In a recent column at EnduranceCorner, I wrote about “Nine Interesting Facts About the Athlete’s Heart.” The heart is truly amazing!
Cardiac Arrest? Heart Attack? Heart Failure?
I’ve heard from a bunch of readers that our terms cardiac arrest, heart attack, and heart failure are confusing.
Today I thought I’d offer a quick vocabulary lesson. One of the biggest challenges for students of medical school and other health professions schools is learning the 1,000’s of words that medical professionals use, but we end up with words and phrases that are very specific and very descriptive.
Cardiac Arrest. This is an electrical problem of the heart. The electrical activity of the heart stops or becomes disorganized in what we call an arrhythmia. And because of the electrical problem, the heart stops pumping blood. If you’ve attended CPR class, you’ll know that the electrical problems include PEA (pulseless electrical activity), ventricular tachycardia (VT), ventribular fibrillation (VF), and asystole.
When athletes collapse during training or competition, cardiac arrest is usually the problem.
Heart Attack. This is a plumbing problem in the heart. Heart attack is the lay term for the medical problem we call myocardial infarction, or MI. This problem is due to blockages in the coronary arteries–the small arteries that bring bloodflow and oxygen to the heart muscle itself.
In the most common scenario, there is build-up of cholesterol or lipid-laden plaque in the wall of a coronary artery that produces narrowing of the artery and reduced bloodflow in that artery. When that bloodflow is sufficiently reduced, individuals experience chest pain that we call angina. When the angina occurs with exertion, we call it exertional angina. When the angina occurs at rest, we call it unstable angina or rest angina.
Myocardial infarction occurs when one of these plaques ruptures (on the inside of the coronary artery), exposing the plaque material to the bloodstream. The body responds by forming a blood clot at that location, further restricting–and possibly stopping–bloodflow in that artery. With no bloodflow or oxygen, the heart muscle in the area of that artery dies pretty quickly. When heart muscle dies, the process can be detected on the EKG and by the presence of heart enzymes (released into the bloodstream from dying heart muscle cells) on a blood test.
Heart Failure. We use this term when the heart pumping function is weak. This can be either an acute, or short-lived problem, or a chronic, long-term problem. There are many causes, including myocardial infarction, but also including various problems with the heart valves, inherited conditions, and others.
A Useful Video Clip. One of my colleagues at work brought to my attention a great video clip on the topic of Heart Disease and Heart Attacks at The Khan Academy. With the help of some great illustrations at the blackboard, the narrator goes over each of these problems. Take a look.
Coronary Artery Disease: The Essentials
For those of you who have been following along, we’ve talked briefly before about the problem of coronary artery disease (CAD) and illustrated the problem last week with the story of Jim Fixx. And I’ve mentioned previously that CAD is the most common cause of sudden death in athletes over the age of 40. Today, we’ll talk about CAD in a little more detail. This should provide the foundation for future discussions that we’ll have about the many aspects of maintaining heart health as we age.
To put the problem of CAD into some perspective, you should realize that this is the most important chronic medical condition that Americans face. In fact, CAD affects more than 13 million Americans today. It’s the leading cause of death in the United States, with nearly 1 person dying every minute from this condition.
The Anatomy
The heart, as you know, is simply a muscle….but one that is in constant motion, usually beating 60-100 beats each minute, or upwards of ~140,000 times each day. And like other muscles of the body, it requires a generous blood supply to furnish the needed oxygen to keep things going. As the aorta leaves the heart, to take blood flow to the rest of the body, the first 2 branches are the left and right coronary arteries….the arteries that supply blood flow to the heart muscle itself. The left coronary artery branches into the left anterior descending and the circumflex coronary arteries. We often say, then, that there are 3–not 2–important coronary arteries.
We use the term CAD to refer to the progressive (over many years time) narrowing of the coronary arteries, the arteries that supply the heart muscle with its blood supply. This process, called atherosclerosis, usually starts with fatty streaks on the inside surface of the coronary arteries, but over years’ time progresses to larger, more space-occupying deposits of various lipids. The situation is not much unlike a typical plumbing problem, where a pipe might become clogged with unwanted material, thereby limiting blood flow.
What problems does CAD cause?
Individuals with CAD often experience no problems until the narrowing in the coronary arteries becomes severe. When the arteries become narrowed to less than 25-50% of their original diameter, the reduction in blood flow to the heart muscle can produce symptoms. At first, the symptom might be chest pain or discomfort (that we call “angina”) or perhaps unusually severe shortness of breath with exertion. Any of these symptoms should be a warning sign….and prompt you to be evaluated by your physician.
The plaques on the inside of the coronary arteries can sometimes rupture, leaving a raw surface exposed to the bloodstream, and lead to the formation of a blood clot at that site. This can produce chest pain at rest (unstable angina) or even acute myocardial infarction (MI), the situation where there is irreversible damage to the heart muscle.
Who gets CAD? What are the risk factors?
Much time and effort has been devoted to understanding who gets CAD. As you can imagine, this is the starting point for figuring out how to prevent CAD. We’ve learned that there are a handful of so-called risk factors, indicators of how likely it is that an individual will develop CAD. Some of these risk factors can’t be changed, but others can be modified to help reduce somebody’s risk.
