Should You Say No to Non-emergency Coronary Bypass Operation?
Majid Ali, M.D.
This is an important question. Should You Say No to Non-emergency Coronary Bypass Operation? This question is equally important for individuals who have had a coronary bypass operation.
Below is a part one of my five-part series entitled “The More-Plaques-Fewer-Deaths Paradox.”
The More-Plaques-Fewer-Deaths Paradox
First of five-segment Series
Majid Ali, M.D.
More arterial plaques are associated with fewer deaths from heart attacks and strokes. No, you did not misread the sentence. I write precisely what I mean: people with less intense plaque formation have higher mortality from cardiovascular diseases. I anticipate harsh frowns from doctors on the title of this tutorial. The idea that plaques in arteries cause heart attacks and strokes is deeply etched in doctors’ belief systems, and through them in the consciousness of the general public. The very notion that more plaques are associated with fewer heart attacks and strokes is likely to be considered preposterous.
Strong Claims Require Strong Evidence
Neglect of the scientific facts of arterial plaques leads to more disastrous treatment errors than any other neglect except that of insulin toxicity that sets the stage for obesity and diabetes. This is a strong claims and requires strong evidence. I devote this five-part series to do just that. I present personal autopsy, microscopic, biochemical, and clinical observations to expose the folly of both the plaque theory and cholesterol theories of coronary heart disease. I also cite the neglected published work of others to further support my assertions.
In past publications, I presented extensive evidence for debunking the “cholesterol theory” of coronary heart disease. In this series, I marshal evidence to debunk the “plaque theory”—the notion that plaques cause heart attacks—to offer readers a liberating and scientifically sound challenge to the dictums of the bypass-stent industry for cardiac conditions that do not threaten life in crisis setting.
The More-plaques-fewer-deaths Paradox
I introduce the term “more-plaques-fewer-deaths paradox” to highlight six essential points.
☞ First, in general fewer coronary heart and stroke deaths are associated with greater degrees of arterial plaques. Surprise!
☞ Second, we have choice: We can keep the inner “endo region” of the arterial wall healthy and live longer, or we can obsess on cholesterol deposits and plaques in the outer region of the arterial wall and live less. Another surprise!
☞ Third, countless lives are lost when non-drug oxygen therapies to restore “endo health” are opposed and blocker drugs (beta blockers, calcium channel bloclers, etc) are used to suppress symptoms caused by injury to endo cells.
☞ Fourth, coronary bypasses and stents do not remove arterial plaques. Stents close up with high frequency and bypasses less often.
☞ Fifth, many people live long healthful lives after coronary bypasses and stents but only when they address issues of foods, environment, an dstress that keep the inner linings of arteries non-sticky and negatively charged.
☞ Sixth, drugs save lives in crisis situations but do not reverse plaque formation to any meaningful degrees. By contrast, the focus on the inner endo region, where the circulating blood interfaces with the arterial wall, prevents heart attacks, strokes, and deaths.
An Iron Pipe With Inner Aluminum Lining
Imagine an iron water pipe with a delicate inner aluminum lining. The lining is so delicate that it is easily injured and leaks water. The lining also has a magical capacity for self-healing. It readily plugs its own micro-holes and prevents further water leakage. However it cannot prevent slow and steady corrosion of the outer strong part of the pipe made of iron by water which leaks through it before it self-plugs.
One part of the iron-aluminum pipe is burried in the soil. With passing years, the corroded iron part of the wall develops microscopic holes and some water leaking through tears in the aluminum lining,escapes into the soil surrounding the pipe. With time, the leaked water feeds mold spores in the soil and other microbes to create moldy, mulch-like suds around the pipe. A CAT scan of the pipe at this time reveals a thickened pipe wall—muddy mulch suds appear like plaques. However, the technology of CAT scanning is not yet advanced to reveal self-healing tears in the inner delicate aluminum lining. When the water flowing through the pipe is checked, it is clear.
Evolution’s Intelligent Design for Arteries
The structure of arteries is one of Nature’s marvel. It is a self-cleansing and self-healing structure. My grandfather forgot to die on time. I do not know whether he lived for 101, 102, or more years. My grandmother lived a similarly long life. They did not have any heart attacks or strokes. The Japanese in Okinawa Islands live for 120 or more years without heart attacks or strokes. That means Nature’s intelligent design for arteries can prevent plaque formation for hundred or more years, if only toxicities of foods, environment, and thoughts can be avoided.
The arterial wall has the following four layers:
1. Inner endothelial (endo for short) lining composed of a single-celled layer
2. A thin layer of loose connective tissue beneath the endo cells.
3. A strong and resilient muscle layer
4. A thin outermost layer of loose connective tissue
The inner endo layer s is smooth and electronegatively charged. It forms the “inner region” and prevents the blood cells and plasma from sticking to it. The outer region is where muscle and surrounding tissue develop cholesterol crystals, calcium deposits, and plaques. The endo region directly faces the circulating blood while the outer region is removed from it. The endo cells have strong healing ability since they are directly supplied by oxygen and nutrients. By contrast, the outer part damaged by scarring and plaques have limited ability to heal and restore their normal structure.
The “action” in events that trigger heart attacks, strokes, and kidney failure occurs in the endo region—the “endo-blood interface” seems an appropriate designation—and is always regulated and preserved by factors related to oxygen homeostasis (balance). This simple fact is readily validated by high-resolution phase-contrast microscopy. Regrettably, it is completely neglected by doctors controlled by the “heart disease industrial mega-complex.” Please ask yourself, when did I last see an “endo commercial” on TV? Or, when did The New York Times publish a large “endo article”? Or, The New Enron Journal of Medicine fight back the ”statin monsters” who want everyone to be on drugs like Lipitor, Crestor, Zocor, Pravaco and others prescribed to lower blood cholesterol level?
What Do Arterial Plaques Really Mean?
In cardiology literature, those who profit from the plaque preoccupation seldom, if ever, duly recognize and consider evidence against their model of the plaque-death relationships. Below are some quotes from recent cardiology journals that reveal the dimension of the problem that are seldom, if ever, duly considered in the matters of plaque-death relationships:
1. Atherosclerotic plaques that lead to acute coronary syndromes often occur at sites of angiographically mild coronary-artery stenosis. Lesion-related risk factors for such events are poorly understood (N Engl J Med 2011; 364:226-235).
2. Currently, there are no available methods that can reliably predict when or if an atheroma will rupture. ( Journal of Invasive Cardiology 2010;22: 406-411, September 2010).
3. The study by Stone et al. provides conclusive evidence that current morphologic assessments of vulnerable coronary plaque do not predict major adverse cardiovascular events
4. Study4 have confirmed that positive remodeling was a predictor of future acute coronary events, independent of plaque characteristics.
5. In response to the comments of Maseri and colleagues (writers of a letter to the Editor) we agree that the lesion-specific characteristics that we identified were sensitive but not specific for future major adverse cardiovascular events.
6. The 13 infarctions (areas of tissue death) that were related to culprit lesions were caused by stent thrombosis.