What Causes Heart AttacksIn this article, I lay out the case

that the spectrum of heart diseasethat includes angina, unstable angina,and myocardial infarction (heartattack) is better understood from theperspective of events happening inthe myocardium (heart) as opposedto events in the coronary arteries (thearteries that supply the heart). As weali know, the conventional view ofthe cause of heart disease is that thecentral events occur in the arteries.In this article, I will go into moredetail about why the conventionaltheory is largely misleading, and thenI will describe the precise and well-documented events that do lead toheart attacks.

This new understanding is crucialbecause, as the past 50 or 50 yearshave shown, pursuing the coronary-artery theory has cost th is nationbillions of dollars in surgical costs -most of which are unnecessary - andbillions in medications that cause asmuch harm as any benefits, and hasled many people to adopt a low-fat dietand which only worsens the problem.In contrast, by understanding the realpathophysiological events behindthe evolution of Mls, we will be ledto a proper "Nourishing Traditions"-style diet, the use of the safe andinexpensive medicine g-strophanthin,and rnost important, we will be forcedto look at how heart disease is a truemanifestation of the cost of modernlife to human health. To overcomethe epidemic of heart disease, weneed a new medical paradigm, anew economic system, and a newecological consciousness; in short,a new way of life. The coronarytheory misses ali of this, just as it

by Dr. Thomas Cowanmisinterprets the actual pathologicalevents. .

In writing this article, I am indebtedto the work of Dr. Knut Sroka andhis website www.heartattacknew.com. For ali who are interested inthis important subject, it is advisedto read the entire website and watchthe video on the website. For healthprofessionals and researchers, yourunderstanding of this subject isincomplete without reading andstudying two items found in theprint version of the website: TheEtiapathagenesis oi Caronary HeartOisease: A Heretical Theory 8ased anMarphalagy, by G. Baroldi, and "Onthe Genesis of Myocardial Ischemia,"by Sroka.

Rebuttal of the Conventional TheoryUntil recently, it was thought that

most Mls were caused by progressiveblackage created by plaque buildupin the major arteries leading ta theheart (there are four major coronaryarteries). The plaque was thought tobe cholesterol buildup in the arteriallumen (inside of the vessel), whicheventually cut off blood supply toa certain area of the heart, resultingin oxygen deficiency in that area,causing first pain (angina), thenprogressing to ischemia (heart attack).The simple solution was to unblockthe stenosis (blockage) with either anangioplasty or stent, or, if that wasnot possible, to bypass the area withcoronary bypass grafting (CABG).Simple problem, simple solution.

However, problems becameapparent through a number ofavenues. First, a story related by acardiologist at a Northern California

heart symposium, at which I was aspeaker, points to the first problem.He told us that during his residencyhe was part of a trial conducted inrural Alabama with black men. Inth is trial, angiograms (injections ofdye into the coronary arteries todetect blockages) were done on alithe men presenting with chest pains.For the ones who had a single arteryblocked, no treatment was prescribed,and the researchers predicted in theirnotes which part of the heart wouldhave a subsequent heart attack ifone occurred. Of course, they alipredicted that it would be in the partof the heart supplied by the blockedcoronary artery. Then they waited.

Eventually, many of the men didreturn and did have Mls, but to theresearchers' surprise, less than 10%had a heart attack in the area of theheart supplied by the original blockedartery.

Second, a large study conductedin 2003 by the Mayo Clinic on theefficacy of bypasses, stents, andangioplasty concluded that:

a. bypass surgery relieves symptoms(chest pain);

b. bypass surgery does not preventfurther heart attacks;

c. only high-risk patients, thosewhose lives are in acute danger,benefit from bypass surgerywith regard to a better chance ofsurvival.

