Strophanthin Urtinktur Natur pur ( Strophanthus gratus) 120ml

Coronary artery disease is currently the leading cause of death in the United States.  Despite the increasing sophistication of surgical techniques, the introduction of new techniques such as balloon angioplasty, and a number of new drugs (e.g. beta blockers, calcium antagonists), it is estimated that over 1 million heart attacks will occur this year, resulting in 500,000 deaths.  In short, we do not have an adequate therapeutic solution to the problem of myocardial infarction (heart attack).

The cornerstone of therapy for treatment and prevention of myocardial infarction is to remove blockages in coronary arteries that are thought to be the cause of the infarction.  This adheres to the widely accepted coronary artery thrombosis theory of infarction; that is, arteries become clogged with plaque, damaged from such things as smoking or high cholesterol.  A clot forms a fissure in the plaque.  The clot may shut off the blood flow of the coronary artery, causing a heart attack.  It is deceptively simple:  The coronary arteries are clogged.  No blood can flow, so the muscles of the heart cannot be supported, and heart metabolism stops, leading to death.

In Germany, another theory of myocardial infarction has been proposed by Dr. Berthold Kern (1911-1995).  Dr. Kern, while performing autopsies in Germany in the 1930s and 1940s, observed that the findings of these autopsies did not corroborate the coronary obstruction hypothesis.  He began researching the literature, looking for clues as to an alternative etiology.  What he found was not only a new theory that may provide the missing piece of the coronary obstruction theory, but a therapy now being used by over 5000 physicians in Germany with reportedly remarkable success.

Dr. Kern’s claims, as set forth in his 1971 informational paper, Three Ways to Cardiac Infarction, can be summarized as follows:

1. The coronary obstruction theory cannot adequately explain observed facts.

2. The major etiologic factor underlying myocardial infarction is a primary chemical destructive process, cause by unchecked metabolic acidosis (accumulation of acid) in the left ventricular tissue and substantially unrelated to coronary artery disease.

3. The regular, clinical use of oral g-strophathin (a cardiac glycoside derived from the West African plant strophanthus gratus):

• Prevents lethal myocardial tissue acidosis, and thereby
• Substantially reduces the incidence of myocardial infarction and completely prevents infarction deaths.

Dr. Kern’s observations that most myocardial infarctions occur in patients without significant obstruction of the coronary artery supplying the infracted tissue finds great support in the American peer-reviewed literature.  Since 1948, over a dozen reports of post-mortem examination of infracted hearts have consistently failed to corroborate the coronary artery thrombosis theory of myocardial infarction.  That is, victims of fatal heart attacks have had no evidence whatsoever of coronary occlusion.

An example of the degree of non-confirmation can be ascertained by the following quote from a 1980 article on Circulation:

“These data support the concept that an occlusive coronary thrombus has no primary role in the pathogenesis of a myocardial infarct.” The reviewer went on to note, “These reports also present clear refutation of the most common explanation used today to dismiss autopsy findings which detect no coronary thrombi, i.e. that thrombi existed at infarction but have since lysed, embolized or washed away.”

There does not appear to be any literature that effectively refutes these autopsy findings.

Another source of inconsistent data are the many reports in the literature of myocardial infarction in patients without coronary artery disease, as deduced by normal coronary angiograms.  Other autopsy data has revealed widely scattered areas of necrotic tissue that produces a substantial incongruence between the area of infarction and the arterial supply.

In a 1988 editorial published in the New England Journal of Medicine titled “Twenty years of coronary bypass surgery,” Thomas Killip observed that “Neither the VA [Veterans' Administration] nor CASS [the National Institute of Health's Coronary Artery Surgery Study] has detected a significant difference in long-term survival between the two assigned treatment groups [surgical vs. medical] when all patients have been included…”

More recent work with coronary angioplasty and anti-thrombolytic agents has also failed to demonstrate any clear cut improvements in survival.

Dr. Kern went a step further.  In his review of the literature, he came across the notion of collaterals (or anastomoses), a finely-meshed network of small blood vessels that act as natural bypass channels in the heart muscle.  These collaterals have been made visible by Professor Giorgio Baroldi in studies at the Armed Forces Institute of Pathology.

