Contrary to popular belief, no specific correlation has been found between clogged arteries and fatal heart attacks in autopsy studies. Stringent clinical observations have documented that plaque build-up in coronary arteries and incidences of myocardial infarction (heart attacks) occur for very different and unrelated reasons. This raises an obvious question about the need for heart bypass operations, which are expensive, painful, and far more common in the United States than any other nation. In fact, there were over 500,000 coronary bypass procedures in the U.S. in the year 2000 with costs ranging from $40,000 to $60,000. This means that we may be spending $25 billion dollars each year for no appreciable benefit.
Coronary Artery Bypass Surgery
Coronary artery bypass surgery is based upon the belief that patching leg veins around occluded (blocked) arteries will improve blood flow and prevent heart attacks. The interesting thing is that, when left alone, the body performs its own version of bypass surgery to keep the heart supplied with blood. As arteries become occluded, the body generates a series of new blood vessels, called collaterals, that bypass blockages to join the heart.
Collateral artery provides blood to occluded artery:
Above: coronary anastomoses or collaterals. A) intercoronary ventricular and (B), atrial. C) homocoronary anastomoses. Note the innumerous collaterals joining different intramural branches at any level of their course. They have frequently a corkscrew aspect (D) visible also histologically (E), as adaptation to cardiac contraction-relaxation cycle.
This isn’t common knowledge because collaterals don’t show up clearly on x-rays, but Professor Giorgio Baroldi of the Armed Forces Institute of Pathology in Washington developed a technique to make these collaterals visible, revealing the entire structure of blood vessels in the heart. His research helps explain why autopsy data is inconsistent when it comes to arterial blockages and heart attacks.
Some of the autopsies in question were performed by Dr. Berthold Kern of Germany in the 1930s and 1940s. Dr. Kern observed that the findings of these autopsies did not substantiate the coronary obstruction hypothesis. Instead, he found that heart attacks occur in patients without significant obstruction of the coronary arteries. A separate study spanning twenty-five years showed that only 25% of patients who died from a severe heart attack had arterial blockage, with the remaining 75% lacking arterial blockages.  Additionally, in 1980, the journal Circulation reviewed 100 patients who had a confirmed death from myocardial infarction and concluded as follows: “These data support the concept that an occlusive coronary thrombus has no primary role in the pathogenesis of a myocardial infarct” . In other words, a blockage in the coronary artery is not the cause of heart attacks.
The process of angiogenesis (growth of new blood vessels) ensures sufficient blood flow to the heart, despite the occurrence of coronary artery blockages. This process is natural and essentially makes a heart bypass operation unnecessary. Another study, published in the April 1, 1988 issue of The American Journal of Cardiology, confirmed the work of Dr. Kern. The results once again challenged the widely held belief of the coronary artery blockage theory. 
In an editorial, Dr. Stephen Epstein of the National Heart, Lung and Blood Institute summarized the findings of the authors by stating the following: “They found that in an advanced state of the narrowing of the coronary arteries, the supply of blood to the heart muscles is fully assured via collaterals that enlarge naturally in response to the blockage. Interestingly they observed that the more the coronaries narrow, the less danger there is of heart infarction.” Research has also shown that arterial blockages often occur after a heart attack but prior to death. In fact, the longer the time between an acute heart attack and death, the more likely a blockage will occur and the greater the obstruction. Therefore, the blockage is a consequence of the heart attack, not the cause. .
What Really Causes Heart Attacks?
In the 1940’s, Dr. Kern proposed his own hypothesis on the cause of heart attacks, which he believed to be a metabolic disorder known as metabolic acidosis.
Metabolic acidosis is a destructive process that involves the accumulation of lactic acid in the left ventrical of the heart, depriving it of oxygen and energy in the form of ATP (Adenosine triphosphate). Insufficient oxygen and ATP in tissue causes cell apoptosis (programmed cell death) of the heart tissue, resulting in a “heart attack,” while the lactic acid is responsible for pain felt during the event.
Lactic acid is a natural metabolic waste product of energy metabolism in the muscles. Provided there is sufficient oxygen and energy in the form of ATP, the muscle cells can convert lactic acid into pyruvate, and in turn produce more ATP. Any condition that impairs available ATP or oxygen will increase the risk of metabolic acidosis, and the risk of heart attack.
As to the root cause, metabolic acidosis is the result of an underactive thyroid. The thyroid gland affects the respiration of all cells in the body and when it’s not functioning properly, cells do not properly utilize oxygen. This inhibits the oxidation of organic acids, allowing them to build up and change the body’s pH. The process involves the release of lysosomal and cytosolic enzymes, causing a breakdown in tissue and eventual heart attack. 
