A PRIMER ON CORONARY ARTERY DISEASE
Anatomy
To understand how narrowed or blocked arteries affect the heart, you need to know how your heart works and how its structure is suited to its function.
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Your heart's job is to pump blood - the sole source of oxygen and nutrients -- to
your brain, kidneys, muscles -- wherever it's needed. Blood gets to its destinations through arteries and returns to the heart via veins (Figure 1.).
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The heart's main pumping chamber is the left
ventricle(Figure 2). It does most of the work, consumes about
90 percent of the energy and is the part most affected by coronary artery
blockage. There are three other
chambers of the heart - another ventricle and
two atria-but for the sake of
understanding coronary artery disease, you can regard these parts as
comparatively passive conduits through which blood passes before reaching the
left ventricle. They are only
indirectly affected by coronary artery disease.
Size and orientation
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Your left ventricle lies behind your rib cage between your left nipple and your
breastbone. You can get an idea of its size and orientation by making a fist
with your left hand and holding it in front of your chest as in Figure 3. The left ventricle is an oblong chamber
about the size of your fist. Its
muscular walls are roughly the thickness of your fingers.
Now spread the first three fingers of your right hand over your left fist as in Figure 4. Your coronary arteries wrap around your left ventricle like your fingers cover your fist. In this position, your right hand is attached to the top your left fist like your body's largest artery, the aorta, is affixed to your left ventricle. Your coronary arteries arise from the first part of your aorta, doubling back to reach your heart.
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Conveniently for surgeons, coronary artery blockage is usually confined to parts of the vessels that lie on the surface of the heart rather than in the offshoots that penetrate into the heart muscle. To perform a coronary by-pass operation, the surgeon takes a vessel from another part of the body, sews one end to the aorta and attaches the other to the narrowed artery downstream from the obstruction. The technical aspects of coronary bypass surgery will be discussed in more detail in the next chapter.
To get an idea of what the left ventricle does, squeeze your hand a few times as if you were compressing a rubber ball. With every heartbeat, the left ventricle squeezes blood into the aorta through a one-way valve. Between beats it relaxes, opens up and fills with blood coming in through another valve. (Don't confuse valve problems with artery disease. They are entirely different diseases.)
As you squeeze your fist repetitively, imagine how much work your left ventricle has to do to keep your body supplied with blood. It has to pump about five quarts per minute to supply enough blood for you to just sit and read. It must generate enough pressure to push blood up to the head and through all the other arteries of the body. If it stops pumping even for a few seconds, the pressure in the arteries falls, blood stops flowing to the organs and consciousness is lost. After about five minutes, damage sets in, first to the brain and then other organs.
The three main coronary arteries
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Spread your fingers over your fist again.
The position of your fingers corresponds roughly to the paths of your
three main coronary arteries. Notice
that one artery, represented by your middle finger, supplies the front of the
heart; and the other two wrap around to supply the back (Figure 5.).
If you could remember the names of the three major coronary arteries, you'd be able to hold your own in a conversation with a cardiologist, but you don't have to know the terminology to understand what happens when they become blocked. Notice that the front of the heart is dependent on a single artery while the back gets blood from two. That's why an obstruction in the front artery is usually more serious than a blockage in one of the other two.
As for their names, the artery represented by your middle finger--the one that supplies blood to the front of the heart--is called the anterior descending coronary artery (nicknamed “LAD” for left anterior descending.) The one corresponding to the index finger is the circumflex coronary artery. The ring finger is the right coronary artery.
Notice that the front artery and one of the back ones actually arise from a common root, the left main coronary artery. Blockage here is less common than in other parts of the coronary arteries, but as you can imagine, such an obstruction would interfere with blood supply to an especially large amount of heart muscle.
Figure 6 is a “plumbing diagram” of your coronary arteries that illustrates the way blood travels to your left ventricle and indicates the approximate percentage of muscle that is dependent upon flow through each artery.
