The puzzle of improving care and reducing costs in American medicine and in vascular conditions (that is, diseases associated with blood vessel metabolism) in particular – these are responsible for 60 percent of all cost – has been in part due to the nature of medicine itself. Physicians are at their core scientists. Our undergraduate degrees are in the scientific disciplines of biology, chemistry, physics. We have been educated in the culture of science and that is the environment in which we practice.
Thomas Kuhn’s The Structure of Scientific Revolutions perfectly describes a central problem in cardiovascular diseases. A scientific community cannot practice without a set of core beliefs. These central constructs are, in Kuhn’s terms, the foundation of the “educational initiation that prepares and licenses the student for professional practice.” The student’s instruction is “rigorous and rigid,” with the purpose of ensuring that these beliefs are firmly fixed in the student’s mind.
Scientists go to great lengths to defend the idea that they know what the world is like. It should come as no surprise then that “normal science,” – that is, the framework to explain the world used by the scientists who lead the current paradigm – will often suppress novelties that undermine its foundations.
So research often is not about discovering the unknown, but rather “a strenuous and devoted attempt to force nature into the conceptual boxes supplied by professional education.” A generally-accepted paradigm, essential to effective scientific investigation, requires “some implicit body of intertwined theoretical and methodological belief that permits selection, evaluation and criticism.” That paradigm, in turn, forms the basis of a new profession or specialty, like Interventional Cardiology, and from this follows the establishment of journals, societies, and a special place in the medical academic structure. The articles in those journals are intended for professional colleagues who share the the field’s knowledge and who are the only ones capable of fully understanding them.
A shift in the accepted scientific construct occurs when research aimed at further developing that formulation of the evidence runs into an anomaly — a fact that does not fit the paradigm and cannot be explained away. When anomalies pop up, they typically are not welcome and may be ignored. The current paradigm’s scientists may make little or no effort to formulate a new theory to explain the phenomenon. They are also likely to be intolerant of practitioners who try to do so.
All the same, the discovery of anomaly is the stimulus that leads to a new paradigm. The failure of existing beliefs and rules is the necessary but insufficient platform for the development of new scientific and practice structure.
The leaders of an entrenched paradigm strongly resist alternate systems of science and practice. Only in crisis can that resistance be overcome. No better example of this can be found than the current situation in the treatment of cardiovascular and arterial disease.
The fixed blockage is the dominant paradigm today for both the science and practice of cardiovascular and arterial disease management. In other words, it is viewed as a plumbing problem. This paradigm has persisted because it made so much sense.
Angina is a historical diagnosis – particularly in a man. Just talk to the patient and you can make the diagnosis. If a man walks and gets chest pain that is relieved by rest, he has angina. Almost all of those men have a blockage of 70% or greater.
If the cardiologist does a catheterization he will demonstrate the blockage. If he opens the blockage with a stent the pain will go away. But many men with angina go on to have heart attacks – it is high risk. So it is no surprise that blockage became the dominant scientific paradigm. To this day, virtually the entirety of the science, practice, and financing are organized around this idea: Heart attacks are caused by a progressive blockage. If we open that blockage before it becomes complete, we will save the patient.
Now the anomaly. In 1988, WC Little and his colleagues at Wake Forest performed a study “to help determine if coronary angiography can predict the site of a future coronary occlusion.” If the plumbing model were correct and a progressive blockage of the artery caused myocardial infarction, the findings on coronary angiography should predict the site of heart attack. It did not.
Little and his colleagues studied 42 consecutive patient records of patients who had had coronary angiography before and up to a month after having a heart attack. In 19 of 29 (66%) patients, the artery that occluded subsequently had less than a 50% occlusion on the first angiogram. In 28 of 29 (97%) the stenosis (or narrowing of the vessel) was less than 70%, even though it takes a stenosis of 70% or greater to justify angioplasty with stenting.
“Because it was difficult to predict the site of subsequent occlusion in our patients from the initial coronary angiogram, coronary bypass surgery or angioplasty appropriately directed only at the angiographically significant lesions initially present in almost all of our patients would not have been effective in preventing the majority of infarctions…instead effective therapy to prevent myocardial infarction may need to be directed at the entire coronary tree…”
And, in keeping with Kuhn’s description of the scientific revolution, the best arterial disease scientists quickly developed a new paradigm that provides a much better explanation of the mechanism of heart attack and other vascular events. Within 7 years of the first anomaly, Erling Falk, Prediman K Shah and Valentin Fuster, leading academic cardiologists, summarized four studies that came to the same conclusion as Little. Only 14% of heart attacks occur in an artery that was 70% blocked on the previous catheterization. Only 14% of heart attacks occurred in an artery with enough obstruction to cause angina and justify bypass surgery or stenting. Falk and his colleagues described the new paradigm very simply:
“plaque disruption with superimposed thrombosis (obstructive clot) is the main cause of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden death.”
Peter Libby is Chief of Cardiology at Boston’s Brigham and Women’s Hospital, one of Harvard’s teaching hospitals. One of the world’s foremost authorities on the science of heart attack and plaque rupture, he quite literally “wrote the book” on the topic. In the volume of Harrison’s Principles of Internal Medicine, the standard reference text for the discipline, that sits on my desk, Peter Libby wrote the chapter entitled The Pathogenesis of Atherosclerosis.
In 1995, the same year as the Falk article, Libby wrote a piece called “The Molecular Basis of the Acute Coronary Syndromes.”
“Bypass surgery or transluminal angioplasty (dilation of the artery and then, propping it open with stents) provide rational and often effective therapies for these fixed, high-grade stenoses (blockages). However, these treatments do not address the non-stenotic but vulnerable plaque (which may rupture and suddenly block the artery with clot). It is of interest in this regard that despite the well-accepted benefit of coronary bypass surgery on anginal symptoms, this treatment aimed at severe stenoses does not prevent myocardial infarction. To reduce the risk of acute myocardial infarction, one must stabilize lesions to prevent this disruptions, particularly the less stenotic plaque.”
In other words, heart attack is not caused by a gradual narrowing of the artery, but rather is the result of sudden cholesterol plaque rupture with subsequent clot formation, which blocks off the artery and cuts off blood flow.
Today, 14 years later, we can dramatically stabilize plaque and reduce plaque progression by smoking cessation and reduction of cholesterol, triglycerides, blood pressure, and blood glucose. We can prevent clot formation with aspirin and other medications.
The scientific revolution in vascular disease is 20 years old and the new paradigm firmly in place and supported by the very best vascular scientists. Still, the practice paradigm persists as if the science never changed.
Just last year, I heard a brilliant talk by Valentin Fuster, one of the co-authors on the Falk article. Afterward I asked him what it would take to move the practice paradigm forward. He responded that it would take the time required to replace current practitioners wi
th the next generation.
Can we afford to wait for that? Several years ago, I heard Dr Libby speak at a national meeting of the American Society of Hypertension. I later asked him, “Dr Libby, I read your article from 1995, saying that bypass and stenting do not prevent heart attack, do you still hold that view.” He became very animated and enthusiastic and said he was convinced that the new science was valid and required action to move it forward.
The science has become irrefutable. Yet the defenders of the old science still carry the day. I fear that medical scientists will not move this forward and it will require changes in payment and support for research coming from outside the professional community to bring the latest science to patients.
We have to recognize the suppression of anomalies and new paradigms in medicine. Only then can we develop mechanisms that can bring the latest evidence-based science to patients.
Bill Bestermann is Medical Director, Integrated Health Services at Holston Medical Group in Kingsport, TN.