The New Science of Vascular Disease

This article, published almost two years ago on C&C, we’ll refer to these as Recycled but Relevant – is a perfect opening to our Urgent Science section.

If you agree that this kind of review article can be useful to clinicians, let us know. If you would like to write one like this about another topic, or know someone who would, let us know that as well.


Originally Published on The Health Care Blog, 1/28/09

Vascular disease and the conditions that produce arterial problems consume roughly one- third to one-half of the $2 trillion annual spend in American health care. The science and systems exist today to dramatically improve the quality and cost related to cardio-metabolic conditions but almost nothing has been done to implement these new tools since the Institute of Medicine (IOM) published “Crossing the Quality Chasm” in 2001.

The most glaring example of the failure of medical and political leadership in these matters can be found in the treatment of chronic conditions, which consume 70 percent of our health care dollars. “Crossing the Quality Chasm” was a stinging indictment of American medicine, describing a system that is in need of fundamental change, with many professionals and patients concerned that the care delivered is not the care that we need. The report described a system that harms too frequently and routinely fails to deliver its potential benefits.

It went on to say that we should be able to count on care that is based on the best scientific knowledge, but that there is strong evidence that this is frequently not the case. It takes 17 years for new scientific evidence to be widely implemented and even then there is excessive variation. The report said “current care systems cannot do the job, Trying harder will not work. Changing systems of care will.”

Hard business, but make no mistake. Half measures will not work here. Improvement will require a thorough re-engineering of the way we care for chronic conditions. The way we handle cardio-metabolic disease offers the most striking example of how this indictment is justified.

Virtually every new patient we see at Holston Medical Group in our chronic disease clinic understands artery disease to be a plumbing problem. And little wonder. A billboard in town sponsored by a local hospital recently proclaimed “more procedures equal better outcomes” in heart disease. So naturally, the public understands coronary artery disease to be like scale in a pipe, a progressive blockage.

The current system of cardiac care works like this: If a patient has a 60% blockage of an artery, it does not interfere with blood flow. It does not cause chest pain. The patient is thought to be safe, and nothing much is done for or to the patient.

If the blockage is 70% or greater, it begins to interfere with blood flow, it may cause pain, the patient is thought to be in danger, and this level of disease activates our entire system of stress tests, cardiac catheterizations, stents and bypasses. 100% blockage is a heart attack and if we catch the blockage before it becomes 100% and open it with a bypass or a stent, then we have made the patient safer. We have saved him from a heart attack. This is the way most patients and clinicians currently understand the problem of coronary artery disease and it is the way our system operates.

The plumbing model of coronary artery disease has been thoroughly discredited in stable patients, beginning with the landmark work of WC Little and others summarized by Erling Falk, PK Shah, and Valentin Fuster in Circulation in 1995. This article reviewed 4 investigations that compared the results of two heart catheterizations done in the same patient. The first catheterization had shown a blockage (stenosis). Some of these patients went on to have a heart attack, and then a second heart catheterization was done at the time of the heart attack.

The results of the second catheterization were shocking. The original blockage was there, but it had not caused the heart attack. The myocardial infarction was caused by complete blockage of the artery by clot, frequently in a different place and surprisingly often in a totally different artery. In the studies summarized by Falk, only 14% of heart attacks occurred in an artery which had shown a 70% or greater stenosis on the first catheterization. Since it generally takes a 70% blockage to produce angina, this explains the reason that most heart attacks occur as the first cardiac symptom. The patients did not have enough vascular obstruction to cause chest pain beforehand.

The WC Little article was published in 1988, 21 years ago. Dr. Little did a very good job of describing the new vascular paradigm in this pioneering work in the discussion at the end of the article:

Because it was difficult to predict the site of the 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 myocardial infarctions. 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 arterial tree, not just at obstructive lesions. Such therapy to prevent myocardial infarction might rationally include avoiding smoking, reducing serum cholesterol, administering agents that alter platelet function such as aspirin, or possibly fish oil, and pharmacologic agent to prevent spasm of the coronary arteries.

These early landmark articles have informed the work of leading authorities in cardiology.

So how does a heart attack happen? LDL-cholesterol (or bad cholesterol) plaques build up in the wall of the arteries. They do not belong there and the body attacks these plaques with white blood cells (pus cells). These plaques become highly inflamed collections of LDL cholesterol and pus. They function like little boils or abscesses and they rupture.

When the contents come in contact with the blood within the vessel, it causes the blood to clot. This is why aspirin, an anti-coagulant, prevents heart attack. It is why tissue plasmin activator, a clot buster, will stop a heart attack in progress by breaking up the clot and restoring flow to the artery.

