What’s the Real Cause of Heart Attacks?

Rebuttal of Conventional Theory

Until recently I believed, along with most physicians, that most heart attacks were caused by the progressive blockage caused by plaque buildup in the four major coronary arteries leading to the heart.

These plaques were thought to be composed of cholesterol that built up in the arterial lumen (inside of the vessel), which eventually cut off blood supply to a certain area of the heart, resulting in oxygen deficiency in that area, causing first pain (angina), then progressing to ischemia (heart attack).

The simple solution was to unblock the stenosis (the blockages) with either an angioplasty or stent, or, if that was not possible, then bypass this area with coronary bypass grafting (CABG). Simple problem, simple solution.

The problems with this approach became apparent to me through a number of avenues. The first emerged in a story related by the head of cardiology during a northern California heart symposium at which I was a speaker. He told us that during his residency he was part of a trial conducted in rural Alabama on black men.

In this trial, they did angiograms (injecting dye into the coronary arteries to detect blockages) on all the men presenting with chest pains. For the ones who had a single artery blocked, they did no interventions, only noting which part of the heart would have a subsequent heart attack if one occurred.

Of course, they all predicted it would be in the part of the heart supplied by that particular coronary artery. Then they waited. Eventually, many did return and did have heart attacks, but to the researchers’ surprise less than ten percent had a heart attack in the area of the heart supplied by the original blocked artery.

This means, of course, that had they performed the usual angioplasty, stent, or bypass on that artery, the patient would have received no benefit. The second occurrence that helped change my mind was the publication in 2003 of a large study conducted by the Mayo Clinic on the efficacy of bypass surgeries, stents, and angioplasty.

The study concluded that bypass surgery does relieve symptoms (chest pain); that bypass surgery does not prevent further heart attacks; and that only high risk patients benefit from bypass surgery with regard to a better chance of survival. In other words, the gold standard for treating arterial blockages provides at best only minimal benefits.

If you watch the video on www.heartattacknew.com and go to the FAQ called “The Riddle’s Solution,” it becomes clear why this is so. Large stable blockages, that is, sites that are over 90 percent blocked, in almost all cases compensate for the blockage by developing collateral or additional new blood vessels.

In fact, the view that the four coronary arteries supply all the blood to the heart is completely wrong. Starting soon after birth, the normal heart develops an extensive network of small blood vessels called collateral vessels that eventually compensate for the interruption of flow in any one (or more) of the major vessels.

As Sroka correctly points out in the below video, coronary angiograms fail to show the collateral circulation; furthermore the procedure creates spasms in the coronary arteries through the injection of heavy dye under high pressure. Thus, coronary angiograms are notoriously inaccurate at assessing the amount of stenosis in the vessels as well as the true blood flow in the heart.

To this day, most of the bypasses, stents, and angioplasties are performed on minimally symptomatic patients who show a greater than 90 percent blockage in one or more coronary artery. These arteries are almost always fully collateralized; it is not the surgery that restores blood flow, because the body has already done its own bypass.

If tests found a major coronary artery 90 percent blocked, with only 10 percent flow “squeezing through the bottleneck,” how could you possibly still be alive if you did not have collateral blood vessels? And are we really to believe that the decisive thing that will cause the eventual heart attack is when the stenosis goes from 93 percent to 98 percent?

This is an insignificant difference, and the premise that this small increase will cause a heart attack is completely nonsensical. Yet this is what most of the procedures are meant to accomplish, to unblock the stenosis, which as the video on heartattacknew.com shows, does not actually improve blood flow.

It is no wonder that in study after study, these procedures fail to provide any significant benefit to the patients. For these reasons, conventional cardiology is abandoning the stable plaque model in favor of a different model for the etiology of heart attacks one that, as it turns out, is equally invalid.

We can now all agree that the entire focus of cardiology—upon the stable, progressing calcified plaque: the thing we bypassed and stented for years, the thing we do CT scans of arteries for, the thing they told us is created from cholesterol buildup in arteries, the thing “alternative cardiology” like the Ornish program focused on eliminating—all this is not so important after all.

Dr. Cowan – at this point – proceeds to debunk the approach of using statin drugs to prevent the combination of inflammatory “buildup” and LDL-cholesterol, the exact two components that are targeted by statin drugs. And the approach that everyone should be on statin drugs to prevent this unfortunate occurrence, and the suggestion of putting therapeutic doses of statins in the municipal water supplies.

Another observation that puts into doubt the relevance of the coronary artery theory of heart attack is the fact that the proposed etiological mechanism of how thrombosed arteries cause ischemia is through cutting off the blood supply and thereby the oxygen supply to the tissues. To the enormous surprise of many investigators, the reality is that when careful measurements are done assessing the oxygen level of the myocardial cells, there is no oxygen deficit ever shown in an evolving heart attack I.  The oxygen levels (measured as pO2) do not change at all throughout the entire event. I will come back to this fact later when I describe what does change in every evolving MI ever studied.

If this is so, what then does cause heart attacks?

continued on next page

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