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Recently, there has been much discussion and debate about what causes the atherosclerosis that builds up in our arteries. The western medical explanation is that high cholesterol in our blood causes cholesterol to get clogged in arteries and if that clogging becomes significant enough then it can restrict blood flow to an area of the heart. It is thought that this will cause tissue to die like we see in a heart attack. I have written about why high cholesterol is not the cause of atherosclerosis (here) and why high cholesterol in our bodies can actually be a good thing (here). But is atherosclerosis even relevant when is comes to heart attacks? It is time we ask ourselves if atherosclerosis of enough significance is what causes a heart attack at all? Also, we need to discuss if the breaking off of a piece of an atherosclerotic plaque and creates a clot is a cause of heart attacks?


If you follow my blog you can probably guess that I am going to argue that a stenosis or a clot is not the cause of the majority of heart attacks. I am going to do this mainly by summarizing the work of Dr. Giorgio Baroldi. He was a medical doctor and coronary artery pathologist who spent his career researching the causes of heart attacks.


Dr. Baroldi did many, many autopsies of hearts over his career, and had strongly opposed the stenosis/clot theory of heart attacks based on his work. His work began in the 1950’s during the heart disease mania that was President Eisenhowers’ heart attack and the subsequent blaming of saturated fat and cholesterol by Ancel Keys’ bad science. Due to all this no one was listening to Baroldi. In his work, he studied the hearts of people who died of heart attacks, who died of other non-heart related diseases, and who had no medical ailments but died in accidents. His findings were perplexing.


In one study, (r) he found that in some of the victims who died of accidents and were healthy, with no medical history of heart disease symptoms, had “old total coronary occlusions” despite having no clinical signs of heart disease before death. They also had no evidence of myocardial ischemia upon autopsy. How could these people who had a total occlusion of an artery of the heart that had been there well before they died have no signs of heart disease from reduced blood flow and no tissue death from that blockage? In fact, of the 217 healthy patients who died of an accident in this study, 46 had mild stenosis present and 171 had severe stenosis present. Of the 46 who had mild stenosis a clot was found in 5 of them and of the 171 with severe stenosis a clot was found in 68 of them. Yet, in all cases there was no evidence of tissue death from these findings. How could stenosis and clots be present without causing a heart attack?


In another study (r), Baroldi and his colleges looked at a group of men in the Armed Forces. The group consisted of “208 acute infarct cases, 116 unexpected sudden coronary death cases, and 112 expected coronary death cases”. In these men who died of a heart attack, a clot of some sort was present in less than 50% of the cases. Of the cases where there was a clot, most of them were located in the area of a pre-existing stenosis of >70% narrowing. There was also evidence that the clot found was a secondary event of the heart attack, meaning that it happened after the heart attack started and did not cause it. Baroldi would later find research showing this. (r) Further, in the cases where there was a clot there was a “lack of correlation between the age of the infarct, and the age of the thrombus”. This means that the clot they found had been there well before the heart attack occurred. These findings are not matching up with the theory that stenosis or clot formations cause heart attacks.


To begin to clear this up, I want to discuss yet another study by Baroldi (r) that will shed some light on some of this. He did what is called his plastic cast studies. In these, he would fill the arterial system of the autopsied hearts with a plastic (neoprene or latex) material and then warm it so the material would harden. Then he would dissolve the rest of the tissue away with hydrochloric acid until he was left with just a plastic cast of the arterial system of the heart. When he studied these, he found two pretty striking things. On was that if the heart he was studying did suffer from a heart attack often times there was a clot, but it was in an entirely different area of the heart than where the heart attack occurred. This is shown below.


He also found that anywhere he saw a greater than 70% stenosis of a coronary artery the body had built a vast network of collateral arteries that essentially bypassed the stenosis. He found anywhere from 5 to 22 collateral arteries around a single stenosis with an average of 16 per stenosis. Then heart had created its’ own bypass.


This explains a few things. One, because the body builds its’ own bypass, it explains why large studies of the clinical outcomes from heart bypass surgery show that they are largely ineffective and don’t prolong life or prevent heart attacks. (r,r,r,r) Secondly, in the study of the men in the armed forces who died of heart attacks, it explains what was going on when he found clots in stenotic areas yet the heart attack didn’t happen in those areas. The heart had already built a bypass around the stenotic area so a clot forming there wouldn’t affect blood flow.


At first, Baroldi questioned whether the blood supply from these collateral arteries would be sufficient enough to supply the necessary blood to the needed tissues. He would later find that these collaterals can form very quickly, within days, so as not to leave the heart without blood in the case of a stenosis (r,r). He also concluded that since many of the subjects he studied who had died of an accident had no heart diseases symptoms before death but also had severe stenosis on autopsy, that these collaterals must have been enough to maintain adequate supply to heart tissue. (r) He discusses at length the inability of an angiogram to visually show the existence of collaterals. Though this video proves they must exist. Case studies have shown that people are able to run marathons with severe blockages of coronary arteries so the blood supply must be pretty strong. (r)


To summarize, we have discussed how, in the presence of stenosis and clots, there is evidence that they were not the cause of heart attacks. Also, that sometimes the person had clot/stenosis and a heart attack was not even the cause of death. Further, sometimes not a single stenosis or plaque was found in someone who had died of a heart attack. After all these findings Baroldi concludes saying, “Therefore, in their natural history, acute coronary syndromes may begin in the absence of a functional stenosis and in the majority of cases, in the presence of old critical obstructions compensated by collaterals. What, then, is the meaning of the coronary heart disease/atherosclerosis association?” (r)


What does all this mean? It means that the clot/stenosis theory of heart attacks is not as sound a theory as we are told. While a clot can cause a heart attack, the work of Giorgio Baroldi has shown us that in the vast majority of cases they are not to blame. This begs the question of what does cause a heart attack. I have given a brief explanation of what does cause a heart attack in other posts. But in my next post I will lay out all the details and explain the series of events that cause a heart attack without it having to be precipitated by a stenosis or clot. Stay tuned!


Stay healthy out there!


Want to learn more fascinating information about the heart? Click here to find out more about my heart course, or click here to order my book, Understanding the Heart.


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