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Is Heart Disease a Plumbing Problem?

The Oxygen Model of Cardiac Myocytic Disease


First of Three-part Series on CMD

Majid Ali, M.D.


Most people look at heart disease as a plumbing problem. Celebrities talk about their coronary stents. Presidents exalt their coronary bypass procedures. On public television, highly esteemed hosts exhort the virtues of Lipitor and related drugs to lower blood cholesterol levels (once I heard Charlie Rose ask in his program, “Why don’t we all go out and put ourselves on Lipitor?”)  Many people wear their coronary stents not in their chests but on their chests as badges of honor—as a distinction of having reached some zenith of personal enlightenment. So it is no surprise that people worldwide look at heart disease as a plumbing problem. (Oh, please, please Google “Statinex” to read my dream on the subject.)
 

 
Patients of New York Cardiologists Are Immune to Toxins
 

Do you know that the patients of New York cardiologists are immune to toxins? No, this is not a trivial question. I do not seek cheap thrills. The hearts of  the patients of New York cardiologists are immune to toxins. I can prove that.
  
Once at a dinner with friends, I sat close to a young New York City cardiologist. She enthusiastically stated her mission: to identify risk factors for heart attacks and prevent them. Her primary weapons were drugs, statins to lower blood cholesterol levels and blood pressure drugs were clearly her top priorities. It would have been impolite for me to ask how much training had she received about attacking the trio of toxicities of foods, environment, and thoughts that torment hearts, sicken them, and cause heart attacks. I practice in New York City and care for a large number of patients with failed coronary stents and bypasses. I have yet to see a patient whose heart was cared for by a practitioner of nutritional or environmental medicine at any of New York's university hospitals. Perhaps because the hearts of their patients are immune to toxicities of mercury, lead, mold toxins, industrial pollutants, and poisons in the food, water, and air.  Also those doctors must think their patients never develop functional nutrient deficiencies. Otherwise why wouldn’t they detect such insults to the hearts of their patients with appropriate tests and address them with robust efforts.

 
Seven Crucial Questions
 
To highlight the importance of MCD (cardiac myocytic disease) and distinguish it from coronary artery disease (CAD), I invite you to ponder the following questions:
 

*  Henry Kissinger, President Nixon’s Secretary of State, lives an active life 29 years after his triple coronary bypass operation. Most  people know about individuals who, like Secretary Kissinger, lived long useful lives after triple coronary bypasses.  Most people also know of someone who died within months or a few years of  two or more coronary bypasses. How might reconcile such differences?
 
* Nearly one in two people who suffer a heart attack have low blood cholesterol level. How might that be explained?
 
* The incidence of the “stiff heart syndrome”—a common form of heart failure—is rising. Many patients with this syndrome do not have significant coronary artery blockages. Why do their hearts become stiff and fail?
 
* At autopsy, over 50% of individuals, who died of acute heart attacks within six hours of hospitalization, do not show fresh blood clots in their arteries while nearly all patients who die after 48 hours of hospitalization for acute heart attacks show such clots. How can this be explained?
 
* At autopsy, all patients dying of heart attacks show dead and dying individual heart muscle cells. Many of them do not show blockages of coronary arteries. How might their condition be explained?
 
* Many patients with congestive heart failure do not show blockages of coronary arteries. How might their condition be explained?
 
* The heart fails when it is overloaded with iron, amyloid proteins, abnormal lipids (fats) or other materials. Most people with this condition do not have significant coronary artery blockages. Why do their hearts become stiff and fail?
 
* In a condition called cardiomyopathy (cardio - myo - pathy), the heart fails and, if not treated, results in death.  At autopsy, all patients dying with cardiomyopathy show dead and dying individual heart muscle cells. In most  cases, there is no acute coronary artery occlusion. What takes their lives?
 
The prevailing plumbing (cholesterol-plaque model) of coronary artery disease (CAD) cannot rationally and scientifically provide sound answers to any of the above questions. 
 
The Dead Can Teach the Living Only If ....
 

For the correct answers to the questions I raised, I return to the lessons taught to me by my friends on my autopsy table and by my friendly microscope. In 1982, as a young pathologist I recognized the death of individual heart muscle cells as the basis of congestive heart failure. I coined the term cardiac myocytolysis for it (myo for muscle and cytolysis for death). In collaboration with  my colleagues in the departments of pathology and nephrology, I correlated the degrees of cardiac cellular death and resulting fibrosis (scarring) with cardiac failure as determined with ejection fraction by ultrasound studies. We published our data in The American Journal of Cardiology and Kidney International. The pictures showing the patterns of death of individual heart muscle cells in autopsy specimens are presented at the end of this article.

