Chapter 1 - A Cardiologist’s Story
Updated on February 1, 2003

I am a cardiologist. I have cared for thousands of patients with heart disease. For most of my career, I did what most cardiologists do. I specialized in the diagnosis and treatment of symptomatic heart disease. In the middle of the night, I would rush to the emergency room and battle closing arteries. I would infuse clot busting drugs and thread delicate catheters through the body and into the arteries of the heart. I would open closed arteries with balloons and stents. It was difficult, but immensely rewarding work. Each successfully treated patient reinforced my passion for helping those with heart disease.

Then I began to think about larger issues related to heart disease. Yes, it’s true; cardiologists can perform near miracles with the arsenal of drugs and devices at our disposal. But why, I wondered, could we not do a better job at preventing heart disease? How could we identify the heart attack candidate well before the event and treat the underlying problem? On the one hand, it seemed we knew a great deal about the disease called atherosclerosis, the disease that gradually infiltrates the arteries, suddenly closing them off with potentially devastating consequences. We also seemed to know a lot about the risk factors associated with atherosclerosis. The famous Framingham study, named after the town in Massachusetts, had followed thousands of people for decades, measuring all sorts of bodily functions and then relating these measurements to heart attacks and strokes. Out of this study came the Framingham risk factors. The most important one is age. The older we get, the higher our risk. The other risk factors are total cholesterol, HDL cholesterol (the good one, with an inverse relationship to risk), cigarette smoking, diabetes and gender (men have a higher risk). Since the discovery of the original Framingham risk factors, more have been discovered.

But even with all our knowledge of risk factors, people continue to develop heart disease. Why is this? As I pondered the question, several reasons came to mind. The most important was that most people who get heart attacks do not have a particularly dangerous risk factor profile. Most victims have cholesterol levels that are in the mid-range for Americans. Most do not have diabetes, and most do not smoke. Most have just high normal or mildly elevated blood pressure. The vast majority of heart attack victims are in the medium risk range. Framingham risk factors work very well for the small numbers of people with very high cholesterol and other risk factors, and for those with very low cholesterol and no other risk factors. But most of us are somewhere in between.

Another reason is the poor job we physicians do at convincing our patients to lose weight, exercise, eat a healthy diet, and medically treat their risk factors. It seems that prevention, which requires education, tracking, behavioral psychology and constant vigilance, does not fit the usual paradigm for health care in America, which is focused on treating symptomatic disease.

But perhaps the most important reason is the fact that atherosclerosis is silent until the most advanced stages. Why is that? In recent years, doctors have made several new discoveries about atherosclerosis (also known as plaque). Instead of narrowing as the plaque develops, arteries actually expand outward. This process, called compensatory remodeling, protects the blood flow by keeping the artery channel at its normal width. Normal blood flow means no chest pain, no symptoms whatsoever. Silently growing, the plaque infiltrates more and more of the artery wall. It grows and expands, accumulating fatty and inflammatory material. By the time symptoms do develop, the arteries usually have advanced disease. So the key to prevention, it seemed to me, would be not to measure risk factors, but to measure plaque itself. If we could measure plaque in the early and mid stages of development, we could stop its progress through medical and lifestyle treatments, and prevent it from reaching the advanced stage.

How, I wondered, could plaque in the coronary arteries be measured? Luckily, I was not the only one thinking about this. A small company in South San Francisco was making machines capable of seeing plaque in the coronary arteries. The company, Imatron, had discovered a new way of taking very rapid pictures of the heart. The machine, called an electron beam CT scanner, used focused electrons to generate x-rays and shoot them through the body at speeds fast enough to freeze the motion of the arteries. No other CT scanner in the world was nearly as fast as this machine. All CT scanners produce images that are slices of the body just millimeters thick. But traditional scanners have parts that swivel around the body to produce the image. This mechanical swiveling limits the speed of the machine. Pictures of the heart end up being blurred. The coronary arteries swing through an arc while the x-rays cross them. The inside of the artery wall gets stretched and distorted. The Imatron scanner reduced this motion to a minimum.

The scientists at Imatron wanted to measure the amount of calcium in the coronary arteries. For many years, doctors had noticed calcium in arteries that were diseased. Chest x-rays will sometimes reveal large deposits of calcium in the aorta, the large vessel that delivers blood from the heart to all the organs of the body. Traditional CT scans of the abdomen can show calcium in the lower portions of the aorta. Observational studies had shown that people with these calcium deposits in the aorta were more likely to suffer heart attacks and strokes. The Imatron team believed that if one could freeze the coronary arteries and obtain very thinly sliced images, it would be possible to precisely measure even small quantities of calcium in the artery wall. They worked closely with cardiologists at medical centers around the country. Dr. Agatston, at the University of Miami, developed the first method for measuring arterial calcium (the Agatston Score). Dr. John Rumberger, at the Mayo Clinic, did elegant studies showing that the measured calcium correlated almost perfectly with the amount of atherosclerosis found by traditional staining techniques used by pathologists to study atherosclerosis.