There are some risk factors that you simply can’t change. One such risk factor is age. Men over the age of 45 and women over the age of 55 are more likely than their younger counterparts to have CAD. Unfortunately for men, men are just more likely than women to have CAD. And lastly, a family history of CAD in close relatives is a risk factor. As you can see, each of these risk factors is beyond your control.
On the bright side, though, several risk factors are under your control….and should be paid very special attention as we age:
1. Obesity (or even just being overweight)
2. High blood pressure
3. Smoking
4. High levels of blood cholesterol
5. Diabetes
6. Physical inactivity (although I’ll bet that most readers here are active!).
We’ll cover these risk factors in greater detail in upcoming posts.
Diagnosis and Treatment
Most patients with CAD come to medical attention because of symptoms such as angina or shortness of breath. Many others come to attention because of acute MI. And, sadly, some come to attention because of sudden death….and an autopsy shows CAD.
A stress test (which can be done in a variety of ways) or a cardiac CT scan can indicate the likelihood of CAD. The diagnosis is established, though, with coronary arteriography….a test in which dye is injected into the coronary arteries and motion picture x-rays are made. This creates a roadmap of the coronary arteries and shows any blockages.
If blockages in the coronary arteries are not severe, patients can be treated with medicines. Patients with severe blockages can be treated with angioplasty and stenting (to push the blockages aside) or with coronary artery bypass surgery.
That’s CAD in a nutshell. Like I said, I hope that this information provides the necessary foundation for us to have more detailed discussions about various topics down the road.
Aortic Stenosis and Bicuspid Aortic Valve
I operated on a young man (in his early 30’s) a couple weeks ago for aortic valve replacement. It reminded me that valvular heart disease is not limited to older folks. This particular patient wasn’t an athlete, but I have a cycling acquaintance here in Jackson who also needed aortic valve replacement in his 30’s.
The aortic valve is the valve that lets blood flow out of the heart, from the left ventricle (the heart’s main pumping chamber) into the aorta (the large blood vessel that carries blood to the rest of the body). Ordinarily, this valve has 3 leaflets that are arranged to produce a pattern much like the Mercedes Benz emblem, if you look at the valve from above. With each heartbeat, the leaflets open nearly completely, allowing for unobstructed blood flow out of the heart.
There are 2 main problems that happen with heart valves….the valve can leak or it can become obstructed. Today, we’re going to focus on narrowing of the aortic valve, that produces obstruction to blood flow, and this is a condition that we call aortic stenosis. We’ll leave the leaking valves to another day.
There are several causes of aortic stenosis, but, by far, the most common cause is age-related calcific degeneration of the valve. That is, over years and years, calcium deposits build up in the valve leaflets, making them immobile. The leaflets eventually become so stiff that they do not open properly….and produce obstruction to blood flow exiting the heart. Aortic stenosis is usually a problem for patients who are in their 60’s, 70’s, or even older. Because the problem develops gradually over many years, patients sometimes don’t notice the effects, but the 3 primary symptoms are: 1) shortness of breath with exertion; 2) chest pain; and 3) syncope (blacking out).
Patients come to medical attention because of one or more of the hallmark symptoms or occasionally because a physician hears a heart murmur. There is a characteristic sound, or murmur, associated with aortic stenosis and your physician can hear this murmur in a very particular location on the chest—just to the right of the sternum, above the level of the nipples. An echocardiogram (ultrasound) is used to make detailed pictures of the heart valves and can be used to quantify the degree of stenosis, or obstruction, as mild, moderate, severe, or critical.
Aortic stenosis is a serious medical problem. Patients with severe or critical aortic stenosis require valve replacement. There is no other treatment (ie, medicines) that can correct the problem. For patients with breathing difficulties because of their aortic stenosis, the average life-expectancy is less than 2 years without valve replacement. Major heart surgery is needed to replace the valve with a mechanical (eg, carbon fiber and metal) or tissue (eg, the aortic valve “borrowed” from a pig) valve.
But like I mentioned above, aortic stenosis can sometimes be encountered in a much younger patient….sometimes as young as in the 20’s. And this is often due to a congenital abnormality of the aortic valve in which there are only 2—and not the standard 3—leaflets. This occurs in 1-2% of the general population. For some reason, this arrangement predisposes the individual to earlier calcification and stenosis of the valve as well as leaking of the valve. This is relevant to the athlete because problems are likely to develop during the very active portion of a typical athlete’s active lifetime.
The second important consideration in patients with bicuspid aortic valve is that they are much more likely to develop enlargement (aneurysm) of the beginning portion of the aorta, as it leaves the heart. Over time, the aorta can enlarge from its typical diameter of less than 3 cm to 5 cm or more, the aorta and the aortic valve should be replaced….again, with major heart surgery
Professional triathlete, Torbjorn Sindballe, was recently in the news when he retired from competition because of bicuspid aortic valve and mild aortic enlargement.
Decisions about continued participation for patients with these conditions will need to be individualized, but should only be made after careful consideration of the risks involved. Athletes with mild to moderate aortic stenosis, and who don’t have symptoms, probably can participate fully in athletic activities. Those with severe aortic stenosis should refrain from strenuous activity as treatment plans are made with their physicians. Athletes with bicuspid aortic valve and enlargement of the aorta should refrain from strenuous activity.