In the past decades, the fight against an epidemic of heart disease has spurred the development of a diverse range of pharmaceuticals, such as cholesterol-lowering drugs and beta blockers, and surgical techniques, including bypass, stents and angioplasty. Yet heart disease is still a killer. According to the National Heart, Lung and Blood Institute and the British Heart Foundation, coronary heart disease ─ the most prevalent form of heart disease ─ is the leading cause of death in the US and UK. Why? With an impressive array of medical advances, why are people still dying of heart attacks at an alarming rate?
To shed some light on this question, we need to examine the conventional theory of heart attack, the coronary artery obstruction theory. The basic premise here is that blocked arteries cause myocardial infarctions (the medical term for heart attacks). There are four main arteries that supply oxygen-rich blood to the heart. Deposits called plaque can build up in one or more arteries, causing them to become narrowed and constricted (a condition known as atherosclerosis), limiting blood flow to the heart. In time, a portion of plaque can rupture, forming a clot, further limiting or even completely blocking blood flow, leading to angina (chest pain), damage or death to heart tissue, and heart attack.
Let’s backtrack to the 1930’s and 1940’s, the years when the brilliant German cardiologist Berthold Kern (1911-1995) repeatedly observed, while performing autopsies, that most of the heart attacks he investigated had occurred with little evidence of coronary artery blockage; in other words, the basis of the coronary obstruction hypothesis appeared to be unsupported in these cases. Kern’s findings (i.e., the occurrence of heart attack in the absence of blockage) were later corroborated in the medical literature: various studies concluded that “intracoronary thrombus [blockage] contributes little to the pathogenesis of [the] average acute myocardial infarction” (1), and similarly, “an occlusive coronary thrombus has no primary role in the pathogenesis of a myocardial infarction.” (2)
If not by blockage, Kern must have pondered, then by what mechanism does heart attack occur? In his myogenic theory, Kern suggested that it is the accumulation of lactic acid in the heart that is the primary culprit in myocardial cell death and infarction. Various insults such as stress, diabetes, and smoking result in deficits in oxygen and nutrients transported through small blood vessels such as capillaries and arterioles. Instead of producing energy via the usual route, aerobic respiration, heart cells revert to anaerobic metabolism in the absence of oxygen, producing lactic acid as a byproduct, resulting in a chain reaction that leads to myocardial cell death. The progressive necrosis of heart tissue due to acidosis triggers infarction. In 1978, it was demonstrated that in myocardial infarction, the pH of heart tissue drops significantly; (3) it was later determined that a drop below pH 6.2 leads to irreversible damage. (4)
Was there a way to counter this destructive chemical process? Even in Kern’s time, it had been known for centuries that medicinal tonics known as cardiac glycosides (compounds with the four-ring chemical structure of steroids) had a therapeutic effect in heart disorders. Digitalis (common foxglove) is a source of digoxin and digitoxin, drugs which have been used extensively worldwide. Another plant, Strophanthus gratus, an African vine that produces seeds with a milky, oily substance from which the glycoside g-strophanthin (also known as ouabain) is derived, gained the attention of European doctors in the nineteenth century as a cardiac tonic.
When used intravenously in high doses, these compounds increase the output of the heart and strengthen contraction of the cardiac muscle – known as a positive inotropic effect. (4-6) However, the increased power of contraction can put further stress on the heart muscle, leading to undesirable effects such as arrhythmia. (4) Kern searched the medical literature and uncovered studies from the 1920’s demonstrating that g-strophanthin, when administered orally in low doses, did not produce this positive inotropic effect, a result that was confirmed in more recent studies. (4,6). What’s more, Kern estimated that the glycoside could be used orally to prevent or reverse lactic acid accumulation in cardiac tissue and so ward off angina, arrhythmia and heart attack.
g-Strophanthin acts by several mechanisms. It has been shown to stimulate myocardial metabolism and reduce lactic acid accumulation in myocardial tissue and in the blood. (4) Administration of g-strophanthin in an animal model of heart attack raised the pH of acidic cardiac tissue within a few minutes. (4) g-Strophanthin also effects fatty acid metabolism in the heart (4,7) and reduces the concentration of fatty acids in the blood. (4) Interestingly, it also increases endurance performance in animals and humans. (4) g-Strophanthin appears to be unique among cardiac glycosides: none of these physiological actions and therapeutic effects are produced by low-dose digitoxin. (4)
Kern administered oral g-strophanthin to over 15,000 patients with heart disorders in his clinical practice in Stuttgart over a two decade period, from 1947-1968. In this large group, remarkably, no fatal and only 20 non-fatal heart attacks were reported, compared to statistical predictions of over 120 fatal and over 400 non-fatal heart attacks for this population size. (8)
Many decades of use – predominantly in Germany – have demonstrated the benefits of g-strophanthin in treating and preventing acute heart attacks, as well as other cardiac conditions such as angina and arrhythmias. In fact, oral low dose g-strophanthin has even been used to treat the arrhythmia induced by digitalis derivatives (4,9) and may also lower blood pressure in patients with heart diseases. (4)
Several clinical studies conducted in Germany, and published in German, reported highly successful outcomes in the treatment of cardiovascular diseases with orally administered g-strophanthin. (10-12) One study showed that oral g-strophanthin reduced angina symptoms in 81% of patients. (8)
In another trial of 150 patients suffering from heart disease, g-strophanthin was effective in stopping the progression of heart attacks in 85% of cases, and with remarkable speed, between five and ten minutes after oral administration. (8) In fact, due to its fast onset of action, it was used by German physicians in the so-called “strophanthin quick test”: patients suspected of having heart disease were administered two 3-mg tablets that were thoroughly chewed and distributed in the mouth. The diagnosis of heart disease was confirmed if symptoms disappeared within five to ten minutes. (4)
In 1991, g-strophanthin was identified as an endogenous hormone produced by the adrenal glands to support cardiac metabolism and sodium transport, (4,5,13,14) among other more recently discovered roles such as cell growth regulation, apoptosis, modulation of immunity and even central nervous system function. (15) This fascinating discovery has led to a re-examination of the glycoside, its mechanisms of action and physiological functions. The high degree of tolerability reported with g-strophanthin is likely due to its natural production in the body. (4)
In the 1970’s, enteric-coated g-strophanthin formulations were introduced to optimize absorption. Today, one such formulation is registered in Germany for insufficiency of left ventricle (the chamber of the heart that pumps blood to most of the body) and sold as the prescription drug Strodival® (available from International Antiaging Systems). Strodival® is reportedly used successfully by over 5000 physicians in Germany today. (8)
It’s unfortunate that knowledge of this remarkable cardiotonic has been landlocked in Germany and has only recently begun to gain the international recognition it deserves – much of the original research, including Kern’s work, was performed in that country and remains untranslated, in German. As mentioned, conventional medicine, by adhering to the blocked artery theory of infarction, has “missed the boat” and largely failed to address the daunting rate of heart attacks, despite a vast array of drugs and surgical techniques. Strodival®, with its high degree of tolerability, markedly fast onset of action, and broad application in relieving a variety of cardiac symptoms, is a major breakthrough in the treatment of heart disease.