Baroldi developed a technique for filling the arteries of the heart with artificial blood, a chemical substance that thickens in the blood vessels.  When later the tissues were dissolved in acid, the entire structure of blood vessels in the heart was revealed.  Kern hypothesized that bypass grafts were created naturally by the body via the collaterals whenever a coronary artery became blocked.  Therefore, heart bypass would be redundant to a large degree.

A study by Rentrop et al in the April 1, 1988 issue of The American Journal of Cardiology has produced results completely at odds with the coronary artery blockage theory, and consistent with Kern’s hypothesis.  In an accompanying editorial, Dr. Stephen Epstein of the National Heart, Lung and Blood Institute summarizes Rentrop and colleagues’ “extremely important observations.”  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.

Dr. Kern’s second claim, i.e. his proposed new theory of metabolic acidosis, can be summarized as follows: Metabolic conditions in the most healthy of hearts are, at best, marginal in the constantly beating left ventricle.  This is the part of the heart responsible for pumping blood to most of the body, the right ventricle merely supplying the lungs.  Oxygen and energy requirements are always perilously close to available supplies, and any of the several stressors may cause an oxygen/energy deficit, with deterioration in oxidative metabolism, and consequent development of acidosis.  Lack of oxygen sets off the process of zymosis or fermentation metabolism, an anaerobic process, in order to produce energy in the cells.  This, in turn, lowers the pH.

This lowering of the pH sets off a destructive chemical process, literally a suicide reaction of the cell.  Lysozymal enzymes are released, causing cell self-digestion.  This starts as a single point in the muscle, then many points, which eventually join to form a small area of necrotic tissue.  Finally, a critical mass is reached, no bigger than the head of a pin, which triggers larger and larger areas of damaged tissue, resulting in infarction (heart attack).

Ideally then, the remedy to address infarction would be a restoration of pH balance to the heart muscle, thereby preventing tissue damage and fatal infarction.  The problem Kern faced was how to accomplish this without causing positive inotropy [increasing the strength of the muscular contraction], i.e. without putting further stress on the contracting heart muscle itself.  The cardiac glycosides, including digitalis and the strophanthin byproduct known as ouabain, are known to produce such a deleterious effect, and this is why they are not effective against infarction.

This is where Kern made an important re-discovery.  In reviewing the literature, he came across the work of Dr. Edens, who in the 1920s had reported on a qualitatively different effect of strophanthin given intravenously versus orally.  Specifically, the positive inotropic effects [that is, increasing contraction] that accompanied intravenous administration were not observed with oral administration.

This important observation has been confirmed in a study by Belz published in theEuropean Journal of Clinical Pharmacology in 1984.  Utilizing a randomized, placebo-controlled, double blind methodology, the researchers found that the intravenousouabain (strophanthin) produced the expected increase in cardiac inotropy.  However, the investigators stated quite definitely that, “… the single sublingual (oral) dose of ouabain did not exert a positive inotropic effect.”

The postulated mechanism of action, based on animal research done by Adams, Powell and Erdmann, is that there are two receptors in the heart: “High affinity” and “Low affinity.”  It is thought that intravenous administration triggers low affinity receptors, and thus positive inotropy.  High affinity receptors, on the other hand, react to small concentrations of g-strophanthin via oral administration, thereby avoiding the dangerous effect of positive inotropy.

Dr. Kern reported results of his clinical practice in Stuttgart over the period 1947-1968 involving over 15,000 patients.  His patients treated with oral g-strophanthin experienced no fatal infarcts and only 20 non-fatal heart infarcts.  These patients included many suffering infarction prior to entering the study.  In contrast with these results, government statistics for the same time period would have predicted over 120 fatal heart attacks and over 400 non-fatal infarctions in a group of patients this size.

Currently, there are approximately 5000 M.D.s in Germany using and prescribing oral g-strophanthin.  The booklet Eine Dokumentation ambulanz-kardiologischer Therapie Ergebnisse nach Anwendung oralen g-strophanthin represents the results of a survey wherein 3645 medical doctors made statements on use of this remedy in their practices from 1976 to 1983.  Of these, 3552 gave exclusively positive testimony with no reservations.  No one gave a negative response.

