From 1993 to 2001, Bill Clinton held the most high pressure job in the world. He had access to the best medical care: How many of us have our own personal doctor at our side most of the day? His health was regularly monitored, including his heart healthâ€”since his family had been afflicted by heart disease and he was known to have high cholesterol. As far as anyone could tell, his health was fine.
Following his presidency, he continued a very high pressure life, and continued to feel healthy.Â In July 2004, he appeared trim and vibrant when he delivered an impassioned address to the Democratic National Convention.Â Less than a month later, the former president was undergoing emergency heart bypass surgery.Â
Maybe youâ€™ve had experience with something similar. As a doctor, I sure have had patients who have.Â I remember one man in his 50s who competed for two hours in a summer soccer tournament in 95 degree heat without any problem, and had a heart attack some days later while watching television.
How can it be that we can live with a â€œtime bombâ€ like heart disease within us, and not even know it?Â And what can we do about it?
Today, we have a much better understanding about why heart disease can be a time bomb than we did when I was in medical school.Â Back then, we got the basics right, but we got some other important details very wrong.
What did we get right? We knew that the most common kind of heart diseaseâ€”coronary artery disease, or atherosclerosis (often called â€œhardeningâ€) of the coronary arteriesâ€”eventually interfered with the supply of blood to the heart muscle.Â Like your biceps, your heart muscle needs a blood supply to work without hurting.
We knew thatâ€”for those of us in the developed nationsâ€”atherosclerosis started at an early age.Â The very first signs appeared in men in their 20s and 30s, and in women in their 30s and 40s. First, a little bump on the inner wall of the artery formed. Then, over time, the little bump grew larger (into what is called a â€œplaqueâ€), making it harder for blood to flow through the artery. Thatâ€™s what we got right.
This is what we got wrong: We thought that plaques had three stages, each logically and gradually following the next. Â During stage 1, the plaque was so small that you didnâ€™t even know it was there; it didnâ€™t cause any symptoms. In stage 2, the plaque slowly grew big enough (blocking about 70% of the blood supply) that the heart muscle would not get enough blood when the body was asking it to work hardâ€”like when you were exercising or angry, for example. If you slowed down, or calmed down, the symptoms would go away. The most common symptom was angina (a kind of chest pain).Â When stage 3 coronary artery disease was present, the blockage grew big enough to totally shut off the flow of blood to a part of the heart served by the diseased artery, causing a heart attack.
The problem with that explanation was that it didnâ€™t explain Bill Clinton, or my friend the soccer player. Â And it surely didnâ€™t explain the peopleâ€”hundreds of thousands of them every year around the worldâ€”who never have any symptoms of heart disease until one day they just drop dead.
We now think we understand what is happening, because we have a better understanding of what atherosclerotic plaque is. Each artery is a little pipe, with a circular wall and a space in the middle through which the blood flows. We used to think that the plaque always grew into the space in the middle, blocking blood flow. We now know that some plaques can grow not inward, not into the space in the middle, but outwardâ€”beyond the outer part of the wall. That means that they can grow quite large without blocking the flow of blood.
The second and most important new thing we now understand is that the plaque is not just an inert lump, but a complex structure with several key parts. The outside part of the plaque, the part that pushes toward or into the space in the middle of the pipe, is called a fibrous cap (a cap made of fibers). Inside the plaque is a pool of cholesterol. But thatâ€™s not all. The inside of the plaque also can contain natural chemicals that cause inflammation. Some plaques are â€œquietâ€, and some are inflamed. When a plaque is inflamed, the inflammation can eat into the fibrous cap, weakening it. If the cap ruptures, the cholesterol and chemicals of inflammation spill out into the center of the artery. That can cause a blood clot to rapidly form. If the clot is large enough, it can suddenly cut off the blood supply from that artery.
In summary, plaques that are inflamed can be small enough not to block the flow of blood and cause any symptomsâ€”unless and until they rupture, suddenly causing a marked blockage. Thatâ€™s a perfect example of a time bomb: Something that just sits there doing no damage until it explodes.
What can we do about it? Doctors are working hard on tests to detect such time bombs before they go off. No imaging tests yet achieve the ideal goal: detecting a plaque that may not be blocking the flow of blood at all right now, but that has the potential to suddenly have its plaque rupture. Other doctors are working on simple blood tests that can spot such time bombs by the chemical traces that they leave in the blood. Unfortunately, these tests are not yet good enough for routine use.
In the absence of such tests, there is still a lot you can do to protect yourself against heart disease: observing a heart-healthy lifestyle, and getting treated for any conditions (like high blood pressure, high cholesterol or diabetes) that increase your risk of heart disease.
Are you doing all you can to keep your heart healthy?
Anthony Komaroff, M.D., is the Simcox-Clifford-Higby professor of medicine at Harvard Medical School (HMS), and editor-in-chief of Harvard Health Publications at HMS. He is a practicing senior physician and was formerly director of the Division of General Medicine at Brigham and Women's Hospital.
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