This is often the case when you hear about a college athlete or marathon runner dropping dead from a heart attack. These people may have a heart defect, but many times it’s simply that their body has reached beyond its aerobic capacity, resulting in acidification of the left ventricle and damage to heart tissue.
Preventing Heart Attacks
Invariably, a person at greatest risk for heart attacks will have a thyroid condition, although often without official diagnosis. One easy test for thyroid health is whether you suffer from diabetes (all type 2 diabetics have impaired thyroid function) or have blood sugar problems.
Treating Metabolic Acidosis
Dr. Kern determined that the decline in pH can be averted and fully restored in the heart muscle, preventing metabolic acidosis and fatal heart attacks, through the oral use of ouabain, also known as strophanthin gratus, a cardiac glycoside that can raise the body’s pH. Cardiac glycosides can be produced in the body, as oubain is, or ingested from a plant called strophanthin gratus. When produced in the body, cardiac glycosides function as a hormone which is secreted from the adrenal glands, activating tissue proliferation and heart contractility. 
In the following chart, you can see Dr. Kern’s results with strophanthin gratus. The first two columns show heart attacks in patients using strophanthin gratus and the second two show expected heart attacks for the patient population.
Dr. Kern treated over 15,000 patients suffering from heart conditions between 1947 and 1968 with oral strophanthin gratus. During this time, no patients experienced fatal heart attacks and only 20 had non-fatal heart attacks. Many of these patients already exhibited a history of heart attacks prior to the study and, based upon government statistics, the population should have experienced 120 fatal and 400 non-fatal heart attacks during that time.
Strophanthin gratus has been used extensively in Germany with very positive results from several thousand doctors prescribing it for oral use. Based on a survey of 3,645 physicians spanning from 1976 to 1983, all comments were positive . It is commonly believed that cardiac glycosides, such as strophanthin gratus, block the action of the sodium pump. However, such is not the case in small doses, only large doses. In small doses, strophanthin gratus improves the action of the sodium pump,  which is important, as can be seen in our salt article. Although strophanthin gratus is a simple, effective treatment, it is important to note that the best way to prevent a heart attack is by improving thyroid function and aerobic capacity. Please note that injecting strophanthin gratus creates the opposite effect, therefore strophanthin gratus should only be used orally.
How to Use Strodival (strophanthin gratus)
Take Strodival on an empty stomach. In case of an emergency or for immediate effect, it can be crushed and chewed to assure maximum absorption through the mucous membrane. Strodival has no known side effects, see label for further information on usage and dosing. Strodival (G-Strophanthin/Ouabain) can be purchased at http://www.
Other Risk Factors for Heart Attacks
Dr. Edzard Ernst at the University of Vienna recognized another important risk factor for heart attack – thick blood. Observing patients suffering from recurring myocardial infarctions over the years in a rehabilitation center in southern Germany, he realized that the risk for heart attacks was highest in those with the most viscous blood. Dr. Ernst determined that after a heart attack there is severe deterioration of the flow properties of blood, and that blood thickness and the clumping of red blood cells are relative to the increased risk of heart attack . Therefore, if blood viscosity can be reduced, the risk of heart attack will also be lessened. An accurate way to measure viscous blood is to check fibrinogen levels. Studies have indicted that fibrinogen is pathophysiologically related to cardiovascular events .
How to fix viscous blood
How does one improve blood flow? Enter Nattokinase. Nattokinase is an enzyme extracted from Japanese natto, which is a fermented soybean delicacy made from a culture of Bacillus subtilis. Researchers hypothesized that nattokinase could reduce certain factors of blood clotting that are associated with an increase risk for cardiovascular disease. An open-label, self-controlled clinical trial was conducted on three groups of subjects: healthy volunteers, patients with cardiovascular risk factors, and patients undergoing dialysis. All groups ingested two capsules of nattokinase, containing 2000 fibrinolysis units, daily for two months. At the conclusion of the study, nattokinase positively reduced fibrinogen factors in all groups.  This is significant because high fibrinogen levels are an indication of thickened blood.
Dosage: Two 2,000 fibrinolytic unit capsules of nattokinase per day.
Another fix for viscous blood can be found in the supplement, ecklonia cava, which is a potent inhibitor of antiplasmin. Plasmin is a natural anti-clotting protein that helps to prevent viscous blood.
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