The fundamental, underlying event in myocardial infarction is plaque rupture. Coronary artery calcium is a reflection of healed plaque rupture. In early disease, multiple discrete dots of calcium can be seen. The more you have, the higher your risk. A test called a calcium score assigns you a risk level based on how much plaque you have.

The Tim Russert story is an unfortunate reflection of how these dynamics play out in our system. Ten years before he died, Mr. Russert had a calcium score of 200, which roughly translates to 40 plaque ruptures. A few months before his heart attack, his stress test was normal, probably indicating a low risk from obstruction. On autopsy, one of the arteries was completely blocked by clot. The Russert example fits the new paradigm perfectly.

Our system does too little too late. In cardiovascular disease, the care model is built around opening blockages in patients with late disease, which relieves symptoms, but does not prevent heart attack.

Leading experts now agree that preventing heart attack requires identifying patients at high risk and then stabilizing plaques by aggressively treating blood pressure, high cholesterol, triglycerides and glucose with diet, exercise and evidence-based medical treatments.

Remember, investigators laid this out in 1995 based on studies going back to 1988. We are now at 20 years and counting. We have passed the 17 year mark, and most patients still don’t get the care they need.

The science of vascular disease has changed dramatically, though the evidence shows that aggressive application of this science makes a real difference. The COURAGE trial’s purpose was to prove that, when added to “optimal medical treatment” – that is, an optimal drug reigmen – stents further protected the patient. Patients with stable angina and blockages greater than 70% received optimal medical treatment for blood pressure, cholesterol and diabetes. Then the patients were randomly assigned to receive the appropriate stents or no stents. At the end of 5 years, there was no difference in the number of cardiac deaths and heart attacks. Even more interesting, 70 percent of patients who did not receive stents experienced complete relief of their pain, most in the first year.

The Courage Trial confirmed the findings of a great deal of research that addressed the same issue. An article in last year’s Journal of Managed Care summarized 13 studies since 1993 that compared optimal medical treatment alone and combined with stents. In stable angina patients, there was no benefit of angioplasty with stenting over optimal medical therapy alone. The authors thought the findings of their analysis might “engender additional support for a policy cognizant of the lack of marginal benefit of PCI (stents) over that of MT (medical therapy) alone in nonacute cases.”

Everything bad that happens to an adult onset diabetic is vascular. At diagnosis, the type 2 diabetic has an 80% lifetime risk of heart attack and stroke. Again, we do too little too late. Guidelines emphasize checking for the late consequences of diabetes and vascular obstruction: doing eye exams for retinopathy; foot exams for ulcer, nerve damage and poor arterial supply; doing special tests looking for arterial blockage in the leg.

In the Steno 2 study, 160 type 2 diabetes patients were divided into 2 groups: optimal medical treatment (where the emphasis was on controlling risk factors) versus usual care. At the end of 7 years, there was a substantial difference between the two groups in terms of diabetic complications and everyone was moved to aggressive care for the next 6 years.

Nonetheless, there were major differences in outcomes. In the usual care group, 40 out of 80 people were dead vs. 24 out of 80 in the aggressive care group. The usual care group experienced twice as many cardiovascular deaths, 4 times as many heart attacks, 5 times as many strokes, 11 times as many stents, over 3 times as many amputations, and 6 times as many people were placed on dialysis. The usual care group averaged 2 vascular catastrophes each over a 13 year period.

We need to divert resources from an ineffective system of dealing with the late complications of diabetes and focus on producing the optimal medical therapy that will keep those problems from happening in the first place.

In the face of this irrefutable new science, some stent advocates and other naysayers have said, “that is all very well, but optimal medical therapy does not exist, and so these studies do not apply to the real world.” They are wrong. Thousands of diabetics in Holston Medical Group have risk factor control rates that are very close to those achieved in Steno 2 and Courage. We and others have “Crossed the Quality Chasm” in cardiometabolic conditions and are continuing to improves.

The solutions are at once terribly complex and very simple. Systems produce the results they are designed for. We need to rework our cardio-metabolic care system. Because that system produces what it pays for, we need to start paying for treatments that actually produce the results intended. In this case we need to pay a premium for optimal medical treatment as an initial strategy in high risk patients and in patients with stable vascular disease, with a priority placed on proven, evidence-based treatments.

We need to stop paying for stents and bypasses in stable angina patients until they receive a trial of optimal medical therapy. Until we do that good people will continue to die and suffer needlessly. We are putting our own friends and family at risk. We have robbed Tim Russert’s grandchildren of the opportunity to know their remarkable grandfather.

William Bestermann MD is a Preventive Cardiologist and Medical Director for Integrative Services at the Holston Medical Group in Kingsport, TN.

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