Angina, Heart attack, Ouabain, Strophanthus, Atrial fibrillation, Heart failure, Stents, Bypass surgery [FB]

Strophanthus: The Insulin of the Heart

By Thomas Cowan, MD

In 2003 the Mayo Clinic published a major review article whose intention was to understand the risks and benefits of coronary artery bypass surgery. It came to the following conclusions:

1. Bypass surgery can effectively relieve symptoms.

2. Bypass surgery does not prevent further heart attacks.

3. Only high-risk patients benefit from bypass surgery with regard to better chances of survival.¹

In other words, having a bypass operation with its attendant mortality risk is effective only at relieving symptoms in the vast majority of the patients who undergo this procedure. There is no evidence of prevention of future heart attacks (MI), nor of extending life.^2,3

Similar results have been found for the more common procedure of stent placement. Instead of surgery to place new grafts in the heart, the blockages are mechanically opened, and stents are placed in the coronary arteries to keep the vessels open. Again, while this procedure is effective for symptom relief, it does not reduce the likelihood of a future heart attack nor confer a longer life to the patient.⁴

One would think that cardiologists and internists armed with this information would doggedly pursue other avenues for treatment, avenues that would help prevent heart attacks and increase functional lifespan. However, sadly, since these results were published, the numbers of these procedures have increased rather than decreased, reaching a peak of 4.5 million worldwide in 2016.⁵ Something is seriously amiss in the halls of our modern cardiology wards.

One clue to understanding why bypass grafting and stent placement have not delivered on their promised results comes from the work of Italian pathologist Giorgio Baroldi. In his groundbreaking book The Etiopathogenesis of Coronary Heart Disease: A Heretical Theory Based on Morphology,⁶ he concluded that after doing autopsies for 40 years on patients who died of heart attacks, only 41 percent of these patients had a significant stenosis (plaque build-up) in the artery leading to the area of the heart affected by the heart attack. And 50 percent of these stenoses came AFTER the heart attack occurred, not before, as one would commonly assume. These results suggest that approximately 80 percent of heart attacks have some other cause than simply a “blocked” or stenosed artery. Given this information, it is no wonder that, in the majority of cases, unblocking arteries — no matter how thoroughly or carefully done — will never be the solution for our nation’s epidemic of heart disease.

In my book Human Heart, Cosmic Heart,⁷ I reviewed the existing literature on the controversy about the cause of heart attacks and suggested three other causes of heart attacks. I assert that these possible causes must be addressed if we are to have a thorough approach to the prevention and treatment of angina, unstable angina and heart attacks. Briefly, these three other causes are autonomic nervous system imbalance, microcirculation, and metabolic acidosis.

Autonomic nervous system imbalance. With the advent of heart-rate variability testing, a sensitive and accurate way to assess the autonomic nervous system activity, we now know that a large percentage of patients who go on to have an MI have decreased parasympathetic activity in the days, weeks, and months leading up to the MI. Baroldi suggests that the majority of MIs are caused by the combination of chronically low parasympathetic activity and a temporary stressful event, which furthers this imbalance.

The important point here is that although they are similar, decreased parasympathetic tone is not the same as excessive sympathetic activity. Decreased parasympathetic tone is a consequence of chronic stress, diabetes, hypertension, smoking, and lack of physical activity. Increased sympathetic activity, which conventional cardiology focuses on with its use of beta-blockers, is more of a short-term imbalance and doesn’t have the same predictive value in determining whether an MI will occur. Cardiology is in need of a strategy that will support the patient’s parasympathetic nervous system while he or she implements long-term strategies to transform the causes of parasympathetic dysfunction.

Microcirculation. Typical anatomical drawings of the heart suggest that all of the blood flow to the myocardium goes through the three major coronary arteries. Although these arteries are certainly important, it turns out that, even from a young age, the heart is endowed with a rich supply of blood vessels that make up the microcirculation of the heart. If you go to Figure 1 in the FAQ section of the heartattacknew.com website, under the heading “The Riddle’s Solution,” you can see a perfectly illustrated depiction of the normal cardiac microcirculation.