In other words, the gold standardfor treating arterial blockages has,at best, only minimal benefits.If you watch the video on theheartattacknew.com website andgo to the FAQ called "The Riddle's

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of Mls was done in Heidelberg inthe 19705.1 The conclusion was thatthrornbosis sufficient to cause theMI was found in only 20% of cases.Saroldi, in the largest such study everdone, found sufficient thrombosisin 41 % of cases.' He also found thatthe larger the area of the MI, themore often a stenosis was present,and the longer the time between MIand death, the higher the percentageof stenosis. These two facts allowsome researchers to "cherry-pick" thenumbers and make the stenosis ratehigh, as they choose to study onlythose with large Mls and who live thelongest after the MI event. Later in thisarticle, I will explain how the stenosiscomes about as a consequence of theMI.

Another observation that castsdoubt on the relevance of thecoronary artery theory of MI has to dowith the proposed mechanism of howthrombosed arteries cause ischemia,which is by cutting off the bloodsupply and thereby the oxygen to thetissues. The real ity is that when carefulmeasurements are done assessing thep02 (oxygen levei) of the myocardialcells during an MI, to the hugesurprise of many, there is no oxygendeficit ever shown in an evolvingMI.3 The p02 levels do not changeat ali throughout the entire event. Iwill come back to this later when Idescribe what does change in everyevolving MI ever studied. Again, thequestion must be asked, if this theoryis predicated on the lowering of thep02 in the myocardial cells, and infact the p02 doesn't change, thenexactly what did happen?

The conclusion is that thrombosisassociated with MI is a realphenomenon, but in no pathologicalstudy has it been found in morethan 50% of deaths, which raisesthe question, why did the other50% even have an MI? Second, it'sclear from ali pathology studies thatthrombosis of significant degreesevolve after the MI occurs, againleading to the question of whatcaused the MI in the first place. Thefact that thrombosis does occur also

Heart Attacks>Sol.ution," it becomes clear why thisis 50. Large, stable blockages - thoseover 90% - are in almost 100% ofthe cases completely compensated bycollateral blood vessels. In fact, theview that the heart gets its blood onlyfrom the four major vessels is itselffalse. Starting soon after birth, thenormal heart develops an extensivenetwork of small blood vessels calledcollateral vessels, which eventuallycompensate for the interruption offlow in any one (or more) of the majorvessels.

As Sroka correctly poi nts outin the video, coronary angiogram- by failing to show the collateralcirculation, and by creating spasmsin the coronary arteries through theinjection of heavy dye under highpressure - is notoriously inaccurateat assessing the amount of stenosis inthe vessels as well as the true bloodflow in the heart. To this day, most ofthe bypasses, stents, and angioplastiesare done on minimally symptomaticpatients who show a greater than90% blockage in one or morecoronary arteries. These arteries arealmost always fully collateralized; thesurgery does not restore blood flowbecause the body had ai ready doneits own bypass. Ask yourself: If it weretrue that an artery more than 90%blocked had no collateral circulation,how would that person still be alive?And does it really make sense thatthe eventual MI is caused when thestenosis goes from 93% to 98%?This is an insignificant differenceand is completely nonsensical. Yetthis is what most of the proceduresare meant to accomplish, to unblockthe stenosis, which, as the videoshows, actually has no blood-flowrepercussions. It is no wonder that instudy after study these procedures fai Ito provide any significant benefit topatients.

For these reasons, the stable-plaque model is being abandoned byconventional cardiology, in favor ofa different model for the etiology of

Mls, which, as it turns out, is almostequally invalid.

