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State of the Heart

The Future of Cardiology

By Sean Henahan, Access Excellence
Copyright Info

Cardiovascular disease accounts for nearly fifty percent of deaths in both the developed world and in developing countries. Indeed, the risk of dying from heart disease is greater than the risk from AIDS and all forms of cancer combined. (Source: WHO) Worldwide, cardiovascular diseases cause 12 million deaths in the world each year. It is the leading cause of death in the US, killing some 950,000 people each year. It also accounts for a significant amount of disability and diminished quality of life.

The news is not all bad. The incidence of some forms of heart disease appears to be declining. New screening tools are allowing cardiologists to recognize problems earlier and new treatments are slowing the course of life and improving the quality of life of millions of people. Lifestyle education efforts and the use of aspirin to prevent heart attacks is also improving the public health outlook. In the research fast lane, everything from the human genome project, stem cell research and the recent implantation of the world's first completely implantable artificial heart indicate significant progress on many fronts. (link to oz)

Sean Henahan got an update on the battle against heart disease in an interview with Dr. Rose Marie Robertson, former president of the American Heart Association and director for the Women's Heart Health Institute at Vanderbilt University Medical Center.

Q: What is the status of the battle against cardiovascular disease, how are we doing?

A: Oddly enough, the trends are moving in two directions at once. Some 60 million people in the US have heart disease, including hypertension, stroke and coronary artery disease. As the population ages there are more people who have heart disease. However, the death rates from many forms of heart diseases are actually falling. We have become much better at treating patients who have had a heart attack, in some cases stopping a heart attack in its tracks. We have gotten better at treating people with heart rhythm problems, or heart failure. So we can give people many more years of high quality life even though they have heart disease. Also, we now know many ways to prevent heart disease.

Q: How are we doing in terms of improving diagnosis and screening for ethnic minorities, poorer populations, and women?

A: We are not doing as well there. Heart disease is a big problem for women, and it is a problem they don't recognize. In fact if you look at mortality rates from heart disease in this country, almost all of the benefit is seen in men. For example, the number of men dying each year from heart attacks has been steadily decreasing each year since 1979. Over that same time period, the number of fatal heart attacks among women has gone up. Since 1979, every year but one, more women have died from heart attacks than men. Most women don't realize the risks of heart disease. When we survey women, the great majority fear and worry about breast cancer or cervical cancer. We've done a good job of encouraging screening there. But very few women conceive that heart disease might be a problem. The statistics tell us that 1 in 27 women will die of breast cancer, but nearly one in every two women will die of cardiovascular disease.

We are also not doing as well as we should with our diverse population. The American Heart Association, the Surgeon General, the CDC, the National Heart Lung and Blood Institute are all involved in efforts to reduce disparities in health care so that every one has appropriate access to both preventive and therapeutic medical care.

Q: Let's start with atherosclerosis, or hardening of the arteries. How have basic and clinical research improved our understanding of this aspect of heart disease?

A: We have seen tremendous progress in our understanding in this area. For a long time we have understood that atherosclerotic plaque- i.e. fatty deposits in the coronary arteries, were the basis of coronary artery disease and heart attack, and that rupture (cracking) of those plaques was a critical feature when patients have a heart attack. We have learned a lot more about the factors that make those plaques rupture, so that we can now look at plaque and say, this plaque is a vulnerable plaque. That is important. For many years people would go to the doctor's office and have an exercise test or another screening test, appear to be fine, and then days or weeks later, have a heart attack.

This is easier to understand when we know that plaque is not something that is gradually laid down until it finally fills up a blood vessel, then you have a heart attack. In fact, it turns out that plaque is laid down in very different ways from one person to the next. In some people it is laid down in a soft fatty component in a very thin cap over the cholesterol or fat deposit. In that case that cap is quite liable to rupture, so if the artery is subjected to undue stress, e.g. a sudden surge in blood pressure, that plaque is much more likely to rupture than one that is more stable. We know that harder plaque with a lot fibrous tissue is less likely to crack. Once the plaque cracks it is extremely thrombogenic (that is, it encourages the formation of blood clots).

Another thing we've learned is that inflammation or infection seems to release compounds that make patients more likely to lay down plaques that are vulnerable. We are still in the early days of understanding that phenomenon. There are markers of inflammation we can measure in the blood that seem to correlate with the development of atherosclerosis and adverse outcomes.

