The COURAGE Trial: How the Media Misled the Public Concerning the Utility of Angioplasty and Stenting Procedures for Stable Coronary Disease

You may have heard a lot in the news recently about a recent study published in the New England Journal of Medicine concerning the use of percutaneous coronary intervention (PCI) procedures (aka angioplasty and stenting) in stable coronary artery disease. In this article, I will describe how the media has taken it upon themselves to present this study to the public in a misleading way, and how the study really does not tell us anything which we have not already known for years. It is also the public’s pre-conceived notion of how a heart attack occurs and of the utility of these procedures which is driving this hysteria, and I feel that in order to correct this misperception, they need to be properly educated on the basics of coronary artery disease and the utility of available interventions in treating it.
I want to preface this article by stating the following: A. I am not a cardiologist. B. This article is an opinion piece. Nevertheless, I obviously strongly believe in what I am stating here, as you will see shortly. As well, I feel as if the basic concepts behind this controversy are easy enough for a layperson to appreciate, as you do not need to be a board-certified cardiologist to understand it. Let us begin with a little background on this trial, and move on from there.
Results of The Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial was released early through the New England Journal of Medicine’s website (www.nejm.org) on 3/26/07 as “Optimal Medical Therapy with or without PCI for Stable Coronary Disease” (direct link to article here). Although I won’t describe the trial in extreme detail, the concept of the trial is simple enough: the primary investigators randomized ~2300 patients diagnosed with stable coronary artery disease into a group that received PCI + optimal medical management and another group that received optimal medical management alone, and then followed them for several years to determine outcome (I explain what is meant by stable coronary artery disease below). PCI included angioplasty and stenting with bare-metal stents (this distinction is important, as drug-eluting stents are quickly becoming the standard). The primary outcome measured was a composite of both death from any cause + non-fatal heart attack (myocardial infarction, or MI).
The results of the study, for a reason I cannot for the life of me figure out, we’re deemed “SHOCKING”: There were essentially no differences in the rates of all-cause mortality and non-fatal heart attack between these 2 groups after a follow-up period of 2.5-7 years!! Seemingly, PCI + medical management of stable coronary disease was no better than medical management alone in preventing these outcomes!! The media immediately jumped on this, claiming that the results of the trial questions the utility of PCI with angioplasty and stenting. Accusations followed: interventional cardiologists were doing unnecessary procedures; the makers of the stents were making enormous profits at the expense of patients, so on and so on. In fact, here are some of the headlines spewed out over the papers and internet:

“Heart patients want answers after stent study”

“Heart study questions stent use”

“Heart experts question value of stent therapy”

“Stent Shocker: They Don't Stop Heart Attacks”