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The plumbing diagram will come in handy later when you are trying to understand the effects of blockage in different parts of the coronary arteries. It will help you see why the guidelines recommend treating some narrowings differently from others. For example, notice that a blockage of the left main coronary artery interferes with flow to approximately three fourths of the left ventricle, an obstruction of the first part of the LAD compromises flow to about half and an occlusion of either of the others, to a quarter. In general, the guidelines recommend artery-opening procedures for narrowing of the left main and anterior descending coronary arteries but not necessarily for blockages in the other branches.
Angina
When you're exercising the muscles of your arms and legs consume more oxygen than when you are at rest, so they need more blood. To meet that demand, your left ventricle has to beat harder and faster. At maximal exertion, it beats about twice as fast as when you are resting and pumps approximately twice as much blood with each beat.
The heart muscle has to work harder during exercise, so it needs more fuel and oxygen. The only way blood can get to the heart muscle is through the coronary arteries. If those vessels are narrowed or blocked, blood flow to the heart might be adequate at rest but deficient during exertion. Interference of blood flow to the heart muscle during exercise causes a characteristic kind of chest pain called angina pectoris, or just “angina”.
Angina is usually described as a sensation of pressure under the front of the chest or down the left arm, although the character and location of the pain may vary among individuals. Typically, angina comes on only during exercise and subsides after ten or fifteen minutes of rest.
The severity of angina pain varies widely. Some people barely notice it; for others it's disabling. it's the main symptom from which patients with coronary disease seek relief with medications, angioplasty or surgery.
Heart Attacks
While narrowing of a coronary artery can cause chest pain during exertion, this alone rarely damages the heart. Autopsies have shown that the heart muscle can remain healthy despite years of angina.
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However, it's another story when a
coronary artery blocks off suddenly and completely. Unless there's an alternate route for blood to get to the heart
muscle, it will sustain some damage (Figure 7).
The medical term for damage to any organ caused by blockage of a blood vessel is infarction. The word for heart muscle is myocardium, so damage to the heart muscle from artery blockage is called myocardial infarction, or “M.I.,”which is what is generally meant by the layperson's term “heart attack”.
You can imagine what could happen if a person's heart muscle were severely damaged by a heart attack. The left ventricle would fail to maintain adequate blood pressure, blood supply to other organs would cease and death would follow. In actuality, most heart attacks don't cause death; patients often survive one, two or even more attacks. Eventually, however, if enough heart muscle is damaged, the victim may become disabled or die.
It takes less than twenty minutes for a sudden and complete blockage of a coronary artery to cause irreversible damage to the heart muscle. However, peripheral parts of the damaged area, called “border zones,” often take longer to suffer irreparable injury. If blockage can be removed and blood flow restored within three or four hours of a heart attack, some muscle can often be saved.
Sometimes heart attacks damage only a small amount of heart muscle, and patients recover completely. If they are lucky there may be no after-effects at all. Often, however, they are left with some degree of disability. Typically, the heart performs okay rest but is unable respond normally to the increased demands of exercise. That may result in varying degrees of shortness of breath and fatigue during exertion.
What determines the severity of a heart attack? To some extent, it's a roll of the dice. If the blockage is in a small artery or one for which there is an alternate route for blood to reach the heart muscle, there might be no damage at all. If it strikes a large vital artery, it might cause massive, even fatal damage.
A lot depends on how good the other arteries are. If they are wide open, they are better able to supply blood through alternate routes, or “collaterals,” to compensate for a blocked one. In addition, the rapidity with which blockage develops makes a difference. Obstructions that occur in long-standing narrowings cause less damage than blockages that strike wide-open arteries.
How much damage can the left ventricle sustain before it fails? Nature has provided some muscle to spare, so it can survive some damage. Pathologists have determined that if the amount of injury, whether from previous heart attacks or a new one, adds up to less than 15 percent of the total muscle of the left ventricle, the patient will usually suffer no disability. If 15 to 40 percent is injured, symptoms vary from mild to crippling. Damage of over 40 percent is usually incompatible with life.
Patients often do okay after their first heart attack, but the second one pushes them over the line. That's why treatment to prevent heart attacks is especially important for people who have already had one.
