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A New Understanding of Coronary Heart Disease and What Puts You at Risk

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.

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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