Heart Failure or Therapy Failure? Toxins Cause Cardiomyopathy

Written by Dr. Thomas Levy on November 14, 2023. Posted in Current News

Cardiomyopathy simply means heart muscle disease. [1]

It can occur as a primary affliction of the heart muscle, from a secondary condition negatively impacting heart function, or from a combination of both these clinical conditions. [2,3]

Relatively recent changes in the definition of cardiomyopathy have been put forward that differ somewhat with these long-standing categorizations of heart disease.

However, for the practicing clinician, the most important considerations in approaching the cardiomyopathy patient with clinical heart failure are:

• Is the heart muscle itself diseased?
• Is the heart muscle normal but being forced into failure by non-cardiac factors?
• Is the clinical presentation a combination of both these conditions?
• Is the treatment protocol aimed only at relieving symptoms or also at resolving the underlying pathology resulting in the clinical heart failure?

Because cardiomyopathy presenting as clinical heart failure is a condition typically involving multiple factors, there is no single clinical protocol that can be considered the optimal treatment plan.

Furthermore, heart failure rarely occurs by itself without other diseases and co-morbid conditions being present and contributing to symptoms as well. [4,5] However, all presentations of heart failure share features that should always be addressed clinically, regardless of whatever other treatments are being administered.

The huge public health impact of heart failure cannot be overstated. In Germany, for example, heart failure is the most common primary inpatient diagnosis. [6]

Heart Failure Pathophysiology

When the function of the heart is impaired sufficiently to decrease the amount of blood that should be pumped with every heartbeat (cardiac output), a clinical picture of heart failure will eventually emerge.

As the body can clinically compensate reasonably well for early heart failure, it is only when the decreased function is severe enough and chronic enough that heart failure symptoms become clear-cut.

Because of this, even seemingly mild heart failure symptoms should be taken very seriously, with a complete diagnosis (especially in the ongoing pandemic setting), and the application of scientifically-based treatments for supporting and improving heart function.

Common symptoms of heart failure include the following, due basically to the abnormal accumulation of fluid in the lungs and the rest of the body from inadequate heart pumping ability: [7,8]

• Shortness of breath at rest or too quickly with exertion
• Shortness of breath when lying flat
• Waking up suddenly short of breath
• Fatigue
• Swelling in feet, ankles, and eventually legs and/or abdomen
• Accelerated heart rate, palpitations

Heart muscle cells do not just fail and “wear out” for no reason. When oxidative stress increases inside the heart tissue, inflammation by definition then exists as well. Also, part of that increased oxidative stress is the result of decreased ATP (adenosine triphosphate) production in the mitochondria of the heart cells.

As ATP is the main energy-providing molecule in the body, those heart cells that have compromised ATP production have more oxidative stress, which results in a clinical picture of inflammation, or myocarditis.

When the factors increasing oxidative stress are intense and acute in onset, rapid heart enlargement with poor heart contraction (congestive cardiomyopathy) will result. However, when the factors increasing oxidative stress are less intense and more chronic in nature, the heart will generally first “adapt” by increasing the heart wall thickness without enlargement of the left ventricular dimensions (hypertrophic cardiomyopathy).

A clinical picture of heart failure will still be present and continue to evolve as the heart wall thickening makes the left ventricle stiffer and less compliant. This results in that heart chamber not filling up as readily (diastolic heart failure, or heart failure with preserved ejection fraction). [9,10]

Effectively, this form of cardiomyopathy actually consumes more ATP trying to fill the heart than to empty it. [11]

With this resistance to chamber filling, the amount of blood pumped with each heartbeat decreases while the blood supply coming into that chamber “backs up,” resulting in the heart failure symptoms noted above.

To be discussed below, toxins cause both forms of cardiomyopathy. Left untreated, the terminal stages of hypertrophic cardiomyopathy evolve into a congestive cardiomyopathy, with substantial enlargement of the left ventricle and very poor contractility.

This will result even when the heart was not enlarged or poorly contracting at the onset of the myocardial inflammation. The initial clinical presentation of heart failure is roughly split equally between hypertrophic and congestive cardiomyopathy. [12]

Limited blood flow in the heart (ischemia) is commonly considered to be the cause of congestive cardiomyopathy most of the time. This is certainly a major reason for heart failure when multiple heart attacks with death of heart muscle and fibrotic scarring are present in place of contracting heart muscle.

However, heart biopsies in consecutive patients with advanced coronary artery blockages and clinical heart failure indicated otherwise. The microscopic evaluation of these biopsies indicated that myocarditis was the underlying cause, and heart function in some of these patients improved dramatically with anti-inflammatory measures.

In the absence of active ischemia or old heart attacks with extensive loss of heart tissue, it is erroneous to consider ischemia as a primary cause of congestive heart failure. The important takeaway point is that myocarditis is not necessarily an obvious diagnosis.

There must be a lower threshold for taking heart tissue biopsies, as missing the diagnosis of a treatable condition greatly increases morbidity and mortality for many patients. [13]

Toxins and the Heart

While toxin accumulation in the heart muscle can be the singular cause of advanced heart failure, it will much more often be one of several factors contributing to decreased heart contractility.