In addition to accumulating clinical experience, a number of studies have demonstrated excellent results with oral g-strophanthin.  One fascinating report in a real-life setting took place at a German coal mine.  During the period 1972-1974, miners suffered episodes of acute chest pain 229 times.  Medical help was a two-hour ride away, and 11 miners died during this period.  From 1975-1980, all miners who experienced acute chest pain (280 episodes) were immediately given oral g-strophanthin.  During this period, which was twice as long as the comparison period, no miners died after the onset of symptoms.  No toxic side effects were observed.  Many variables were studied, i.e. age better access to treatment, different working conditions, etc to ensure comparability of observation periods.

A rigorous, double blind, randomized control study of oral g-strophanthin in the treatment of angina showed impressive results at statistically different levels.  After fourteen days, 81% of patients in the treated group experienced a reduction in attacks, while in the control group, 72% receiving placebos registered an increase in attacks.

In a study of 150 seriously ill heart patients, who altogether had 254 heart attacks, oral g-strophanthin was successful in 85% of the cases.  Dr. Dohrmann, who conducted the study, observed, “A positive result was registered when the severe heart attack abated at least five minutes after the g-strophanthin capsule was bitten through, and after ten minutes at the latest, they disappeared completely.”

A consistent feature of clinical reports using oral g-strophanthin is the absence of side effects.  The cost of this remedy, which is currently available to German physicians and their patients, is approximately $30 per month for typical use.

At this point, every indication suggests that oral g-strophanthin may be a significant breakthrough in the treatment and prevention of myocardial infarction.  What is needed is a definitive American clinical trial.

At an annual meeting of the American College of Cardiology in New Orleans, it was mentioned that every year one million US citizens suffer a heart attack.  Of these, about 60 percent get to the hospital alive.  About 16 percent never leave the hospital, and a further 10 percent die within a year.  This should be keen motivation for a complete and intensive investigation of the benefits of g-strophanthin.

The prospect of replacing heart bypass surgery with a safer, more effective, and less expensive treatment may be another reason to interest other parties in funding American research on oral g-strophanthin.