Again, as Baroldi points out, the normal heart is perfectly well suited to do its own bypass in the event of a chronic disruption of flow through one or more of the coronary arteries. This ability is why thousands, maybe millions, of Americans are walking around with arteries greater than 90 percent occluded, yet with no symptoms whatsoever. The body, using its robust capillary network, has done its own bypass, and the heart is protected. It is only in the case of chronic disease, in particular, diabetes, with its well-known microcirculatory pathology, that MIs start to show up. Clearly, stents and bypasses confer no benefit to those with microcirculatory disease. Modern cardiology is clearly aware of this issue, as this is the rationale for the use of Plavix and aspirin in cardiac patients. Both affect the microcirculation and increase blood flow therein. Both, of course, have their own toxicity, which limits their use and the ability of patients to tolerate these drugs.

Metabolic Acidosis. This situation is perhaps the most important and most overlooked reason that people suffer from angina, unstable angina and MIs. The production and build-up of lactic acid in the myocardial tissues is the final common pathway in all cases of angina, unstable angina and MI. What happens is that, because of parasympathetic disease, coupled with micro-circulatory problems, the heart finds itself in a stressful situation, one in which it is forced to undergo what is called a glycolytic shift. This shift means that the heart is unable to generate energy in the usual manner, which is through mitochondrial-based respiration, and instead begins to ferment sugars to obtain fuel. A similar shift is thought to underlie the cancer process and is becoming well known as an important etiology in chronic disease. Once this glycolytic shift happens, the cells start to build up lactic acid in the surrounding tissues. The same process happens in your leg muscles as the result of over-exercising. However, in contrast to leg muscles, the heart muscle can’t relax, so the lactic acid continues to build up. It is at this point that the familiar feeling of angina or chest pain begins to occur.

As the process continues, the lactic acid continues to accumulate, which then causes a localized metabolic acidosis (lowered pH) to occur. The lowered pH prevents the influx of calcium into the myocardial cells, essentially preventing the contraction of the heart muscle fibers. This result can be seen on the stress echo or nuclear-perfusion tests used to diagnose heart disease in modern cardiology. As the process continues and the lactic acid continues to accumulate, eventually there is a necrosis of the surrounding tissue, which is what we call a MI.

Along with the destruction of the myocardial tissue, the dyskinetic or akinetic areas of the heart create shear pressure on the embedded arteries, which results in clots forming after the MI occurs. This sequence of events perfectly describes the events that occur as the MI is progressing. Modern cardiology has no tools in which to address this central pathology of the build-up of lactic acid in the myocardial cells.

Strophanthus: The Insulin of the Heart

An effective treatment for angina, unstable angina and heart attack prevention must address each of these three areas to be truly successful. Luckily, such a medicine already exists and has been both widely used and sorely overlooked during the past century.

An African perennial vine called strophanthus makes seeds that contain the active ingredient referred to as g-strophanthin in Europe and ouabain in the US. Ouabain is a copy of a hormone made by our own adrenal cortex, and it has many functions that are useful in treating patients with heart disease. Used as the main treatment for the prevention of MIs in Germany for many decades, ouabain has been shown to support the parasympathetic nervous system, improve the micro-circulation and, crucially, convert the lactic acid in the myocardial tissue into pyruvate, which is the preferential fuel of the heart.^8,9 With the conversion of lactic acid into a nutrient for the heart cells, the cycle of pain and subsequent necrosis of the myocardial tissue is broken. In the majority of cases, the patients will experience relief from their angina as well as improvement in heart function.

During the past decade, I have treated heart patients with either g-strophanthin capsules or, more recently, an extract of the strophanthus seed extract with positive effects on their overall sense of well-being, and, specifically, on their heart function. Since the book was published, we have started a program to make strophanthus extract available to all heart patients who wish to use it. We ask each patient to find a health-care practitioner who will order the medicine from us and supervise its use. By doing this, we hope to develop a network of practitioners who are well versed in its use. The results from practitioners are beginning to come in, some of which are showing remarkable benefit. Below are some of those cases (either written by the practitioner or the patient him or herself).

If you are interested in learning more about the use of strophanthus for heart disease, please contact our office at (415) 334-1010 to schedule a free, 15-minute phone consultation on the use of strophanthus and how to order it.

