By Chuck Gebhardt, MD
Copyright statement: I wish to exert no copyright for this document. I only ask that I be given due credit if it is copied and distributed in any format.
My topic for today is a disease often called atherosclerosis. The two most common results of this disease are heart attacks and strokes. It causes other very serious disease processes also, such as abdominal aortic aneurysms, peripheral vascular disease and others with very dire consequences. This is quite an important process for us to understand so that we can do whatever is in our power to prevent it or at least minimize its devastating results.
This article is targeted towards two groups of people: the average reader without a medical background and physicians, particularly primary care physicians and specialists in cardiology as well as cardiac or vascular surgery. I have provided sub-topic headings so that physicians or other medically trained readers can bypass the basic information necessary for the non-medical public. Here is the list of topics:
THE BASICS OF ATHEROSCLEROSIS IN A NUTSHELL (non-physicians)
HOW DIET AND DRUGS AFFECT THE RISK OF ATHEROSCLEROSIS (non-physicians)
VERY EFFECTIVE SCREENING FOR ATHEROSCLEROSIS (everyone)
You might wonder what a non-academic internal medicine specialist might have to say that is of value to these other specialists. (Actually, I do have some experience in both research and teaching within the field of medical nutrition, but my primary focus for over twenty years has been direct patient care and the prevention of disease.) My main goal in deciding to enter medical school and become a physician was to teach nutrition to physicians. I realized very early on in my career, though, that one of the most important consequences of our food habits was their impact on the atherosclerosis process. My career focus changed to a very aggressive approach to the management of atherosclerosis Along with other diseases impacted by our diet. I am going to encapsulate over twenty years experience into this article as briefly as I can while still being effective. There is something here for everyone, physician and non-physician alike.
THE BASICS OF ATHEROSCLEROSIS IN A NUTSHELL
Atherosclerosis is a systemic disease. What I mean by this is that it is a disease that can affect every part of the arterial system on which every part of every tissue throughout our body is dependent. This system supplies oxygen and nutrients to our tissues and if any part of the blood supply is blocked, the tissues will die, often very quickly. The death of tissue in this way is called an “infarction.”
The heart and the brain are the two main organs where infarctions or symptoms of inadequate blood flow (called ischemia) first show up when atherosclerosis is developing. This is not a hard and fast rule, though, since sometimes a different pattern such as pain in the legs from ischemia due to peripheral vascular disease, for example, may be the first sign of atherosclerosis. Once clear signs or symptoms of atherosclerosis develop in one part of the body, it is a safe bet that it exists in other parts. Remember, it is a systemic disease. Often, once symptoms show up in one area, the disease is quite advanced in other areas even if problems have not become obvious there as yet.
It is also important to be very aware that you can have very advanced disease and feel completely well. Almost half of the time that this process is discovered, the way it is discovered is that the victim dies suddenly from a heart attack or stroke with no prior warning. This disease process is definitely one where it would be far better to find it early rather than late. Before I get into how this might be done, though, I need to develop more of a background about the disease process for you.
We have long known that the damage to the lining of the body’s arteries starts as very mild defects in the inner lining of our arteries and usually develops very slowly. We know that it usually takes six to ten years, or even longer, for a plaque to grow from its earliest form that pathologists call “fatty streaks,” to advanced blockages that cause ischemia or devastating infarctions.
You should see this as very good news! It means if we have reliable means to test for these early plaques in a way that is safe and affordable, we can follow the disease progression and possibly intervene to slow or stop it. This leads me to the second part of the good news: we have developed very effective treatments to do just this: slow or stop the disease. We know a lot about diet, control of blood pressure, control of diabetes and the use of potent drugs to decrease the atherosclerosis forming tendency of our blood. Before I go on to the main point of this article, how we can effectively monitor the disease as it forms and proliferates in our arteries, let me lay a little more ground work in discussing the topic of the atherosclerosis forming tendency of the blood.
Cholesterol and triglycerides (fats) are not water soluble. This means that the body needs special particles (called lipoproteins) to carry these essential body components to where they are needed. In this article, I will only focus on two of the four main lipoproteins in the blood since they are the two most important in the formation of artery plaques. Low density lipoprotein (LDL) has the potential to be very damaging. Having some is essential to body metabolism, but the higher the levels in the blood, the more atherogenic (or plaque forming) they are. In general high is bad and low is good. This is because LDL leaks through the inner lining of the artery and builds up unless it can be removed by specially structured lipoproteins that help do just that. The higher the LDL in the blood, the more that leaks in and the more stress is put on the body’s ability to remove it and protect the viability of the artery to perform its essential work.
The second lipoprotein I will discuss is often labeled the “good” one: high density lipoprotein (HDL). This lipoprotein is part of the process that removes fat and cholesterol from inside the artery lining where it does not belong and can wreak havoc. Another part of the protection system are a type of white blood cell called a macrophage which is found in the lining of the artery where is cleans up the LDL remnants and other debris. If these macrophages pick up too much fat and cholesterol before the HDL system can remove it, they will burst open and their toxic contents will begin to destroy the artery by forming plaque. In general, the higher the level of HDL the less likely atherosclerosis will develop and if it does, the slower it will proliferate.