As I read about EBCT, and reviewed the growing scientific literature validating the technique, my excitement grew. Here at last was a technique for measuring plaque! Best of all, the technique was noninvasive. No needles, no contrast agents, no catheters, no complex or time consuming procedures. The simplicity of the technique was stunning. The patient simply lay on the CT scanner table fully clothed for about forty seconds. Electrodes placed on the body triggered each of forty images to the instant in the heart cycle with the slowest cardiac motion. The images were sent to a work station. A doctor could then use 2D slices or 3D pictures to see the calcium. Calcium deposits as small as several pixels could be detected. Each area of calcium could be accurately measured. The sum of all areas gave a coronary calcium score. Each person’s calcium score could be compared to others in the same age group. If you had high amounts of calcium, or if your score was high for your age group, you needed to take prevention seriously.

I decided to visit Imatron in South San Francisco. I caught an early shuttle from San Diego and took a cab for the short drive to Imatron corporate headquarters. I toured the facility, observed scanners in various stages of construction, and met with several executives. Connected to the headquarters was a scanning center owned by Imatron. As we walked into it, John, my guide, turned to me and asked if I would like to have my heart scanned. I felt a small shiver of anxiety as I accepted the offer. I fully expected to have a 0 score. I had no strong family history of heart disease, I exercised almost every day, I ate reasonably well, but did not follow a strict low fat diet. I had no diabetes or high blood pressure. I’m thin. I smoked for several years in high school and college, but that was long ago. In short, I considered myself the picture of good health.

I lay down on the scanner table and lifted up my shirt. A technician attached three small electrodes to record my heart’s electrical activity. This information would be used to trigger the exact instant when the scanner would take each picture. The table moved into the doughnut shaped space where the x-ray source and detector rings were located. I was instructed to hold my breath for a quick scan used to locate the top and bottom of the heart. Then I held my breath again and the table pulsed through 40 quick movements, each one coinciding with one slice of x-ray information. That was it. I hopped off the table and tucked my shirt in.

John was in the next room looking at a computer monitor. The scanned images were already available for viewing. “How do I look?” I called out. “Do you see any plaque?” I said this somewhat light heartedly, because I knew he would say no. Instead, he said “Yes, you do have some.” Marilyn, the CT Technician, was starting to score the images. As each slice came up on the screen, she used her mouse to circle the areas of white in the coronary arteries. The arteries were supposed to be grey. Each white spot represented calcium buried in plaque. I looked at the name in the upper right hand corner of the screen, to make sure it was mine. It was.

“Is that a lot?” I asked.
“It’s a fair amount,” responded John.

Marilyn finished totaling the areas. After typing some more information, she saved the report and sent it to the printer. I took it and read through it. I could not believe that in a matter of minutes this machine had looked far beneath my skin into a place that normally would require surgery to see. The information I now held in my hands was like a memo on my destiny. The numbers and graphs revealed the story of my coronary arteries over the past several decades, and intimated on what they would look like many years into the future.

I learned that I had a score of 79. What did this mean? I looked at the explanation and saw several categories, going from no plaque, a 0 score, through minimal plaque burden, a score from 1 to 10, through mild plaque burden, from 11 to 100, moderate plaque burden from 101 to 400, and severe plaque burden over 400. So I was in the mild category. That did not seem to be so bad. Then I looked at a graph with several curves. The graph plotted age horizontally and calcium score vertically. Each curve represented the calcium scores for a given percentile of a known population of men. There was one curve for the 25th percentile, one for the 50th, one for the 75th, and one for the 90th. A small star had been inserted into the graph. This star represented me. It fell between the curves for the 75th percentile and the 90th percentile. That meant my score was higher than the scores of more than 75% of the men in my age group. This suggested that my arteries were more prone to the development of plaque. How could that be? I just did not want to believe what my eyes were seeing.

I left Imatron in a somewhat deflated mood. Yes, I had seen a marvelous machine capable of revolutionizing the prevention of cardiovascular disease. Yes, I felt more certain than ever that my future would be dedicated to using this technology. But my image of myself had changed. I had always assumed that my body was in excellent condition. I looked many years younger than most others my age. I exercised almost every day. I felt great! But now I knew that my perceptions were an illusion. I flew back to San Diego wondering what to do next.