In the following years, my deepening understanding of the antioxidant, anti-inflammatory, cell-protective, and healing roles of cholesterol led to the recognition of the folly of the “cholesterol-plaques-plumbing” model of heart disease. I marshaled evidence against this theory in a series of articles and in Integrative Cardiology, the sixth volume of my textbook The Principles and Practice of Integrative Medicine.  In this series on cardiac myocytic  disease (CMD), I summarize my microscopic, biochemical, and clinical observations to show that CMD is a far more important clinical problem than coronary artery disease (CAD) and that it claims many more lives.  

 
With Apologies to Statiners, Stenters, and Bypassers


Most readers, including cardiologists, are not likely to be familiar with the heart problems caused by the death of individual heart muscle cells (cardiac myocytolysis). Indeed, I anticipate that this article will irk doctors and others who are committed to the cholesterol and coronary artery theories of heart disease. I illustrated the microscopic features of CMD with photomicrographs in Pathology of Maintenance Hemodialysis (1982), which I coauthored with Professor Alfred Fayemi of Mount Sinai School of Medicine, New York. These photographs can be seen at www.wiki-medical.org.  In other articles, I cite my early work with The Dysox Model of Coronary Artery Disease to address the causes of cellular injury— toxicities of foods, environment, and thought—which lead to CMD.  Finally I offer my integrative guidelines for controlling and reversing CMD. In past columns, I published personal data to document the efficacy of integrative protocols that reverse CMD and allow people to live long and productive lives after they were told they have advanced heart disease.

 

Figure 1 

Normal microscopic appearance of cardiac myocytes (heart muscle cells). Note the branching and merging of individual myocytes with dark rectangular and elongatednuclei. The matrix between them is delicate and contains smaller and thinner nuclei.  

Figure 2

An early stage of cardiac cell death (cardiac myocytolysis). The arrows point to a disintegrating cell.

Figure 3

An intermediate stage of cardiac myocytolysis (muscle cell death with focal disintegration of myocytes (center field)

 

Figure 4

An advanced stage of cardiac myocytolysis with a multi-layered  pattern ("Sandwich Effect") of cell loss.

Figure 5

A higher power view of advanced stage of cellular death and disarray. Note that the lost cells are replaced by larger areas of loose connective tissues of the matrix. 

 

Continued with Parts two and Three

 

List of Related Articles

k  Oxygen Model of Coronary Heart Disease

k  Evidence for Oxygen Model of Heart Disease

k  Coronary Heart Disease - Simplified

k  Oxygen Model of Cardiac Myocytic Disease (CMD)

k  Being One’s Own Cardiologist

k     Seeing the Heart

k    Anatomy of the Heart 

k Physiology of the Heart

k Cardiac Myocytic Disease (CMD) 

k What Causes Coronary Heart Disease? utorial He6 Blood Clots and Unclots At All Times

k The More-Plaques-Fewer-Deaths Paradox Part I

k Should You Say No To Non-emergency Coronary Stent?

k  Cholesterol Is Dignified Cholesterol

 

 

 

Figure 6: An area of infarcted (dead) and densely calcified of the heart muscle typically seen after recovery from an acute coronary artery occlusion. Compare with the patterns of individual cardiac myocyte loss shown in Figures 2-5.

 

Figure 6

 

 

 

 

Figure 7

 

 

Figure 8

Microscopic Appearance of Pericarditis

Tutorials

* Cardiac Myocytic Disease (CMD)

* Tutorial GG.12 Ali M. Fischer S, Juco J, et al. The dysox model of coronay artery disease. Townsend Letter for Doctors and Patients. 2006;270/71:110-112.

Tutorial GG.7 Ali M. Oxygen governs the inflammatory response and adjudicates the man-microbe conflicts. Townsend Letter for Doctors and Patients. 2005;262:98-103.

Tutorial GG.31 Ali M. Oxygen, Insulin Toxicity, Inflammation, And the Clinical Benefits of Chelation. Part I. Townsend Letter-The examiner of Alternative Medicine. 2009;315:105-109. October, 2009.

Tutorial GG.32 Ali M. Insulin Reduction and EDTA Chelation: Two Potent and Complementary Approaches For Preventing and Reversing Coronary Disease. Oxygen, Insulin Toxicity, Inflammation, and the Clinical Benefits of Chelation - Part II. Townsend Letter-The examiner of Alternative Medicine. 2010;323:74-79. June 2010.

Tutorial GG.17 Ali M. Limbic breathing. Townsend Letter-The examiner of Alternative Medicine. 2007; 288:160-166.

 

 

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