……The list goes on and on, and the fallout has only just begun as I’m writing this ~4 days after the study was released. I fear what might happen in the days to months ahead based on complete hoop-la!! Boston Scientific stock dropped more than 7% after this study was released (they make the Taxus drug-eluting stent). But the question that should be asked is this: “Did this study tell us anything which we didn’t already know?” Read on.
First of all, in general, the public does not understand what causes a heart attack in the first place. I’ve been complaining a lot about this fact for the last 2-3 years, and to be honest, prior to going to medical school, I misunderstood the mechanism as well. It is one of the greatest misperceptions in medicine. To understand this, you must comprehend the difference between stable and unstable coronary disease, and there are many.
Atherosclerosis, extremely simplified, is a process in which cholesterol is laid down in the inner lining of blood vessel walls. The process is complex, but over time, plaques form which can encroach on the hollow lumen of vessels, causing blockages. In other words, the pipes become clogged.
When this process occurs in a coronary artery, the territory of the heart muscle supplied by that artery can become ischemic (i.e. starved for blood and resultant oxygen). The heart is a muscle, and this muscle has a certain demand for blood. The coronary artery supplies the demands of the heart with needed blood. It is simple supply-demand economics. If the supply is too low to meet the heart’s demand, the heart suffers. Conversely, if the demand is too high for the available supply via the coronary arteries, the heart also suffers. This ischemia is manifested in humans through angina, typically in the form of chest discomfort, among other symptoms.
The process of atherosclerosis thus results in blockages, known in medical terminology as stenoses. A stenosis in a coronary artery can limit blood supply to the heart, although the heart can sometimes compensate for this in various ways, mostly by causing the affected artery to become wider (dilation). Thus, it adjusts its own supply to meet growing demands.
If the atherosclerotic process continues, and the stenosis worsens, eventually the heart can’t compensate for the reduced supply anymore, it becomes ischemic, and the symptoms of angina start to occur. This means that the heart is starving for blood supply.
A segment of the heart usually does not become ischemic until a stenotic plaque blocks approximately ~70%-99% of the affected coronary artery.
These plaques that cause 70-99% stenoses are usually stable. They will usually continue to grow as the atherosclerotic process continues, but a patient almost always will manifest anginal symptoms and present for treatment before this slow process leads to complete occlusion of the affected coronary artery. The symptoms help determine the problem. Stress the heart, and the angina may become more apparent, because the heart has a higher demand when it is stressed, and the supply of a severely stenotic coronary artery cannot meet this demand, even after dilating as a compensatory measure. Therefore, stable angina usually manifests itself as chest discomfort in the setting of stress upon the heart, such as exertion.
The 4 determinants of cardiac demand include heart rate, contractility, and the lesser known entities of afterload (related to the systemic blood pressure that the heart must contract blood against), and preload (related to the amount of blood the heart fills with). Change any or all of these 4 determinants enough, and the heart muscle will demand more blood. If it can’t receive it due to severe stable stenoses, stable angina occurs. In summation, it is a supply-demand mismatch problem.
THIS is what the COURAGE trial studied. It does not have ANYTHING to do with how a heart attack occurs. But THAT is the misconception. A majority of the public believes that it is this process which leads to a heart attack, and that fixing these stable stenoses will prevent a heart attack from occurring. They think that the stenoses keep worsening and worsening over time until the affected coronary vessel is 100% blocked, a heart attack occurs, and the heart muscle dies. That is NOT how it works. Let me set the record straight.
A classical heart attack is caused by unstable plaques. Unstable plaques are usually associated with stenoses in the 40-60% range, NOT usually the 70-99% stenoses, which tend to be more stable as described above. There are many determinants of an unstable plaque as compared to a stable one, which I will quote below directly from the published COURAGE trial manuscript.
Atherosclerotic plaques usually stabilize with something known as a fibrous cap, material which keeps the cholesterol core of the plaque from being exposed to the blood contained within the vessel. When this fibrous cap ruptures and the cholesterol-core is exposed to the bloodstream, the body attempts to seal it off with a thrombus (a clot). Sometimes this process can get a little out of control, and the clot grows and grows so much that it completely blocks the affected vessel. This is why aspirin and other anti-platelet agents, as well as blood-thinners like heparin, which affect the clotting factors, can help in these cases.