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Meet the Unstable Plaque50, we ali agree that the entire

focus of cardiology - the stable,progressing, calcified plaque, thething that we bypassed and stentedfor years, the thing that we do CTscans of your arteries for, the thingthat we told Vou is from cholesterolbuildup in your arteries, the thingthat "alternative cardiology," suchas the Ornish program, focused on- actually is not 50 important in theetiology of heart attacks. Don't worry,though. We know that the focus of theproblem must be the arteries, or 50conventional thinking goes. Therefore,enter the unstable, or friable, plaque.This insidious fellow doesn't actuallycreate a large blockage; rather, it'sa soft, "foamy" plaque that undercertain situations (we don't knowwhich situations) rapidly evolvesand abruptly closes off the involvedartery, creating a downstreamoxygen deficit, followed by angina,then ischemia. These soft plaquesare thought to be a combination ofinflammatory "buildup" and LDL, theexact two things targeted by statindrugs. Therefore, the thinking goes,because this type of plaque can buildup in anyone's arteries, at any time,everyone should be on statin drugs toprevent heart attacks. (Some peopleeven advocate putti ng therapeuticdoses of statins in municipal watersupplies.) Angiogram studies havebeen presented to show the evolutionof these unstable plaques as proof thatthey are the true cause of the majorityof Mls.

As I will show in the next section,acute thrombosis does happenin patients having Mls, but it is aconsequence, not the cause, of theMI. But how often does it actuallyhappen? Let's look at pathologystudies, which are the only accurateway to determine what actuallyhappened, as opposed to angiograms,which are misleading and create manyartifacts. The first major autopsy/pathology study of people who died

ains why emergency proceduresmber, the only patients who-t from bypass and stents areost critical, acute patients) canelpful immediately post-MI toe flow in those patients whoot have adequate collateralation to that part of their heart.

50 again, ali the existing theories as tothe relevance of the coronary arteriesin the evolution of the MI are fraughtwith inconsistencies.

If this is 50, what then does causeMls?

lhe Etiology of Myocardial IschemiaAny accurate theory of the cause

of myocardial ischemia must accountfor the risk factors most associated

_ with heart disease. These are: beingmale, having diabetes, smokingcigarettes, and experiencing chronicpsychological/emotional stress.

'Interestingly, none of these riskfactors directly link to pathology ofthe coronary arteries. Diabetes andcigarette use cause disease in thecapillaries, not the large vessels, andstress has no direct effect on coronaryarteries that we know of.

In addition, during the pastfive decades or 50, the four mainmedicines of modern cardiology -B-blockers, nitrates, aspirin, and statindrugs - ali have some benefits forheart patients (albeit ali with seriousdrawbacks as well), which must beaddressed in any comprehensivetheory of myocardial ischemia, whichI will attempt to do here.

The real revolution to come inthe prevention and treatment ofheart disease has been inauguratedthrough our understanding of therole of the autonomic nervous systemin the genesis of ischemia and itsmeasurement through the tool ofheart-rate variability. First, some briefbackground. We have two distinctnervous systems. The first, the centralnervous system, controls consciousfunctions such as rnuscle and nervefunction. The second nervoussystem is called the autonomic (orunconscious) nervous system (AN5),which controls the function of ourinternal organs. The autonomic

nervous system is divided into twobranches, which in health are alwaysin a balanced but ready state. Thesympathetic, or fight-or-flight, systemis centered in our adrenal medullaand uses the chemical adrenalineto tell our bodies that danger isafoot, it's time to run. It does so byactivating a series of biochemicalresponses, the center of which are theglycolytic pathways that acceleratethe breakdown of glucose to be usedas quick energy 50 that we can makeour escape.

In contrast, the parasympatheticbranch, centered in the adrenalcortex, 15 the rest-and-digestarm of the autonomic nervoussystem. The particular nerve of theparasympathetic chain that innervatesthe heart is called the vagus nerve. Itslows and relaxes the heart whereasthe sympathetic branch acceleratesand constricts the heart. It is theimbalance of these two branches thatis responsible for the vast majority ofheart disease.