The question of how to intervene in this process is more difficult to answer. We have a number of trials looking at the question of whether infection of blood vessels or endothelial cells or elsewhere in the body can be treated with antibiotics to reduce the incidence of heart attacks.

Q: Are we getting to the point where it is becoming possible to screen at risk populations genetically, to identify those who might have a genetic predisposition to atherosclerotic disease?

A: We are identifying many different kinds of markers of coronary disease risk. This area is just exploding as the Human Genome Project has come to completion. As one of the scientists involved with Human Genome Project said, it wasn't a race to the finish line, it was a race to the starting line. It was race to say 'here is information'. Now we have to take that information and go back into populations and individuals and say 'here is a gene that could cause a problem, let's see if this is so'.

Graphic: Cross section illustration of artery with plaque build-up

For example, researchers recently identified a genetic marker for obesity. You could say this marker is present in 25% of a given ethnic population. And individuals with that marker, given the same intake and lifestyle, are more prone to be more obese. Obesity is an independent risk factor for coronary disease. That is a rather high tech way to find a risk factor. If the individual with that risk factor engages in the kinds of activities we recommend, i.e. 30 minutes of exercise four or five times per week, they could completely overcome the effect of that genetic marker. We'll be able to use genetic markers to select those at increased risk. Some times we will use traditional means to try and reduce that risk. Other times, if we know which gene is involved it will let us be very specific about a particular treatment.

Q: Let's talk about cholesterol, something that is associated with the atherosclerotic process. There has been a positive association between heart disease and elevated cholesterol for some time, yet some patients with normal cholesterol levels develop heart disease, while others with elevated cholesterol do not. Are genetics helping us sort this out?

A: Yes, genetics and biochemistry are helping us to sort that out. For any risk factor, there are those who will have a great resistance to that risk factor, people who say 'my uncle Joe smoked until he was 90 and it didn't do him any trouble', or 'overweight runs in my family, but we don't have heart disease'. But there will also be many more patients who are particularly susceptible to a risk factor.

Sometimes a gene will have a very specific effect. It will cause a protein to be made or not to be made and you will have a specific disease. For example, there are some patients who have an increased heart rate when they stand up, this is not uncommon among younger patients We now know that some of these patients have a specific problem with the receptor on the nerve that pulls norepinephrine (one of the so-called stress hormones) back into the nerve. So when they get a stimulus to release norepinephrine, they get a lot of it out there, and don't sop it up very quickly, so they have a much more profound response to a stimulus. Knowing exactly what the problem is, we can be very specific about our treatment.

Other times there will be genes or clusters of genes that don't do anything by themselves, but make you susceptible to a problem. So a gene that wouldn't have any effect if you were eating a healthy diet might put you at risk if you eat a standard high fat Western diet.

Genetics may also help us to understand situations where people do not have the usual risk factors. This is not a common patient, but we look at these to identify alternative risk factors, things like, homocysteine or Lp(a) or markers of inflammation like C-reactive protein.

Q: One of the huge cardiology stories in the past decade has been treatment of elevated cholesterol with 'statin' drugs. What are learning about these drugs? Do they have effects beyond simply lowering cholesterol?

A: We now have ample evidence that lowering cholesterol either with diet and lifestyle modification, or with drugs, can make a big difference We've seen something very interesting as we give these 'statin' medications. The beneficial effect seems to happen much earlier than we would have expected if this was just a matter of reducing cholesterol. Once the plaque is there in an atherosclerotic artery, even if you reduce the cholesterol, it takes a while to change that plaque. Some may never change, others may change only very slowly over months and years. But the effect of the statins was seen in a period only weeks or months. It seems reasonable to believe the statin is somehow involved in reducing the vulnerability of the plaque by reducing inflammation, or by other mechanisms.

Click here to continue to Part 2 of this inteview


Dr. Mehmet Oz

Dr. Robertson

Primary Risk Factors for Heart Disease

1. Tobacco smoking
3. Physical Inactivity
4. High cholesterol
5. Diabetes Mellitus
6.High Blood Pressure

Source: AHA

If all major forms of cardiovascular disease were eliminated, human life expectancy would increase by 9.78 years.

National Center for Health Statistics

The total costs of cigarette smoking to the Medicare program amounted to $20.5 billion in 1997.


One-third of American adults weigh 20% more than their recommended weight.

Nature Genetics

In an average lifetime, the heart beats more than two and a half billion times



300,000 deaths in the US each year can be attributed to poor diet and inactivity.

The National Institute of Diabetes and Digestive and Kidney Diseases



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