Case Studies

Case 1. From a Physician in Kentucky. Bruce, a 60-year-old male, suffers from atrial fibrillation and severe heart failure. Left ventricular hypertrophy and cardiomyopathy had developed from substantial untreated hypertension. His heart ejection fraction fell to <20%. His main measure of heart failure — BNP — rose to 3000. I had treated him with every supplement that I could contemplate, including ones that normally are very helpful for the heart from L-carnitine, 400mg ubiquinol, d-ribose, cordyceps, hawthorn, and other anabolic botanicals — literally 40 supplements due to his severe situation, along with natural blood thinners. Despite these he was on Lasix 40 mg daily; an ARB produced a highly annoying persistent cough and had to be stopped. 

With the aggressive supplementation, he did improve. However, BNP was still 1316, Bilirubin – 5.3, Alkaline Phosphatase 248, C-reactive protein 29, and d-dimer 2.8; these had all proven to be indicators of his heart failure in the previous two years. But he still was very limited as to physical activity. 

Then I read Dr. Cowan’s report about strophanthus. Out of desperation — all options had been exhausted — it was ordered. Over three weeks he titrated up to 10 drops twice a day. BNP dropped to 1244, CRP to 23.2, Bili to 3.5, Alk phase to 219, and d-dimer to 1.73. He was told to continue to titrate up on the strophanthus until reaching 15 drops twice a day. 

We didn’t hear from Bruce for many months afterwards but heard indirectly that he was doing better. When he did come in six months after the previous visit, he reported only minor physical limitations. His BNP had dropped to 492, CRP to 12.6, Bili to 1.9, Alk phos to 181 and d-dimer to 0.67. His blood pressure that typically was 100 diastolic, and as high as 178 systolic, was essentially normal for the first time at 132/80. 

He reports no side effects from strophanthus (though he does note the taste and smell). After having blood drawn almost monthly for two years with constant adjustment in his regimen, and hobbled from physical activity, Bruce now has his life back with optimism about the future. Strophanthus has proved miraculous in Bruce’s improvement at a time when he had nearly lost hope. 

Case 2. Patient Report. My father had his first heart attack at age 45 and a second one at age 60 while undergoing bypass surgery.  He died on the table. So, I have been careful to watch my diet and lifestyle. About a year ago, I began having left-sided chest and arm pain — only at night, in bed.  A recent ECG had a “dip” that the doctor stated may be a sign of having had a heart attack at some point. I didn’t want to overreact.  I also didn’t want to go down the same path as my father.  I wasn’t going to go “traditional” on this one!
  (My naturopathic doctor) suggested I start taking strophanthus drops twice a day.  After two months of using it, my chest pain is completely gone!  Additionally, I have a very strong sense of peace in my physical body. Not sure how to describe it.
  Case 3. Patient Report. I suffered from cardiac cephalgia angina attacks —35 to 45 per month, even though I was taking 30 mg of isosorbide mononitrate daily and using 0.4 mg nitroglycerin transdermal patches. After taking strophanthus seed extract, I’m down to around five angina attacks per month.
  Case 4. Patient Report. I’ve been diagnosed with a-fib in November last year. After the diagnosis, the additional symptoms were tingling in hands and feet and chest pain and pressure on continuous basis. Everything else was healthy with my heart.

Luckily Dr. Cowan is my doctor. He prescribed strophanthus with vitamin

E and beet juice. This is the month of June. My a-fib symptoms are almost gone.

Tingling is slowly going away, and chest pain and pressure are gradually

vanishing.

Case 5. Patient Report. I had two CT chest scans. The one in October of 2016 had a calcium score of 40. I started the strophanthus in November 2016. The second CT scan in May 2017 had a calcium score of 12.

Case 6. From a Chinese-Medicine Physician in Colorado. On February 7, 68-year-old male was hospitalized with heart failure due to left ventricle damage, rigidity. After stent installed, the ejection fraction was 18 percent. I started him six weeks ago on strophanthus 3 drops bid, and then three weeks later increased to 6, bid.  (I also used ubiquinol, magnesium orotate, proteolytic enzymes, activated B vitamins). Checkup ECG yesterday, ejection fraction now at 47 percent.  The technician commented that in 15 years he never saw this kind of recovery.  Patient feels excellent and says, “I felt my heart moving differently” shortly after starting the strophanthus. I guess so!