Real Cause of Heart Attack - Heart is Not a Pump

January 13, 2016

In writing this article, I am indebted to the work of Dr. Kunt Sroka and his website http://heartattacknew.com.  The video in this website shows how the collateral circulation nourishes the heart even with a severe blockage of coronary artery.  If you watch the video and go to the FAQ (http://heartattacknew.com/faq/) it becomes clear.

 

In fact, the view that the court coronary arteries supply all the blood to the heart is completely wrong.  Starting soon after birth, the normal heart develops and extensive network of small blood vessels called collateral vessels that eventually compensate for the interruption of flow an any one (or more) of the major vessels.  As Sroka correctly points out in the above video, coronary angiograms fail to show the collateral circulation; furthermore the procedure creates spasms in the coronary arteries through the injection of heavy dye under high pressure.  Thus, coronary angiograms are notoriously inaccurate at assessing the amount of stenosis in the vessels as well as the true blood low in the heat.  

 

To this day, most of the bypass, stents, and angioplasties are performed on minimally symptomatic patients who show a greater than 90 percent blockage in one or more coroner artery.  These arteries are almost always fully collateralized; it is not the surgery that restores blood flow, because the body has already done its won bypass.

 

Unblocking the stenosis, which as the video on heartattacknew.com shows, does not actually improve blood flow.  It is no wonder that in study after study, these procedures fail to provide any significant benefit to the patients.  Thus conventional cardiology is abandoning the stable plaque model in favor of a different model for the etiology: unstable plaque theory.

 

Defendants of this theory point to angiogram studies that show the changes in these unstable plaques, claiming them as proof that unstable plaque is the true cause of the majority of MIs (Myocardial Infarctions).  This acute thrombosis does happen in patients having heart attacks, but it is a consequence, not the cause of the MIs.

 

Observations that puts into doubt the relevance of the coronary artery theory of heart attack is the fact that proposed etiological mechanism of how thromboses arteries cause ischemia is through cutting off the blood supply and thereby the oxygen supply to the tissues.  To the enormous surprise of many investigators, the reality is that when careful measurements are done assessing the oxygen level of the myocardial cells, there is no oxygen deficit ever shown in an evolving heart attack.  The oxygen levels (measured as pO2) do not change at all throughout the entire event.  

 

The question must be asked: if this theory is predicated on the lowering of the oxygen levels in the myocardial cells when in fact the oxygen levels don't change, then what exactly does happen?  The conclusion is that while thrombosis associated with MI is a real phenomenon, it does not occur in more than 50% of cases - which leads to the question: why do the other 50%, those without an occlusion in the coronary arteries, even have a heart attack?

 

Any theory as to what causes myocardial ischemia must account for some consistent observations over the past fifty years.  The most consistent risk factors for a person having heart disease are male sex, diabetes, cigarette sue and psychological of emotional stress.  Interestingly, in none of these is there a direct link to pathology of the coronary arteries - diabetes and cigarette use causes disease in the capillaries, not in the large arteries (as far as we know).  

 

Also, we have learned over the past decades that the four main medicines of modern cardiology      beta-blockers, nitrates, aspirin, and statin drugs      all provide some benefits for heart patients and this observation must be accounted for in any comprehensive theory of myocardial ischemia.

 

The real revolution in the prevention and treatment of heart disease will come with increased understanding of the role played by the autonomic nervous system in the genesis of ischemia and its measurement through the tool of heart rate (HRV).  

 

The autonomic nervous system is divided into two branches.  The sympathetic ("fight-or-flight") system is centered in our adrenal medulla; it uses the chemical adrenaline as its chemical transmission device and tell our bodies there is danger.  The centerpiece of which are the glycolytic pathways, which accelerate the breakdown of glucose to be used as quick energy as we make our escape from the bear chasing us.  

 

In contrast, the parasympathetic ("rest-and-digest") branch , centers in the adrenal cortex, uses the neurotransmitters acetylcholine (ACh), nitric oxide (NO), and cyclic guanosine monophosphate (cGMP) as its chemical mediators.  The particular nerve of the parasympathetic chain that supplies the heart with nervous activity is called the vagus nerve.

 

I believe it can be shown that in imbalance in the two branches is responsible for the vast majority of heart disease.  

 

Using the techniques of heart rate variability (HRV) monitoring, which gives a real time accurate depiction of autonomic nervous system status, researchers have shown in multiple studies that patients with ischemic heart disease have on average a reduction of parasympathetic activity of over one-third.  About 80% of ischemic events are preceded by a significant reduction in parasympathetic activities.  By contrast, those with normal parasympathetic activity, who experience an abrupt increase in sympathetic activity (such as  physical activity or an emotional shock), never suffer from ischemia.

 

Presumably we are meant to experience times of excess sympathetic activity; this is normal life, with its challenges and disappointments. These shocks only become dangerous to our health in the face of an ongoing persistent decrease in our parasympathetic (life-restoring) activity.  It is fascinating to note that women have stronger vagal activity than men, probably account for the sex difference in the incidence of MI.  

 

Hypertension causes a decrease in vagal activity, smoking causes a decrease in vagal activity, diabetes causes a decrease in vagal activity, and physical and emotional stress causes a decrease in parasympathetic activity.  All the significant risk factors suppress the regenerative nervous system activity in our heart.  On the other hand the main drugs used in cardiology up-regulate the parasympathetic nervous system.

 

Nitrates stimulate NO production.  Aspirin and statin drugs also stimulate the production of ACh along with NO (until they cause a rebound decrease in these substances).  Beta-blockers work by blocking the activity of the sympathetic nervous system.  The bottom line: the risk factors for heart disease and the interventionsused all affect the balance in our ANS.

 

How Heart Attacks Occur

● First comes a decrease in healing activity of the parasympathetic nervous system- in the vast majority of cases the pathology for heart attack will not proceed unless this condition is met.

 

● Then comes and increase in sympathetic nervous system activity.  This increase in sympathetic activity cannot be balanced because of chronic parasympathetic suppression.  The result is an uncontrolled increase of adrenaline,  which directs the myocardial cell to break down glucose using aerobic glycolysis.  This step shunts the metabolism of the heart away from its preferred and most efficient fuel sources, which are ketones and fatty acids.

 

● 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 heart attacks, with no coronary mechanism requires).  As a result, localized acidosis occurs.  This acidosis prevents calcium from entering the cells, making the cells less able to contract.

 

● This inability to contract causes localized edema, dysfunction of the wall of the heart, and eventually necrosis of the tissue - in other words, a heart attack.  The localized tissue edema also alters the hemp-dynamics of the arteries embedded in that section of the heart, resulting in shear pressure, which causes the unstable plaques to rupture, further block the artery.

 

Please note that this explanation alone explains why plaques rupture, what their role in the heart attack process is, and why they should indeed be addressed.

 

 

About the Author

Dr. Cowan has served as VP of the Physicians Association for Anthroposophical Medicine and is a founding board member of the Weston A Price Foundation.  He is a principal author of The Fourfold Path to Healing and is co-author of The Nourishing Traditions Book of Baby and Child Care.

 

Source: Natural Health Information Article by Dr. Joseph Mercola

http://www.mercola.com

 

 

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