When an intracoronary thrombus occurs due to this plaque rupture, the coronary vessel can become 100% occluded extremely quickly, and the affected heart muscle’s blood supply is completely shut off. This can be catastrophic, especially if it affects one of the main coronary arteries. People can die suddenly due to electrical abnormalities (arrhythmias) which result from this lack of blood supply. Other times, the thrombus stops growing on its own, resulting in a plaque growing from 40-60% to say 80-95% within minutes. This is markedly different than the stable plaques described above. Needless to say, a person will experience unstable anginal symptoms if this happens, often while the patient is at rest, since the supply is severely limited by the resultant clot. As well, since this process is rapid, the heart cannot compensate with improving blood supply well in the short-term, as it can with the slow process of stable plaque propagation by growing new, small collateral vessels to the area around it.
In general, heart muscle starts to die within ~30 minutes or so after the affected coronary artery becomes occluded. Fortunately, the body’s own clot-busting system can re-vascularize (re-open) the artery by partially dissolving the clot. The process may cycle from here, as the clot shuts the vessel down, opens up, closes down, etc. The affected person may experience stuttering of anginal symptoms. This may go on for days, but it is an unstable condition. The unstable plaque will continue to be unstable until the body stabilizes it further with remodeling of the clot and fibrous cap over time, or until the worst happens, when the clot completely occludes the vessel, a full-blown heart attack occurs, and the affected heart muscle either dies or the patient seeks definitive treatment. Needless to say, after the whole affected muscle wall dies, the coronary artery can open up all it wants to re-perfuse its territory, but it won’t matter, since the muscle is dead.
This entire process is known as acute coronary syndrome (ACS). It is a spectrum of diseases encompassing unstable angina, NSTEMI, and STEMI, depending on how the supply of a coronary artery is affected by the formed clot, and the resultant muscle damage. In unstable angina, perhaps the clot is formed, cleared, formed, cleared, etc., but cleared in enough time to avoid death of heart muscle, or maybe the clot forms to an extent that it causes enough of a significant stenosis (70-99%) to cause symptoms, but not enough of an acute supply-demand mismatch to result in death of heart muscle. NSTEMI is caused when this aforementioned process does result in death of some heart muscle, as determined by reduced supply and increased demand, coupled with the time over which this mismatch occurs. STEMI is the classical heart attack, resulting from complete occlusion due to an unstable plaque rupture and subsequent intracoronary thrombus. The entire wall of the heart supplied by the affected vessel dies due to the lack of blood supply.
The difference between the entities of stable coronary disease and unstable coronary disease is KEY to understanding the COURAGE trial and its ramifications. Both the media (at least some of the media) and the public completely misunderstands this difference and also interchanges them. Although it is wrong, they believe that stable coronary disease leads to heart attacks, and thus if stable coronary disease is treated with PCI (angioplasty and stents) to relieve the resultant stenosis, it will prevent a heart attack from occurring. This is completely WRONG (although I do not place the blame on the public for this misunderstanding, as it is due to a lack of education).
Acute coronary syndromes are unpredictable events caused by unstable plaque rupture. The risk of it occurring can be reduced by lifestyle modification (diet and exercise) and specific medications. As well, the progression of acute coronary syndromes to a full-blown STEMI and resultant death of affected heart muscle, if they are caught in time (minutes to days, or even months to years, depending on the instability involved), CAN be prevented, none other than with medications and the same procedure which has been completely lambasted over the past several days, PCI, with better outcomes if stents are utilized!!
This has been PROVEN many many times, demonstrated by studies involving a huge amount of patients who received all manner of available procedures, including both bare-metal and drug-eluting stenting. Both angioplasty with bare-metal, and drug-eluting-stenting procedures save lives in this manner. They save thousands upon thousands of lives every year by treating unstable plaques. If a person is having a STEMI with a completely occluded coronary vessel and presents to a hospital that is fortunate enough to have the skilled professionals which can perform angioplasty and stenting (at all hours nonetheless), they will SAVE their heart (and maybe their LIFE). The faster they can get the procedure done and re-open the vessel, the more heart muscle is saved.
Within the medical community, it is well-accepted and has been proven multiple times that PCI in the setting of all acute coronary syndromes saves lives and reduces the rate of a resultant heart attack. Even if a patient presents with unstable angina (in which a vessel is threatening to shut down), PCI can prevent death and resultant NSTEMI or STEMI, as well as further anginal symptoms, if the unstable plaque can be treated with a balloon and stent before the vessel shuts down and a STEMI occurs.
The point is THUS: The fact that the COURAGE trial showed that PCI does not result in any survival benefit or prevention of heart attacks in stable coronary artery disease due to a stable plaque is ALREADY KNOWN. It has been studied before!! We KNOW that treating these stable plaques with angioplasty and stent only results in relief of stable anginal symptoms and improving exercise tolerance.
All of these considerations are in fact stated in the actual manuscript of the COURAGE trial as follows, in the introduction:

