Jun 04, 2002 (EHE) - According to both the National Center for Health Statistics and the Centers for Disease Control and Prevention, heart disease is the number one killer of women and men in the United States. Each year, more than
one million Americans have heart attacks and about a half million die
from heart disease.
Despite the many advances in the field of medicine, heart disease continues
to pose a significant social and economic burden on our society. There
are new and exciting interventional methods that have been developed
to treat heart disease, especially its most common form: coronary
artery disease (CAD). However, despite their enormous contributions
in promoting relief of symptoms and their life-saving value in certain
instances, none of these modalities have made a significant impact on
either the prevention of heart disease or the occurrence of heart attacks
or coronary artery related deaths.
To understand why this is so, we need to take a close look at the results
of research over the past years. Large studies have shed some interesting
light on what appears to be the real cause of heart attacks and on how
we can prevent the development of cardiovascular disease (CAD and
stroke) in the first place. Traditionally, we have been screening
for and seeking the presence of significant blockages ("tight stenoses")
in the walls of the arteries that lead to the heart and targeting our
therapy against such blockages. It was assumed that these blockages
not only restricted blood flow (and, therefore, oxygen delivery) to
the heart, leading to the development of chest pains (angina pectoris),
but also were responsible for the majority of the resultant heart attacks
and coronary related deaths. Recent research, however, has shown this
not to be the case. In fact, quite the contrary - these "tight
stenoses" are currently classified as "stable."
If significant blockages are not responsible for the majority of heart
attacks, then what are? How do we detect these causes, and what can
we do about them?
Research has shown that more than two-thirds of acute coronary syndromes
(unstable angina pectoris, acute heart attacks, the need for urgent
coronary artery revascularization and coronary-artery related sudden
deaths) occur in areas of the coronary arteries that are not
significantly blocked. Instead, the culprit areas of the arteries are
those which contain what is termed "vulnerable plaques." These
killer plaques form not in the channel of the artery where blood flows
but, instead, remain hidden inside the walls of the arteries. Rather
than being composed of hardened, calcified matter, these plaques are
soft and fatty -- even liquid -- at spots. They most often contain a
large cholesterol-laden core. Most of these vulnerable plaques don't
bulge into the interior of the artery enough to restrict blood flow,
or to show up on angiogram. They lurk, hidden and expanding, until the
fibrous tissue (called the "fibrous cap") holding them in
ruptures. When this occurs, their components are released into the lumen
of the blood vessel touching off a chain reaction ending in the formation
of a clot or "thrombus". This acute disruption of the blood
flow to an area of the heart results in the occurrence of an acute coronary
event.
Since these vulnerable plaques are not usually highly obstructive in
nature, we would not expect them to be evident on non-invasive stress
testing procedures, which are designed to detect significant obstructing
blockages. Nor would they be demonstrated on EBCT (electron beam or
Ultrafast CT scanning), which is designed to visualize calcification
that is not usually present in these plaques. What is most concerning,
however, is the fact that coronary angiography, the gold standard for
detection of coronary artery disease, cannot visualize these plaques.
Only with the use of intravascular ultrasound (IVUS), where an ultrasound
probe is introduced into the coronary arteries can these plaques be
visualized.
Despite the limitations in detecting vulnerable plaques with noninvasive
procedures such as stress testing and EBCT, these modalities are still
invaluable in screening individuals for more advanced coronary
artery disease. Many studies have demonstrated that the presence of
inducible ischemia (i.e., a lack of blood flow or positive result) on
stress testing correlates with increased risk of coronary events and
poor prognoses. Similarly, studies have shown that the presence of a
high calcium score on EBCT is also predictive of future coronary events.
Although not directly detecting vulnerable plaques, these noninvasive
tests are extremely useful in identifying individuals who are most likely
to harbor these plaques.
We have discussed so far that the vulnerable plaques in the walls of
the arteries leading to the heart is the major cause of heart attacks
and cardiac related deaths. But now that we have identified the culprit,
what can we do about it? Fortunately, there is good news to report on
this front.
It seems that the development of the vulnerable plaque is promoted
when the endothelium, or the lining of the walls of the arteries, becomes
dysfunctional. As a result, a complex cascade of events occurs that
allows cholesterol, inflammatory cells, and other cellular debris to
accumulate and develop into vulnerable plaques. The tendency of the
vulnerable plaque to rupture and cause an acute cardiac event is also
promoted by endothelial dysfunction. The major modifiable risk factors
for CAD have one common denominator to them - they all promote endothelial
dysfunction. These risk factors (a risk factor is a condition that increases
your chances of getting a disease) include high blood cholesterol, hypertension,
diabetes, cigarette smoking, obesity, and sedentary lifestyles.
Improvement in any of the known risk factors for CAD, on the other
hand, improves endothelial function, thereby serving to retard the growth
of vulnerable plaques and prevent their rupture. We can now understand
how a prudent lifestyle is so beneficial in the prevention of cardiovascular
disease. A prudent lifestyle includes a healthy diet, achievement of
proper weight, routine exercise, and avoidance of cigarette smoking.
This lifestyle, as we now can appreciate, has direct beneficial effects
on the blood vessels that feed the heart and the brain and thereby helps
to retard the formation of any blockages to these vital organs. Best
of all, the adoption of a prudent lifestyle is at our own individual
discretion and so, is, therefore, our ability to minimize the occurrence
of cardiovascular disease.
A special mention needs to be made with regards to high blood cholesterol.
Recently, new guidelines were established which indicate the need for
more aggressive lowering of cholesterol levels in the adult US population.
These guidelines are based on the results of many studies that were
performed over the past decade which have clearly demonstrated the overwhelming
benefits of such an approach and have especially highlighted the powerful
beneficial effects of medical therapy in significantly reducing the
risk of developing or dying from CVD.
The message, hopefully, should now be clear. We have identified a new
culprit, the vulnerable plaque, as the "perpetrator" for most
of the cardiovascular events and related deaths. Despite the difficulties
in its detection, much evidence has been accumulated to demonstrate
that its devastating effects can be dramatically reduced. It will take,
however, a "team" approach to accomplish this goal. Individuals
must do their "part" and lead a prudent lifestyle. Physicians,
similarly, must also do their "part" by addressing and promoting
the modification of all of their patients' known risk factors for CVD.
They must not only encourage their patients to follow a prudent lifestyle
but also be able to explain to them the benefits of their doing so,
as well as the advantages of appropriate medical therapies when indicated.
Only by adopting this aggressive team approach can we realistically
hope to make a significant impact on the number one killer in our nation.
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Dr. Insel is a board certified
internist and cardiologist and a Fellow of the American College
of Cardiology (FACC). He is the Senior Cardiologist at EHE where
he has been for over 10 years and serves, as well, on our Medical
Advisory Board. He holds a medical degree from the State University
of New York at Downstate Medical Center. Doctor Insel completed
his medical residency in Internal Medicine at Brookdale Hospital
Medical Center and his fellowship in Cardiovascular Diseases at
Lenox Hill Hospital. He holds a teaching appointment at New York
University Medical Center where he is a Clinical Instructor in
Medicine. Doctor Insel maintains a private practice in the Upper
East Side of Manhattan and has admitting privileges at both Lenox
Hill and New York University Hospitals.
Dr. Insel's special professional interest
is Preventive Cardiology, a field in which he frequently lectures
to professional groups, medical facilities and corporations.
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