STROPHANTUS - QUABAIN

Ouabain – the optimal solution for the problem of myocardial infarction (Extracts from the book “Ouabain – the possible victory over the myocardial infarction” by Rolf-Jürgen Petry*)         One of the most necessary things in the contemporary medicine is to call attention to a topic that seems to be unbelievable at first sight: Ouabain (in german: g-Strophanthin), an extraction of an african plant called „strophanthus gratus“, which since 1991 is discovered as an endogenous substance – a new hormone-, prevents angina pectoris and myocardial infarction by nearly 100 percent without side effects. There is an overabundance of studies and documented experiences, so that its effects are quite obvious, even if the great clinical double-blind study is missing. But there is a mighty inscrutable opposition against the therapy with orally administered ouabain. There are two wrong tenets creating an impermeable wall:1) Ouabain is like digitalis classified as a heart glycoside, with the indications „heart insufficiency“ and „arrhythmia“. Because digitalis has negative effects in angina pectoris and myocardial infarction, and „the story goes“ that all glycosides act similarly, the outstanding therapeutical results of ouabain don´t attract any attention at all in the medical establishment.2) In the textbooks is written that ouabain has a very bad oral absorption – but there are over 20 studies which prove the contrary. The worldwide best resultsThe best example for the indeed excellent therapeutic results of oral ouabain in angina pectoris and myocardial infarction is Prof.R.Dohrmann from Berlin (West), who has been the leader of a public hospital, starting 1975 with this therapy. In 1984 Dohrmann & Dohrmann published a study (1) dealing with oral ouabain therapy in unstable angina pectoris. 148 patients with severe stenosis visable in coronary angiography, who received for years all the medicaments modern medicine offers and who are dissatisfied because of continous heart attacks and in part unpleasant side effects, have been switched over (with their agreement after an information discourse) to the therapy with oral ouabain from one day to the other, i.e. the other medicaments including the ß-blockers (!) were discontinued immediately. From these 148 patients 122 were free from angina pectoris after one week, and after two weeks this success could be seen with 146 patients. They were also free from the side effects of the former medication. The other two patients had to stop the therapy because of some irritation of the digestion tract, the only harmless side effect which sometimes occures. (Perhaps a conversion to natural food could help in these cases.) The capsula which is dissolved in the small intestine is sufficient in most cases, and when in spite of this prophylaxis there is a heart attack, the capsula for lingual absorption surely helps in 5-10 minutes in almost every case. With this method every patient can help himself even in the case of acute myoardial infarction, before the ambulance can be present.By the way it is not a necessary condition to discontinue the former medication: there have never been any interactions between oral ouabain and any other medicine, even not with digitalis, on the contrary the experience shows that oral ouabain reduces the side effects of digitalis, when this drug is necessary because of tachycardia.The study of Dohrmann et al. of 1977 (2) deals with sublingually applied ouabain to all patients coming to the hospital with severe heart attacks, acute myocardial infarction (AMI) or suspected AMI. In 170 of 264 cases (= 64 %) the attack was totally stopped within 5-10 minutes, in the rest there has just been an AMI in a relatively late phase in 55 cases, when there is no success to be expected any more, so that only in 15 % of the patients with A.p. (but without AMI) there was no positive result with the first application of ouabain. The above mentioned study (1) shows that the optimal success is reached only within some days.In the therapy of AMI Prof. Dohrmann introduced a new therapy (3) with i.v. cortison to stabilize the lysosomal membranes and i.v. k-strophanthine with great success, although the optimal time for applying ouabain or k-strophanthine in the first minutes of AMI had often just passed by when the patients were reaching the hospital. The quota of nonsurvivors (30 days) after myocardial infarction was previously very high (38 %) because there have been much more elderly people than in (the rest of) Germany. With this therapy he reached the worldwide best rate of survival of that time (in the first year (1977) 17 % nonsurvivors, and 1987, after 10 years, 15 % with experiences with over 1000 patients). A multicenter study of northern Germany reported a quota of 26 % mortality in a comparable period (3 a). Prof. Dohrmann was outnumbered only by Prof.DeMesquita from Sao Paolo (4) who used ouabain i.v. (9%).Another example is a coal mine in Gelsenkirchen/Germany (5) where the average number of workers dying because of AMI in the mine under the surface of the earth was 3 every year; the way to the doctor lasted more than half an hour. After the doctor of the mine in 1974 began with oral ouabain therapy directly in the mine, the mortality concearning AMI was reduced to zero in the following 10 years.In 1984, the small firm "Herbert Pharma" (the former producer of Strodival® – the only available ouabain medicament nowadays  - in Wiesbaden / Germany) had made an inquiry to 3650 doctors with respective experiences (6). Ca. 98,5 % answers were very positive, and 1,5 % were positive with some limitation. Reading the released extract, the answeres of 300 physicians, published with full adress, is really convincing, very often they say: "excellently effective", "no side effects", "better than the rest", "I don't see deadly myocardial infarctions any more" and so on... (There wasn't enough money to corrupt such a great number of physicians to make such definite statements. The author talked to some of them, so that it wasn't a faked inventory)The author could motivate some physicians to use ouabain. Their reports of a good therapeutical success are a good current authentication of the findings in the literature. The anthroposophic “Ita Wegman Klinik” in Switzerland are using ouabain since 2002 with the expected success. There are still about 3000 physicians in Germany who are using oral administered ouabain. Ouabain and Digitalis behave oppositely at the cellular levelThe commonly accepted receptor for heart glycosides, i.e. ouabain and digitalis and some other substances, is the sodium pump, which is present in the wall of every cell in a great number and which is pumping Natrium out of the cell and Kalium into it. This is very important for many fundamental functions of the cell.In all textbooks and articles there is written that heart glycosides are inhibitors of the sodium pump. Ouabain is extensively used in many scientific experiments to block the sodium pump. But for all that, this is more false than true: The inhibition of the sodium pump occurs only with high concentrations of ouabain. On the contrary, the low concentrations of ouabain, which are present in the human body after taking the medicine or naturally because of the endogenous nature of ouabain, have the opposite effect. There are over 50 unnoticed and unrefuted studies, that report of the stimulation of the sodium pump by low doses of ouabain. The last one is Gao et al. 2002 from the University of New York (7).