The net result of all this is that the Higher the LDL and the lower the HDL the more atherogenic the blood is to the arteries. Conversely, the lower the LDL and the higher the HDL the more the arteries tend to be protected from this process. We have two good strategies here that have been proven to be effective in slowing or stopping this process. We can Lower LDL (actually fairly easy to do) or we can raise HDL (often fairly hard to do with current technologies). As you might expect, this is a greatly simplified rendition of what we know, but it carries some of the most important and practical points for you to understand.
Next, it is important for you to understand just how these arterial plaques impede blood flow to cause ischemia or completely block blood flow to cause infarction. The most basic process is the accumulation of fat and cholesterol and the formation of scar tissue that may slowly grow and gradually more and more occlude the artery. When this happens in the heart it often causes angina (chest pain of cardiac origin) and tends to be provoked by exercise or exertion. Cardiologists do imaging procedures called cardiac catheterizations when angina is discovered and may be able to intervene with angioplasties or stents to open up these arteries and re-establish better blood flow.
If this was all there was to it, the disease would not be anywhere near as deadly as it actually is. It isn’t just that the plaque progressively blocks the artery as it grows, it also becomes weak and fragile and the lining that coats the inside of the artery can fracture spontaneously, an event that gets more and more likely as the plaque swells. This sets the stage for two very fast processes that both involve the fracture of the arterial lining. When I say fast, I mean the artery can go from ok to completely blocked in a matter of seconds. This is what usually causes catastrophic large strokes and sudden cardiac death. It may give absolutely no warning. (That is why it is so important to have some way to become aware of this disease process is developing before symptoms occur. More about this later.) One of these very fast process is for blood to leak into the plaque once the surface ruptures. This will often cause the plaque to expand quickly and completely block the artery. The second process is for a clot to develop on the surface of the plaque and begin to grow there. It can grow big enough to block the artery there, or it can break off from the site where it first forms and get carried downstream in the blood stream to block other arteries.
Understanding something about these processes helps us in a number of ways. For one thing, you can see how aspirin works. Aspirin will not stop plaque from forming, nor will it protect its surface from rupturing, but it will do a good job of slowing clot formation on the surface of fractured plaque. I always recommend aspirin for someone who has known atherosclerosis if they can take it safely. Also, by understanding how most clots develop from a fractured plaque surface, you can see why the more artery surface you have involved with plaque, the higher the probability it will rupture somewhere. The probability is related to both how much surface is involved and how thick the plaques are. You can also see that we have several processes to stop once atherosclerosis is in the arteries.. We want to stop the formation of new areas of damage, we want to stop existing areas from getting worse (thicker) and we want to prevent the surface of existing plaque from rupturing.
It would be nice if we could completely reverse this process once we discover it, but this is rarely possible with our current knowledge. We have learned, though, that the same treatments that prevent new plaques from forming, and which prevent existing plaques from getting thicker, also stabilize the surface of the artery covering the plaque and greatly decrease the chance it will rupture! Sometimes aggressive management will shrink the plaque a little, but it is the stabilization of the lining that matters most and this is a fairly quick response to our treatments (days to weeks).
Next. Let’s discuss my special area of expertise, nutrition, as well as the role of drugs in this process.
HOW DIET AND DRUGS AFFECT THE RISK OF ATHEROSCLEROSIS
I think that it is fair to say that most Americans believe that heart attacks and stroke are due to poor food choices that cause us to have high cholesterol levels in the blood. This is partially true. High cholesterol and high fat intake (particularly saturated fats) in someone’s diet do usually increase the atherogenic potential in the blood by raising the LDL level. However, if we could magically put every American on a very healthy low fat, low cholesterol diet, I would estimate we would decrease the amount of heart attacks and strokes by only about 20% — at the most. This is because many people have high LDL or low HDL that is not due to diet nor are the abnormal levels very diet responsive. The truth of this was driven home to me when I was the director of an Optifast program years ago. This program placed people on artificial supplements that had almost no fat and no cholesterol. You would have expected that his kind of regimen would normalize everyone’s lipoproteins. I could easily tell who was compliant with the diet program because of the very rapid weight loss and other metabolic changes that resulted from these food replacements. We followed everyone’s lipoprotein levels and many were abnormal before entering the program. A few of the very compliant program member’s profiles got a lot better, but most didn’t. Some even got worse despite rapid weight loss, while, at the same time, diabetes and high blood pressure always got better in these compliant patients who were losing a lot of weight. This was an eye-opener for me.
I don’t want to be negative about diet. Sometimes it is very effective. Also, even if diet alone doesn’t improve the lipoprotein levels it will almost always help medications to be more effective. Unfortunately, though, we need a lot more than diet alone to make the kind of improvements that are possible in these diseases.
