137-6. S. Takase 8 et al. Heart rate variability in patients with diabetes mellitus, ischemic heart disease and congestive heart fallure J E/ectrocardio/. 1992;25:79-88. 6. Sroka. Op cit. 7. Sroka K et a!. Heart rate variability in myocardial ischemia during daily life. J Electrocardio/. 1997;30:45-56 8. Sroka. Op cit. 9. Sroka. lbid. 10. Sroka. lbid. 1L Sroka. lbid. 12. Sroka. lbid. 13. Sroka. lbid. 14. Scheuer J et aI. Coronary insufficiency: relations between hemodynamic, electrical, and biochemlcal parameters. Circu/ation Res. 1965;17:178-189. 15. Schmidt PG et al, Regional choline acetyltransferase activity in the guinea pig heart. Circuieuon Res. 1978;42:657-660. 16. Katz AM. Effects of ischemia on the cardiac contractile proteins. Cerdiolog». 1972;56:276-283. •

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