Also, the chronicity of the heart failure, regardless of cause, will play a large role in determining its reversibility, as more and more inflamed heart cells will eventually die and not just remain in a chronically inflamed state.

Such inflammation is consistently seen on the microscopic study of heart biopsies in toxin- and infection-related cardiomyopathy. [14,15] Many different toxins, including many heavy metals, have been either linked to heart failure or clearly shown to be the direct cause.

Furthermore, one or more of these toxins is nearly always present in high concentrations in the affected heart muscle.

A partial list of such agents includes the following:

• Lead
• Copper
• Iron
• Mercury
• Aluminum
• Cobalt/Chromium
• Cadmium
• Gold/Silver
• Chemotherapy
• COVID Spike protein

Lead: In a 3-year-old girl with chronic lead poisoning, acute heart failure developed that was clinically reversed after four days of calcium EDTA chelation therapy. [16] Children who died from heart failure secondary to acute lead poisoning were documented to have the microscopic findings of myocarditis. [17]

Lead has been shown in other studies to target the heart and the vascular system. [18-21] Animal studies have also shown that enough lead exposure will reliably cause myocarditis and vascular damage as is seen in humans.

These studies show that lead exposure will cause atherosclerosis and high blood pressure as well. [22-24]

Copper: A transition metal necessary for normal cell function but easily pushed to excess and toxic levels in the body, copper is another culprit toxin commonly involved in cardiomyopathy patients. [25,26] E

xcess copper appears to be especially toxic to the heart, as the infusion of copper into the coronary circulation of rats results in impaired heart function in only minutes. [27] Hypertrophic cardiomyopathy has been strongly linked to the excess copper levels seen in Wilson’s disease.

Trientine, a selective chelator of copper, has been shown to improve cardiac function in hypertrophic cardiomyopathy patients. [28]

In a randomized, placebo-controlled trial on diabetic patients with left ventricular thickening (that can lead to hypertrophic cardiomyopathy), copper chelation significantly decreased the heart wall thickening.

This study did not even screen for elevated copper levels. [29,30] Furthermore, trientine chelation in diabetic rats with advanced left ventricular failure over an eight-week period demonstrated significantly improved heart function. [31]

Another heavy metal-removal study in diabetic rats with either trientine or citrate (citric acid) significantly protected heart function. [32] In a case report a patient with scleroderma and a congestive cardiomyopathy improved dramatically on penicillamine, an effective chelator of copper, lead, and mercury.

No copper level testing was reported as part of the evaluation of this patient. [33] These studies further indicate that toxicity from copper and/or other heavy metals in the heart is often a significant contributing factor in patients with early heart wall thickening and then its later decompensation into decreased cardiac function and heart failure.

It appears that a clear diagnosis of copper excess does not need to be made before just treating patients presumptively as having too much copper in their heart, especially when heart wall thickening is present in a diabetic patient. [34]

It has also been shown a copper-overload state is a primary factor in the pathogenesis of damage to any organ in the diabetic. [35] Copper removal has also been shown to decrease the inflammatory response to radiofrequency ablation treatment for liver cancer in rats. [36] These findings strongly suggest that:

The unsuspected presence of excess copper in tissues and organs can impair the resolution of ANY pathology being treated, indicating a positive role for copper removal for nearly all medical conditions.

Iron: Congestive heart failure secondary to severe iron overload in the body has been described. The daily administration of an iron chelator (deferoxamine) in a congestive cardiomyopathy patient over roughly a year dramatically improved heart function and cardiac output, with heart pumping ability more than doubling (ejection fraction from 20 to 48 percent). [37]

Another case report described a 27-year-old woman with “severe heart failure” completely normalizing on an iron removal regimen. [38] Patients with severe iron overload cardiomyopathy have an average survival of only one year when therapeutic phlebotomy (blood donation) and iron chelation are not utilized.

This form of cardiomyopathy begins with restricted filling of the heart (diastolic dysfunction), and then evolving into a congestive cardiomyopathy. [39]

Iron overload cardiomyopathy occurs most commonly in patients with hereditary hemochromatosis or secondary hemochromatosis (as with β-thalassemia and sickle cell anemia). [40] However, excess iron short of that seen in full-blown hemochromatosis can still be expected to inflict its own dose-dependent toxicity.

Most adults already have excess levels of iron in their bodies, as reflected by elevated ferritin levels that erroneously remain regarded as normal in laboratory reference ranges. [25] Excess iron in the heart is also a predisposing factor to developing atrial fibrillation, an arrhythmia that contributes its own increased morbidity and mortality. [41]

In animal studies, excess cellular iron in heart cells has been shown to increase oxidative stress and impair the ability of the mitochondrial electron transport chain (ETC) to produce ATP. As ATP is the primary energy-providing molecule in the body, any decrease in its production always results in compromised cellular function and disease. [42,43]

Of note, resveratrol supplementation has been shown to dramatically improve heart function in animal models of iron overload cardiomyopathy. [44-46] In another animal study, either deferiprone or N-acetylcysteine was effective in decreasing cardiac iron concentration. [47]

Mercury: As the most toxic non-radioactive element, mercury is a heavy metal that causes grave damage wherever it accumulates. A landmark study directly compared toxic heavy metal concentrations in biopsies of heart muscle against control muscle biopsies in patients with idiopathic dilated cardiomyopathy (IDCM), meaning advanced heart failure of unknown cause.