”PCI reduces the incidence of death and myocardial infarction in patients who present with acute coronary syndromes,^5,6,7,8,9,10 but similar benefit has not been shown in patients with stable coronary artery disease.^{11,12,13,14,15}” “Although successful PCI of flow-limiting stenoses might be expected to reduce the rate of death, myocardial infarction, and hospitalization for acute coronary syndromes, previous studies have shown only that PCI decreases the frequency of angina and improves short-term exercise performance.^11,12,15” (italics added)

Please notice the references quoted in the above statement. References 5-10 are from the previous studies that have already demonstrated a benefit of PCI in unstable acute coronary syndromes. Reference 5 itself is the ACC (American College of Cardiolgoy)/AHA (American Heart Association) guidelines on management of STEMI. The other references are from original studies or meta-analyses (which combine multiple studies into one) that show this benefit. So why is it that I am reading a headline that says “Stent Shocker: They Don’t Stop Heart Attacks”? You are right; they DON’T stop heart attacks if used in intervention of stable plaques, since stable plaques don’t cause the heart attacks in the first place!!
Also note references 11-15. They include some studies which compared stenting and/or angioplasty against medical management alone, similar to the COURAGE trial (although there were some differences). AGAIN, these trials showed a benefit in control of anginal symptoms in patients with stable coronary artery disease. Some of these studies (using angioplasty alone, before stents were on the market) are ~15 years old!!
Therefore, the so-called “surprising results” of the COURAGE trial are not a surprise at all!! They are anything BUT a surprise. We have known that PCI does not prevent heart attack or death in stable coronary disease for a very very long time. As well, given the background information I have provided above on the actual pathophysiology of the process, the studies are not a surprise at all anyways. They just prove what we already know via common sense. If I sat down and described to you this process of how unstable plaques lead to heart attacks, and how stable plaques lead to demand ischemic symptoms of stable angina, would you not, via common sense, hypothesize that placing a stent across an unstable plaque would prevent a heart attack from occurring? And that placing a stent across a stable plaque WOULD NOT prevent a heart attack from occurring, but just might help with anginal symptoms? Well, similar investigators thought the same thing (although this pathophysiologic mechanism was not entirely worked out when the first studies came out) and studied the question, confirming these hypotheses.
Therefore, I truly believe that the public is and will remain confused about how a heart attack occurs, and therefore they misinterpret the findings of the COURAGE trial, in still thinking that stable coronary disease leads to heart attacks. Granted, stable plaques may be a marker for other, more unstable plaques elsewhere, but themselves they do not lead to heart attacks. I don’t know how many more times I can say it. In fact, a far majority of stents are placed for acute coronary syndromes, NOT for stable coronary lesions.
Other commentators on this controversy point to inherit study flaws, such as the generalizability of the results (~85% of the study population were men), etc. However, THAT IS NOT THE POINT. The media and public are simply mixing up unstable (acute coronary syndromes) and stable coronary disease. The difference in between these is mentioned perfectly in the manuscript of the COURAGE trial itself!!:

“Our findings may be explained, in part, by differences in atherosclerotic plaque morphology and vascular remodeling associated with acute coronary syndromes, as compared with stable coronary artery disease. Vulnerable plaques (precursors of acute coronary syndromes) tend to have thin fibrous caps, large lipid cores, fewer smooth-muscle cells, more macrophages, and less collagen, as compared with stable plaques, and are associated with outward (expansive) remodeling of the coronary-artery wall, causing less stenosis of the coronary lumen.³⁶ As a result, vulnerable plaques do not usually cause significant stenosis before rupture and the precipitation of an acute coronary syndrome.³⁶ By contrast, stable plaques tend to have thick fibrous caps, small lipid cores, more smooth-muscle cells, fewer macrophages, and more collagen and are ultimately associated with inward (constrictive) remodeling that narrows the coronary lumen. These lesions produce ischemia and anginal symptoms and are easily detected by coronary angiography but are less likely to result in an acute coronary syndrome".^37,38

"Thus, unstable coronary lesions that lead to myocardial infarction are not necessarily severely stenotic, and severely stenotic lesions are not necessarily unstable. Focal management of even severely stenotic coronary lesions with PCI in our study did not reduce the rate of death and myocardial infarction, presumably because the treated stenoses were not likely to trigger an acute coronary event.” (italics, underlining, and bolding added)

