By William H. Bestermann M.D.

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.