Masters of Health Magazine December 2023 | Page 24

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.

Heart Failure or Therapy Failure? Toxins Cause Cardiomyopathy

Part 1

by Dr. Thomas E. Levy, MD, JD