Using heart-rate variabilitymonitoring, which gives a real-time, accurate depiction of thestatus of these two branches of theAN5, it has been shown in fourstudies that patients with ischemicheart disease have, on average, areduction of parasympathetic activityof more than a third. Typically, theworse the ischemia, the lower theparasympathetic activity (5/134).Furthermore, about 80% of ischemicevents have been shown to bepreceded by significant, often drastic,reductions in parasympatheticactivity related to physical activity,emotional upset, or other causes."This finding contrasts with others thatshow that people who have normalparasympathetic activity, then havean abrupt increase in sympatheticactivity (physical activity, or oftenan emotional shock), never sufferfrom ischemia. In other words,without a preceding decrease inparasympathetic activity, activationof the sympathetic nervous systemdoes not lead to MI.7 Presumably,we are meant to have times of excesssympathetic activity: that is normal

Heart Attacks

life. What's dangerous to our healthis the ongoing, persistent decreasein our parasympathetic, or life-restori ng, activity. Th is decrease inparasympathetic activity is mediatedby the three chemical transmitters ofthe parasympathetic nervous system:acetylcholine, NO, and cGMP. Thisis where it becomes fascinating,for it has been shown that womenhave stronger vagaI activity thanmen, probably accounting for thesex difference in the incidence ofMI.8 Hypertension causes a decreasein vagal activity, smoking causes adecrease in vagal activity, diabetescauses a decrease in vagaI activity,and physical and emotional stressalsocauses a decrease in parasympatheticactivitv.":" 50 ali the significantrisk factors have been shown todownregulate the activity of theregenerative nervous system in theheart.

On the other hand, the maindrugs used in cardiology - nitrates

stimulate NO (nitrous oxide)production, which upregulates theparasympathetic nervous system.Aspirin and statin drugs also stimulatethe production of ACH and O,two of the principal mediators of theparasympathetic nervous system (untilthey cause a rebound decrease inthese substances, which then makesthe parasympathetic activity evenworse). Finally, B blockers are calledB-blockers because they block theactivity of the sympathetic nervoussystem. To summarize, the riskfactors and interventions that haveactually been borne out through timeali help balance the AN5. Whatevertheir effect on plaque and stenosisdevelopment is of minor relevance.

50, what is the sequence of eventsthat leads to an MI?

First, and in the vast majority ofcases the pathology wi II not proceedunless this condition is met, thereis a decreased tonic activity of theparasympathetic nervous system. Thencomes an increase in the sympathetic

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Heart Attacks>nervous system actrvity, usually aphysical or emotional stressor, whichraises adrenaline production, whichdirects the myocardial cells to breakdown glucose using aerobic glycolysis(remember, no change in blood flowas measured by the p02 in the cellshas occurred). This developmentredirects the metabolism of the

. heart away from its preferred andmost efficient fuel source, whichis ketones and fatty acids. Thisexplains why heart patients often feeltired before their events. This alsoexplains why a high-fat, low-glucosediet is crucial for heart health. As aresult of the sympathetic increaseand resulting glycolysis, a dramaticincrease in lactic acid productionoccurs in the myocardial cells. Thishappens in virtually 100% of Mls,with no coronary artery mechanismrequired.P-" As a result of the increasein lactic acid in the myocardialcells, a localized acidosis occurs.This acidosis causes the calcium tobe unable to enter the cells, makingthe cells less able to contract." Thisinability to contract causes localizededema, dysfunction of the walls ofthe heart (called hypokinesis, thehallmark of ischemic disease as seenon stress echoes and nuclear thalliumstress tests), and eventually necrosisof the tissue, which we call an MI.The localized tissue edema also alters

the hemodynamics of the arteriesembedded in that section of theheart, causing the sheer pressure thatruptures the unstable plaques, whichfurther blocks the artery and worsensthe hemodynamics in that area of theheart. Only this explanation tells uswhy plaques rupture, whattheir role inthe MI process is, and when and howthey should be addressed; that is, onlyin the most critical, acute situations.Only this explanation accounts for alithe observable phenomena associatedwith heart disease. The true origin ofheart disease could not be more clear.