I called my wife, who was visiting her family in Europe, and told her about my day at Imatron, including the fateful scan. I could tell by the change in her voice that she was also shaken by my report. Within a day or two I checked my lipid panel. My LDL cholesterol, the so-called bad cholesterol, was 140. My good cholesterol (HDL) was 65. An LDL of 140 was a little over the then currently recommended level of 130 or less. My HDL was better than most. My exercise program kept it high. My total cholesterol was 225. My ratio of total to good cholesterol was therefore 3.5. Generally, a ratio under 4 is considered to be reasonably good. My high good cholesterol should have been protecting me from the effects of my mildly elevated bad cholesterol. I had no other risk factors.

Why then, did I have too much plaque in my arteries? Now, several years later, I realize that most people with dangerously high levels of plaque look very much like me. I look back at my naiveté and shake my head. Most Americans, including physicians, place far too much importance on cholesterol as a predictor of heart disease. As I’ll discuss in later chapters, we do not really know what causes plaque. Genes make us susceptible. Our lifestyle also makes us susceptible. But for any one person with a given cholesterol level and a given lifestyle who has a significant plaque problem, I can show you another with the same cholesterol level and the same lifestyle who has no plaque in his or her arteries.

I realized that regardless of why I had a plaque problem, I had to do something about it. Step one was to get my LDL cholesterol down. Never, before my scan, would I have considered myself a candidate for a cholesterol lowering medication. And that’s precisely the problem. Without a measurement of plaque burden, it’s impossible to know accurately who should be really worried about their cholesterol. Unless of course you have already had symptoms of cardiovascular disease. Anyone with a history of heart attack or stroke, or some other manifestation of plaque, should be taking cholesterol lowering medications, regardless of the starting cholesterol level. We call this secondary prevention, or prevention after the fact, and it’s very important to prevent a recurrence. But what I will mostly be talking about in this book is primary prevention. Primary prevention is trying to prevent disease before it reaches the symptomatic stage.

My primary prevention program began with a medication called Lipitor. Lipitor is the brand name for Atorvastatin, a molecule developed by Pfizer. Atorvastatin is one of several medications in the class of cholesterol lowering drugs called statins. All statins have the same mechanism of action. They block a key step in the synthesis of cholesterol by the liver cells. The liver cells react to lower levels of cholesterol by making more receptors for LDL cholesterol. These receptors are on the outside of the cell membrane. The receptors catch molecules of LDL cholesterol in the blood and bring them into the cell. This lowers the amount of LDL cholesterol in the blood, and eventually leads to the removal of cholesterol from plaque.

Statins have other beneficial effects on plaque. In later chapters, I will discuss how plaque evolves. For now, just imagine a plaque in an artery wall breaking through the wall and causing a localized clot to form. This is what happens during a heart attack. The plaque goes from a stable form to an unstable form. Statins stabilize plaque. They appear to have beneficial effects that reduce inflammation in the artery wall, strengthen the artery wall, and prevent clot from forming on plaque.

Lipitor is the most widely prescribed statin in the world. The reason for its success is simple. Compared to other statins, it is almost twice as effective at lowering LDL cholesterol. How effective is it? Two months after I started taking 10 milligrams a day my LDL cholesterol had dropped from 140 to 75. 10 milligrams is the lowest dose. The range of doses goes all the way up to 80 milligrams a day.

Why is low LDL cholesterol important to prevent heart attacks and strokes? Many scientific studies have shown that when you give statins you reduce the number of heart attacks and strokes over the next few years compared to a control group (a group that took a placebo instead). Also, the studies that showed the greatest drop in LDL cholesterol also showed the greatest drop in heart attack rates. Some researchers have speculated that if you can lower the LDL cholesterol down to less than 60, you may be able to prevent 80 or 90% of heart attacks!

So why didn’t I try to lower my LDL with diet and exercise? For two reasons. Most importantly, there are many studies showing that statins lower heart attack rates. There are no good studies showing that eating a low fat diet does the same. Also, I seriously doubted that I could muster the motivation to make the drastic changes necessary to drive my LDL down to where I wanted it. Such a diet would deprive me of many foods I truly enjoy. My wife is French and I have developed a taste for good cheeses, not to mention recipes that may occasionally call for butter or olive oil. I certainly don’t indulge in such things all the time, but I don’t believe we have to deprive ourselves of fat.
I did make some adjustments to my diet. I began to use soy milk instead of cow’s milk in my cereal and coffee. Also, when recipes call for milk, we will often use soy milk. For example, French toast tastes every bit as good with soy milk. In fact, it’s impossible to tell the difference! I substituted margarines with no trans-fatty acids for butter, except for occasional transgressions. Margarines with trans-fatty acids are much worse for you than butter.