Another point is to be made about the COURAGE trial, as I fear that people are going to start to refuse much-needed intervention with stents based upon this trial. Even if a patient does have stable coronary disease, the COURAGE trial suggests that there is no difference between trying medical management alone vs. PCI, and therefore, the patient might ask, WHY would I need a stent then? Justifiably, the question should be asked, right? For one it is a procedure, with its own risks, it costs much more than medicines, and also has some risk (although low) for in-stent thrombosis after it is placed, which leads acutely to a STEMI and sometimes, sudden death (Note: If you haven’t heard, there is another huge controversy involving this potential risk with drug-eluting stents, which I think is blown WAY OUT OF PROPORTION as well, and which would require a whole other article in and of itself).
Even if the patient understands their condition correctly, that they have stable coronary disease and that the COURAGE trial did not show “any difference” between medicines and PCI in management of this disease, they need to THINK (or be counseled) very carefully before they refuse PCI and elect to be treated with medication only. The consideration must be made in terms of the specific outcomes which are measured by the COURAGE trial. As we stated, the trial measures the rates of ALL-CAUSE DEATH and HEART ATTACK in each the medicine group and the stent + medicine group, and it was those outcomes which showed no difference. So how can one say there is no benefit at all in utilizing PCI even in stable coronary artery disease when stable coronary artery disease doesn’t lead to DEATH or HEART ATTACK in the first place? That is what this study attempted to measure, and again, the fact that there were no differences between the two treatment modalities is really no shock at all.
However, maybe there is a benefit after all in treating stable coronary disease with PCI (after all, I already stated that this is well studied and proven, as noted in some of the studies cited in the COURAGE trial as above), and that benefit would be control of demand-ischemia anginal symptoms. So there is still a benefit to PCI in stable coronary disease as compared to medications, in the control of anginal symptoms, and this has been KNOWN and is thus the indication for doing the procedure in the first place. But obviously, even prior to the COURAGE trial, I can say that most patients who received a stent to help treat their stable coronary disease likely thought that it was instead saving their life, or at least, preventing the ~80-90% lesion from progressing to a 100% lesion and (falsely deduced), causing a heart attack. I think it is also a failure on our part as physicians in explaining the true benefit of doing PCI in these cases, controlling their anginal symptoms.
I would still say that this is a noble benefit, and that is why, even in stable coronary disease, PCI definitely has a role. Anginal symptoms are uncomfortable and limit activity, and PCI can control these. I think the issue may be that interventional cardiologists are often quick to use PCI to control these symptoms, rather than trying medical management first in patients. Afterall, there is almost zero risk that the stable stenosis itself is inherently dangerous, since it doesn’t lead to heart attacks!!
Therefore, many patients could probably try medical management first instead of immediately receiving PCI, and we do choose this option for our patients in select cases, after considering the options, especially if we feel that undergoing an angiogram and subsequent PCI may be too risky to justify the benefits. Many of them do fine with no recurrence of symptoms, or if symptoms recur, they are controlled immediately with an under-the-tongue nitroglycerin tab.
Medicines can alter the dynamics of this supply-demand mismatch problem quite nicely. Nitrates and calcium-channel blockers can help dilate coronary arteries for more supply, and medicines which lower heart rate, contractility, and afterload (through blood pressure control) can help lower demand, and patients may remain symptom-free. Nevertheless, if they fail this medical management, PCI is definitive because it completely eliminates the supply-side problem (by opening the artery up completely, at least for a period time, i.e. months to years) of the entire supply-demand equation.
So the COURAGE trial measured a composite of all-cause death and heart attack rates as their primary outcome in comparing the two management strategies. However, as noted in many other studies prior showing a benefit in anginal symptom management with PCI for stable coronary disease, did the COURAGE trial also measure and show this benefit as well? In fact, they did measure this outcome as well, although not much is really mentioned about it (afterall, it has been proven already and this trial attempted to compare death and heart attack rates). In this study, they stated the percentages of patients that were “angina-free” in both the PCI + medicine group vs. the medicine-only group, at time points of 1, 3, and 5 years after enrollment in the study. The PCI + medicine group had slightly higher rates of being “angina-free” at both 1 year (66% vs. 58% of patients) and at 3 years (72% vs 67% of patient). Data for the measurement 5 years after enrollment of the study was not “statistically significant” (put simply, if there was a difference detected between the two management strategies, there is a risk that the difference was not true but simply due to chance, and at a risk that is considered unacceptable by the medical community).
Therefore, in line with previous studies, this study seemed to favor PCI even in control of anginal symptoms (at least in being “angina-free”). Particularly, it is EXTREMELY important to note that the trial was conducted with the use of bare-metal stents for stable coronary disease. Bare-metal stents have a higher re-stenosis rate than the newer drug-eluting stents, meaning that the stable plaque comes back after only several years as the body reacts to the foreign material in the stent and grows over it rapidly (although, some evidence points to the fact that occasionally the re-stenosis plaque can also be unstable). Therefore, this consideration must be taken into account when interpreting the benefit of PCI + medicines on anginal symptoms as compared to medical therapy alone, as the newer drug-eluting stents will allow a greater period of time to go by before a patient has recurrence of stable anginal symptoms and require a “re-do” PCI. If a similar randomized trial was conducted to evaluate drug-eluting stents + medicines instead of bare-metal stents as utilized in PCI vs. medical management alone, and the primary outcome measures were anginal symptoms instead of death and heart attack (as measured in the COURAGE trial), I hypothesize that it would suggest an even greater benefit with an even-wider spread between the percentages noted above, in terms of patients being angina-free at 1, 3, and 5 years. I am unsure however if a specific trial has addressed this clinical question as of yet.
