Thomas Kuhn, The New Scientific Medical Revolution, and Anomalies

These are cross sections of a heart artery. You can see soft inflamed cholesterol deposits that don’t block the artery at all in the middle pictures. To the left, a ruptured plaque causes a clot that blocks the artery acutely to cause a heart attack.

In the last post, I wrote about the new scientific revolution. The structure of scientific revolutions is very well defined and Thomas Kuhn wrote a book on the topic. It is one of the most important scientific books of all time.

Revolutions in science don’t just begin. They don’t come out of thin air. They begin because of anomalies in the prevailing scientific paradigm. Medical scientific revolutions are no different. Anomalies are deviations from the expected or prevailing norm, and they play a pivotal role in the advancement of scientific knowledge.  Anomalies are the key to beginning a scientific revolution. These unexpected findings challenge existing paradigms and force the scientific community to re-evaluate their understanding of natural phenomena.

In science, an anomaly is an observation or experimental result that does not fit within the established theoretical framework. Anomalies are not merely errors or outliers; they are significant because they point to the limitations or incompleteness of the current scientific paradigm. When a scientific theory fails to account for an anomaly, it raises questions about the validity or scope of the theory. These questions, in turn, can lead to the modification or even replacement of the existing theory.

Throughout history, anomalies have played a central role in triggering scientific revolutions. One of the most famous examples is the anomaly of Mercury’s orbit. According to Newtonian physics, the orbit of planets should be perfectly predictable. However, the orbit of Mercury showed a small but consistent deviation from what was expected. For decades, this anomaly puzzled scientists until Albert Einstein's theory of General Relativity provided an explanation. This new theory not only accounted for Mercury's orbit but also revolutionized our understanding of gravity and space-time.

In my last post, I wrote about the well-established scientific revolution in our understanding of heart artery disease and heart attack. It was started by a deviation as striking as the anomaly of Mercury’s orbit. Up until 1988, everyone, and I mean everyone, believed that heart attacks occur because of chronically blocked heart arteries that finally block completely and cut off blood flow downstream of the blockage. That killed the muscle downstream. The answer was obvious under the old paradigm. Opening arteries with heart artery stents and bypasses would prevent heart attack and sudden death.

In 1988, a study at my alma mater Wake Forest uncovered a shocking anomaly that destroyed the old paradigm immediately. I have outlined the scientific method used in this investigation.

Here is the question to be answered:

Can putting dye in a heart artery (coronary angiogram or heart cath) to find blockages predict the site of a future total heart artery blockage that causes a heart attack?

The Experiment:

The heart caths of 42 consecutive patients who had undergone coronary angiography before and up to a month after suffering a heart attack were evaluated.

The Results of the Experiment:

Twenty-nine patients had a newly blocked heart artery. Twenty-five of these 29 patients had at least one artery with a greater than 50% blockage on the initial cath. However, in 19 of 29 (66%) patients, the artery that subsequently blocked had less than a 50% stenosis on the first angiogram, and in 28 of 29 (97%), the stenosis was less than 70%. In every patient, at least some irregularity of the coronary wall was present on the first angiogram at the site of the subsequent coronary obstruction.

That single study destroyed the old scientific paradigm of chronic blockages leading to heart attack and sudden death. It destroyed the validity of opening blocked arteries. To justify opening an artery with a stent s bypass, you must have an artery that is blocked 70% or more. In 28 of 29 patients the blockage was less than 70% and so the opening arteries that are 70% blocked or more would not have prevented the heart attacks.

The cardiologists involved in this study recognized the implications of their work in 1988. “Acute myocardial infarction (heart attack) is usually produced by the sudden total occlusion of a coronary (heart) artery by thrombus (clot), usually occurring at the site of an atherosclerotic lesion (cholesterol plaque). Our study indicates that the lesion (blockage) that will be the site of the thrombotic occlusion (clot blockage) frequently is not severe when evaluated by coronary angiography (heart cath) weeks to years before the infarct in patients with mild to moderate coronary (heart artery) disease; thus, coronary angiography (heart cath) was not able to accurately predict the time or location of the subsequent myocardial infarction (heart attack.) In the majority (66%) of patients in this study, the myocardial infarction occurred because of the occlusion of a coronary artery that did not contain an obstructive (more than 50% diameter narrowing) stenosis (blockage) on a previously performed coronary angiogram. A high-grade stenosis (more than 70% diameter narrowing) was initially present in the infarct-related artery in only one patient.”

These cardiologists immediately realized the implications of their landmark findings. “Because it was difficult to predict the site of the subsequent occlusion (later artery blockage) in our patients from the initial coronary angiogram, coronary bypass surgery or angioplasty appropriately directed only at the angiographically significant lesions (arteries blocked 70% or more) initially present would not have been effective in preventing the majority of myocardial infarctions (heart attacks). This does not indicate that arteries that do not have obstructive lesions should be bypassed or dilated. Instead, effective therapy to prevent myocardial infarction may need to be directed at the entire coronary tree, not just at obstructive lesions. Such therapy to prevent myocardial infarctions might rationally include avoiding smoking, reducing serum cholesterol, administering agents that alter platelet function such as aspirin or, possibly, fish oil, and pharmacological agents to prevent spasm of the coronary arteries.” That is the first description that I have found for optimal medical therapy of heart artery disease.

“In conclusion, an acute myocardial infarction occurred in the majority of our patients because of occlusion of a coronary artery that previously had less than a 50% angiographic coronary stenosis. Furthermore, in most of our patients with mild-to moderate coronary artery disease, the infarction did not occur because of the occlusion of the artery that had previously been found to have the highest-grade stenosis. This suggests that the presence of obstructive coronary artery lesions indicates that a patient is at risk for developing a myocardial infarction but, in the majority of our patients, did not predict the timing or the location of the coronary occlusion that would subsequently produce a myocardial infarction. Thus, therapy such as percutaneous transluminal coronary angioplasty) (stents aimed solely at sites of coronary obstruction may not, by themselves, be able to prevent many subsequent myocardial infarctions.”

As important as this study is, it did not stand alone. There were three other studies between 1988 and 1991 that confirmed these findings and they were summarized in this great article by Erling Falk and his colleagues in 1995. Dr. Peter Libby confirmed that review that same year. These studies occurred 36 years ago. The science has been conclusive all that time, but many stable patients still have their arteries opened and optimal medical therapy is still not widely available.