And, over the years, I subtly altered my eating habits simply because I knew what was lurking in my coronary arteries. The knowledge of plaque transformed me. I may have been a reasonably health-conscious eater before, but I still thought of myself as indestructible. Once I had seen the white speckled areas in my left anterior descending coronary artery it fundamentally changed my perceptions about health and disease. In a sense, I was forced to confront my mortality. Most people don’t confront their mortality until they experience a serious medical problem. Unfortunately, it’s difficult to turn around and undo the damage. EBCT helped me see a disease in an early stage. Coronary atherosclerosis is a relentless process. Once it begins its growth in the artery wall, it tends to multiply and spread. Because the process is silent, we mistakenly assume that we are healthy. All too often, the first symptom of the disease is sudden death or a heart attack.

So, in many ways, I watched myself more closely. I had always exercised, but now I exercised more consistently. I also performed other medical tests. I checked my homocysteine blood level. I looked more closely at my pattern of lipoprotein particles. I measured my CRP level. I even took advantage of some of the newer genomics tests. In later chapters I will tell you all about these exciting tools for precisely diagnosing why we are susceptible to plaque.

But most of all, my own experience showed me a new may to prevent heart attacks and strokes. If I had had a 0 score, I don’t think I would have embraced this technology as passionately as I did. I expected a 0 score, and I didn’t get it. The technology made me painfully aware of my own ignorance. It shocked me, and I realized how naïve most of us are. Even so-called experts, myself included, tend to disregard objectivity. We down play risk, even though the data shows us clearly that we are all at risk. We can’t hide behind “normal” risk factors and pretend that there is no need to worry. Most people who get heart attacks and strokes have relatively normal risk factors. The truth lies hidden in our genes. All we need are several genetic variations and our arteries become less resistant to environmental plaque promoters. As I will show you later, genetic testing can already reveal some of these genetic tendencies. Within a decade, dozens if not hundreds of genetic variations that promote atherosclerosis will be identified.

So began my conviction that EBCT is a key tool for preventing cardiovascular disease. With the scanner, I could diagnose the underlying disease that leads to heart attacks and strokes. I could precisely measure the quantity of plaque in the coronary arteries, in the carotid arteries and in the aorta. This essential information would then guide my therapeutic decisions. Those with no plaque, or low plaque scores, could be reassured and given lifestyle recommendations. Those with higher scores, and therefore higher risk, could be treated more aggressively. Follow up scans would reveal whether treatments were effective. A successful program would lead to plaque regression. If plaque continued to increase, a new set of goals would be implemented.

And so was born the program I call 3D Health. 3D Health provides a framework for optimizing health and preventing heart disease. The three dimensions of the program are Discover, Design and Do. Discover means measuring your unique set of predictive biological markers. Design means goal setting based on your Discover Profile. Do means following specific recommendations to achieve the desired goals. In this handbook, I provide 3D Diagrams to help you through the process. Each 3D E-Diagram (“E” for explain) illuminates a biological or medical concept. Each 3D F-Diagram (“F” for flow chart) tells you exactly how to set up and achieve your goals for improving a biological condition. The starting point for many 3D F-Diagrams is your plaque risk. The more plaque you have, the more important it is that you achieve an optimal result for the key biological conditions that can affect plaque growth.

I have measured plaque risk for over 10,000 people. Each one required a unique plan of action for their unique biological conditions. With low plaque risk, the plan is relatively simple, focusing primarily on various lifestyle recommendations. These are explained under the chapters on 3D Nutrition, 3D Exercise and 3D Emotional Management. As plaque risk increases, the recommendations become more complex. The 3D F-Diagrams simplify each recommendation. They are like little maps that point you in the right direction. You may not have to use all the maps, but there is one for every important biological condition that you may need to think about improving. Simply start at the top and follow your way down to the branch points that describe your situation, and then move from right to left from the Discover column to the Design column and the Do column.

3D Health is a program for life specifically designed to prevent cardiovascular disease. A healthy cardiovascular system goes hand in hand with lower risk for many other conditions, including diabetes, cancer, osteoporosis and osteoarthritis. If you are 3D Healthy, you have vastly increased your chances for a long and disease-free life!