Given everything I have mentioned up to this point concerning the COURAGE trial, I would like to discuss its ramifications. Not, in fact, the actual ramifications of the results of the trial, because again, I do not feel it added much, and it definitely didn’t shock me. I am speaking of the ramifications which are the result of those who misconstrue results of the trial, including the media, the public, and even surprisingly A LOT of physicians, many of them cardiologists (given this, I am sort of worried that I am missing something here, but I know I am not)!
The fall-out from this is just beginning, and to me, it is very frightening. My main concern is that some patients are sure to refuse a much-needed therapy because they do not understand how PCI benefits them immensely if they are having an acute coronary syndrome, due to an unstable plaque. The benefit of PCI in these cases is proven and recommended, but I know that some people will adamantly refuse the procedure because they are confused about the differences between unstable and stable coronary disease, or they will simply quote a headline or TV news segment they saw saying that there is “no difference” between PCI and medical management. There is absolutely no doubt in my mind that many will die or suffer great morbidity due to a heart attack because of this, those who would not have suffered these bad outcomes if they had not read the paper or turned on the TV and witnessed all of the over-blown hype concerning this trial. It is quite sad, and they need to be educated. Many patients may even delay seeking prompt medical evaluation in this regard.
I have already seen this concern manifested, only FOUR days after this trial was released. As I am on a cardiology rotation right now, earlier today a patient who presented with chest pain told us that if we found significant stenoses during his angiogram, he did not want PCI performed, but instead wished to end the procedure and discuss the possibility of medical management vs. PCI first (usually, PCI is performed at the same time as the initial angiogram, since going back and doing a 2^nd angiogram with PCI doesn’t make financial sense and opens up the patient to more risk with an additional procedure). HOWEVER, the patient had presented with symptoms which were more consistent with unstable angina (i.e. rest chest pain, and stuttering, intermittent chest pain), therefore worrisome for an unstable plaque!! Luckily, his angiogram did not show much disease, and therefore, hopefully his chest pain was due to some other cause. Nevertheless, it shows how this over-blown media coverage of the COURAGE trial is already affecting the decisions of patients, albeit in a detrimental way.
Another concern I have is that many physicians may misinterpret the results of the COURAGE trial, and thus the way they manage their patients may change for the worse. I doubt this will happen in hospitals, where access to cardiologists will result in the correct management a vast majority of the time. My concern is particularly with internists, who may see a patient in their office with symptoms consistent with unstable angina, and instead apply the results of the COURAGE trial and treat with medical management first. The results of this could be catastrophic, although I still trust that most internists understand the difference between acute coronary syndromes and stable angina.
To be fair, the COURAGE trial may result in many patients avoiding unnecessary PCI by trying medical management first for their stable coronary disease, and if that doesn’t work, they can subsequently undergo PCI for definitive treatment. Unfortunately, as I stated above, that would usually require two procedures (first an angiogram to diagnosis the stable coronary disease, and subsequently another procedure for the PCI) instead of one, thus more cost, risk, etc. As well, as above, we must still remember that PCI with a drug-eluting stent is likely to result in an even greater benefit of time in which the patient would be “angina-free” as compared to both bare-metal stents as studied in the COURAGE trial and medical management alone.
Another major concern I have is insurance coverage. Will the insurance companies (or Medicare) refuse to pay for PCI procedures in the management of stable coronary disease, unless medical management is tried first? While that may be justifiable, it shouldn’t be justified in light of the results of the COURAGE trial, because again, PCI has NEVER EVER been shown to lower the rates of death or heart attack in the first place, and that is what the COURAGE trial attempted to measure in comparing medical management alone to PCI + medicines. If everybody could just GET THAT THROUGH THEIR THICK SKULLS!!
I also pray that nobody loses their employment or is sued because of the results of this trial. That would truly be a tragedy, but it is bound to happen. Much of the fall-out is still unforeseen at this point in time. Like I said, even Boston-Scientific stock dropped ~7% because of this!! Those people who had invested in the company should get their money back, because people completely overreacted to the results of this trial and sold their stock!!
I think that I have ranted and raved enough on this matter. But in all seriousness, the COURAGE trial has really been blown completely out of proportion. The hysteria is both a result of a misinterpretation of what the trial intended to study in the first place, and in a lack of basic understanding of both how and what type of coronary disease actually leads to a heart attack. Physicians, the media, and the public are all to blame in this. Hopefully, patients will trust their doctors to do what is right for them, and I hope that they will receive proper education concerning what benefit PCI has for both stable and unstable coronary disease. We'll be watching eagerly as this story unfolds further....