The final question is, why isthis understanding of heart diseaserelevant, besides being of academicinterest? The first and obvious answeris that if you don't know the cause, youcan't find the solution. The solutionis to protect our parasympatheticactivity, use medicines that supportit, and nourish the heart withwhat it needs. Nourishing ourparasympathetic nervous system isbasically the same as dismantling away of life for which humans are illsuited. This way of life, in my view,is otherwise known as industrialcivilization. The known things thatnourish the parasympathetic nervoussystem are contact with nature, lovingrelations, trust, economic security (ahallmark of indigenous peoples theworld over), and sex - in a sense, awhole new world.

The medicineaspects of the

that supports aliparasympathetic

Dr. Tom Cowan discovered lhe work of lhe two men who would have lhernost influence on his career while leaching gardening as a Peace Corpsvolunleer in Swaziland, South Africa. He read Nulrition and PhysicalDegeneration, by Weslon Price, and a fellow volunteer explained lhearcane principies 01 Rudolf Steiner's biodynamic agriculture, These eventsinspired him 10 pursue a medical degree. Tom graduated from Michigan StateUniversity College of Human Medicine in 1984. After his residency in familypractice at Johnson City Hospital in Johnson City, New York, he seI up ananthroposophical 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 forAnthroposophical Medicine and is a lounding board member of lhe WeslonA. Price Foundation. During his career he has studied and written about manysubjects in medicine. These include nutrition, horneopathv, anthroposophicalmedicine, and herbal medicine. He is lhe principal author of lhe book TheFourfold Palh 10 Hea/ing, which was published in 2004 by New Trends

. .. Publishing, and is lhe coauthor of The Nourishing Traditions Book of Baby andCbttd Care, publtshed m 2013. He writes lhe' Ask lhe Doctor" column in Wise Traditions in Food Farming andthe Hea/ing Arts, lhe foundation's quarterly magazine, and has lectured throughout lhe US and Carrada. He hasthree grown children and currently practices medicine in San Francisco, where he resides with his wife, LyndaSmith 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 thestrophanthus plant called ouabain,or g-strophanthin. G-strophanthinis an endogenous hormonemade in the adrenal cortex fromcholesterol, whose production isinhibited by statin drugs, that doestwo things that are crucial for hearthealth and are done by no othermedicine. First, it stimulates theproduction and liberation of ACH,the main neurotransmitter of theparasympathetic nervous system.Second, and crucially, it convertslactic acid - the main metabolicpoison in this process - into pyruvate,one of the main and preferred fuels ofthe myocardial cells. In other words,it converts a "poison" into a nutrient.

Perhaps this "magic" is whyChinese medicine practitioners saythat the kidneys (i.e., adrenals, whereouabain is made) nourish the heart.In my years of using ouabain in mypractice, I have not had a singlepatient who had an MI while taking it.It is truly the gift to the heart.

Finally, this understanding ofheart disease leads us to the correctdiet, one that is loaded with healthfulfats and fat-sol uble nutrients, and islow in the processed carbohydratesand sugars that are the hallmark ofindustrial, civi Iized Iife.

Notes1. Doerr W et al, Berlin-Heidelberg- ew York: Springer;

19742. 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, KempHG, Gorlin R. Coronary heart disease. Differentialhemodynamic, metabolic and electrocardiographic effectsin subjects with and without angina during atrial pacing.Circu/ation. 1970;42:601-610.

4. Sroka K. On the genesis of myocardial ischemia. ZCsrdiol. 2004;93:768-783. doi:10.1oo7/soo392-004-0137-6.

S. Takase 8 et al. Heart rate variability in patients withdiabetes mellitus, ischemic heart disease and congestiveheart 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;30:45-568. Sroka. Op cit.9. Sroka. lbid.10. Sroka. lbid.1 L 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 acetyltransferaseactivity in the guinea pig heart. Circuieuon Res.1978;42:657-660.

16. Katz AM. Effects of ischemia on the cardiac contractileproteins. Cerdiolog». 1972;56:276-283.

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