The cardiomyopathy heart muscle had 22,000 times more mercury in it than in normal heart muscle. Versus normal specimens, the same diseased heart muscle had 12,000 times more antimony, 11 times more gold, 13 times more chromium and 4 times more cobalt.

Of great significance, there was no primary screening to detect increased heavy metal exposure in the study group, meaning these accumulations likely represent the finding in most cases of IDCM. [48]

Unless excess exposures to heavy metals are readily apparent, the widespread effects of such poisonings make it very unlikely that such a toxicity will be suspected and then correctly diagnosed. [49]

In another study, the heart muscle in cardiomyopathy patients examined at autopsy revealed significantly higher levels of lead, nickel, copper, and manganese, and significantly lower levels of zinc compared to the heart muscle in non-cardiomyopathy patients.

Mercury and antimony levels were not reported and presumably had not been measured. [50] This study indicates that most patients with IDCM have not only astronomical levels of mercury and antimony, but also significant elevations of lead, nickel, and copper.

If it was not a vital organ, the ability of the heart to selectively remove heavy metals out of the blood and the rest of the body could be considered a protective mechanism for the health of the body! This leads to the conclusion that:

Cardiac muscle in patients with advanced congestive cardiomyopathy is the preferred collection site for most of the heavy metals taken into the body.

Currently, IDCM is the cause of heart failure in over 100,000 people in the United States, and it is the underlying diagnosis leading to 45% of heart transplants. Furthermore, evidence of resolved or ongoing viral infection in heart biopsy specimens are seen in 25 percent of IDCM patients. [51]

Up to 80 percent of IDCM patients demonstrate one or more anti-heart autoantibodies. [52] Such antibodies are commonly the result of occult infections. Heavy metal accumulations and chronic viral myocarditis appear to be pathology-precipitating partners. [53]

While it is unclear whether one factor better facilitates the presence of the other, it appears that heavy metal accumulation, headed by mercury, is a very common cause of IDCM. Based on these studies that have specifically measured heavy metal status in IDCM heart muscle, heavy metal accumulation appears to be the culprit for this advanced form of heart failure MOST of the time.

The IDCM heart would appear to be a chemically attractive site for the accumulation of multiple heavy metals after being primed by an earlier myocarditis-precipitating viral infection, as no other organ in the bodies of IDCM patients appears to similarly concentrate these toxins.

Mercury also works effectively to produce a deficiency state of selenium. Restoring deficient selenium stores can lessen clinical mercury toxicity, although it does not directly promote the mobilization or elimination of mercury.

Congestive cardiomyopathy secondary to selenium deficiency has been reported, and restoring depleted selenium levels can reverse it. [54-57] Based on the data above on mercury and IDCM, a cardiomyopathy associated with selenium deficiency is likely a cardiomyopathy due to the toxicity of excess mercury no longer being negated by a sufficient presence of selenium.

Of note, too much supplemental selenium has its own toxicity, unlike many other nutrient supplements, and should not be overdone.

Aluminum: Aluminum phosphide, an agent used as a pesticide, induced a severe, but reversible, cardiomyopathy after accidental poisoning in an exterminator. [58] Intense supportive care to reverse low blood pressure was shown to facilitate the recovery of other individuals poisoned with aluminum phosphide that resulted in severe compromise of heart contractility. [59,60]

In a hemodialysis patient who expired with heart failure, heavy aluminum deposits were seen in the heart cells upon electron microscope examination. [61] An animal study also showed that aluminum chloride could induce a largely reversible cardiomyopathy. [62]

Organic acids (succinic, malic, or citric) and the iron chelator, desferrioxamine, are agents that can mobilize (solubilize) and eliminate aluminum accumulations. [63]

Cobalt/Chromium: Cobalt is another toxic heavy metal documented as a cause of congestive cardiomyopathy. Elevated blood cobalt levels have been identified in some metal hip implant patients. [64,65]

Elevated blood chromium levels from the implants can be seen as well. [66,67] However, the presence of such elevations is not an assurance that a cardiomyopathy will result. [68] As noted above, IDCM often starts with an undiagnosed viral myocarditis.

Such a myocarditis would appear to inflict the myocardial damage that triggers the almost sponge-like uptake of cobalt and other heavy metals, as described in the section on mercury accumulation in the heart.

An animal study also showed that poor diet (protein restriction) further predisposed the heart to cobalt toxicity. [69] N-acetylcysteine is effective in significantly reducing the blood concentrations of both cobalt and chromium. [70]

Alpha lipoic acid is another effective chelator of cobalt. [71]

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