One of the biggest successes in modern medicine in the last few decades has been the development of very effective medications to modify the lipoprotein levels in the blood. When I first started practicing medicine in my residency training, atherosclerosis was very frustrating to treat. Strokes, heart attacks and similar problems were very, very common. As the new lipid modifying medicines became available, particularly the “statin” class for lowering LDL, I began to see a major improvements that resulted from a careful effort to improve my patient’s lipoprotein profiles. This was the first major improvement, but in the last ten years of so there has been an even bigger improvement with yet another very important advance: new ways to screen patients to find the disease early, when it is most responsive to treatment. In recent years, I still have a few patients with heart attacks and strokes, but only a small percentage of what it used to be. Let’s get into the main point of this article now: the new imaging technologies.
VERY EFFECTIVE SCREENING FOR ATHEROSCLEROSIS
Recall what I said earlier in this article: this disease first starts six, eight, ten or even more years before it begins to cause catastrophic losses of our essential organs. Since we have very effective treatments to slow or stop the disease, what we need most now is to have a safe, effective, cost-efficient way to search for the disease before it becomes advanced to the point that health disasters start occurring. We need to know where the disease is forming, how bad it is and how it is responding to our treatments, and we need this information as soon as possible.
Here is the good news and the bad news on this topic. The good news is that we have excellent techniques that meet all these criteria. The bad news is that, for a variety of reasons, these screening tests are hardly ever being used. This is the reason for this article. I will introduce the technology by going back to the atherosclerotic plaque again.
It turns out that as plaque begins to develop it has a high affinity for calcium which it begins accumulate from the blood. This is not a very important factor in the disease process, but it is a superb marker for the disease, especially since we have several good non-invasive ways to look for this calcium that are already readily available to most of us. Normal arteries have NO accretions of calcium in their lining. Well designed studies have also shown that there is an excellent correlation between the amount of calcium found on certain arterial scans and the extent and severity of the disease process present there.
I use two techniques widely in my practice: carotid ultrasounds to look for calcium in the neck arteries and an ultrafast CT scan of the heart that can provide a picture and a rating score of any calcium in the arteries in the heart (called a cardiac scoring). I try to get every male patient to have these at about age forty and all females at about age fifty, unless I find particularly bad lipoprotein patterns and bad family histories in younger adults, where I do them earlier.
When both of the scans show zero, I feel pretty comfortable that diet therapy is enough for most patients. I will, though, treat very abnormal lipoprotein patterns with medications to try to keep the disease from ever starting, even when the scans are zero. When even a small amount of calcium is found, the disease has gotten a foot hold and very aggressive management is called for, even though the risk for this patient in the near future is still very low. As you should be able to predict by now if you are following all this, the higher the calcium scores the more imperative the treatment and the higher the risk.
Sometimes I can avoid drug treatment for many years in people whose lipoprotein profiles would normally call for medications. I repeat these scans every three or four years, in this circumstance. Sometimes I pick up early disease, treat it aggressively, and find it is gone on the next scan! (Though I have never seen it completely resolve in moderate or advanced disease.) In a few cases, I have discovered advanced disease in completely asymptomatic people, sent them for stress tests, and they went on to have life saving emergency surgery because of the critical nature of the blockages found.
Perhaps the most significant thing I have noted is the large number of fairly “normal” lipoprotein levels (ones that are already at our established national goals without treatment) who already have established disease. Many of these folks are non-smokers, have good blood pressures and no diabetes, yet still have disease. They have virtually no cardiac risk factors, yet the disease is present. What I have learned is that these “normal” patterns are still too high for them. I treat them aggressively with medications and the plaques usually stabilize or resolve.
I have also found some folks who have disease that continues to get worse, as shown by serial scans, despite achieving the most aggressive target levels of lipoprotein levels currently recommended. I have set the goals even lower and often this stops the deadly progression of plaque.
These are my “secrets.” They are secrets that I never wanted to be secret. At long last I have found an effective forum to communicate these things widely to the public.
I have not included references in this article, it is long enough already. Also, while most of the early research in the field of cardiac calcium scanning was quite good, much of the recent research I find to be poorly designed. It seems many researchers are looking to see if cardiac calcification can be used in place of a cardiac cath. This is not the value of these scans. They are best used to find disease very early and to allow very focused and effective treatment to slow or stop it. Cardiac catheterizations are used in advanced disease to search for those who will benefit from angioplasty, stents or surgery. These two goals are very different.
If you are a non-physician and want a CT cardiac scoring done, you will need a doctor’s orders to obtain one, in most states. You may want to share this article with your physician if he or she is reluctant to order it. If there is enough interest on the part of physicians and they are looking for further input, I will write a blog article just for them. And if there is enough interest in the research behind what I say here, I am willing to provide that also.
How many people have to be struck down in the prime of life, or how many of our elderly have to endure preventable disabilities before we begin to effectively use what we have to prevent what can be prevented?