Congestive Heart Failure
Blood travels to the left ventricle through the lungs. When the left ventricle fails as a pump, blood may back up into the lungs and cause them to become waterlogged, or “congested”, a condition called congestive heart failure or “CHF”.
Imagine repetitively squeezing and releasing a dry sponge. Picture how air moves in and out of the small spaces in the sponge with each squeeze and relaxation. That's how air moves in and out of your lung tissue when you breathe. Now think of what would happen if you started dripping water on the sponge. That's how congestive heart failure affects the lungs. As blood backs up into the lungs, they get stiffer and more sluggish, and water starts occupying spaces where air should be. It is easy to understand that why the main symptom of congestive heart failure is shortness of breath.
Congestive heart failure can be a disabling complication of a heart attack. it's often treated with diuretics, which promote urination and help rid the lungs of excessive fluid.
When damage to the heart reaches the point of causing congestive heart failure it's like being behind in a football game by a touchdown going into the fourth quarter. it's not a death sentence but a sign that diligent medical treatment is needed. Twenty years ago, the outlook for patients with congestive heart failure was grim; over half died within three years. In the past two decades, effective new strategies have been developed to relieve symptoms and reduce mortality from CHF as well as to prevent it in the first place.
Ventricular Fibrillation
Unless you're a doctor, ventricular fibrillation is a term you're probably not familiar with. Yet this almost invariably fatal heart rhythm disturbance causes more deaths than cancer or strokes and almost as many as heart attacks.
For purposes of record-keeping, doctors usually considered ventricular fibrillation a mode of death, a way that other diseases--usually heart disease--cause fatality. That is one reason why it hasn't entered common awareness as a way people often die. In addition, because it is so unpredictable and, until recently, so untreatable physicians have adopted a somewhat fatalistic attitude towards it. Most victims never get to a hospital where a physician can treat them. The extent to which a doctor is usually involved is in the signing of the death certificate. While most victims of ventricular fibrillation have heart disease, what actually triggers it is a mystery. Other than thwarting heart disease, there is no way to prevent it.
While damage to the left ventricle can cause it to fail as a pump, it can also fail electrically. Normally, with each heartbeat, a wave of electrical activity travels through the heart activating muscle fibers in a coordinated fashion. If the heart is damaged the electrical properties of the muscle tissue through which the wave travels sometimes becomes disturbed in a way that causes the wave to suddenly and unpredictably shatter. The smooth “wave” becomes a chaotic rip tide (Figure 8.)
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This causes the electrical activity of the ventricles to fall into the state of chaos, which is caused called fibrillation. Ventricular fibrillation causes sudden, profound loss of coordinated heart activity and--almost invariably--fatal cardiac arrest.
The disturbances of electrical activity in the heart muscle that set the stage for ventricular fibrillation are silent and difficult to discern with current technology. The only consistent observation is that some degree heart muscle damage always precedes it. Because coronary artery disease is the most common cause of such damage, it is most often responsible.
When patients with coronary artery disease die suddenly, it is often difficult to tell afterwards if they died of pump failure caused by myocardial infarction or from ventricular fibrillation. Nevertheless, these two complications of left ventricle damage cause most deaths from coronary heart disease.
The possibility of unexpected, sudden death from ventricular fibrillation contributes significantly to the unpredictability of coronary heart disease. Why some patients are prone to this lethal electrical disturbance and not others is largely a mystery. Certainly, extensive damage to the left ventricle raises the risk, and patients who have had enough heart damage to cause congestive heart failure are at especially high risk. Frustratingly, the relationship between damage and risk of ventricular fibrillation is quite variable. Sometimes patients with seemingly minor heart muscle injury are struck while others with severe damage remain unaffected.
Except for preventing damage to the left ventricle, there is, as yet, no reliable way to prevent ventricular fibrillation. Unless the episode is witnessed and the heart immediately shocked back to its normal rhythm with an electrical “defibrillator,” the condition is almost inevitably fatal. In recent years, bioengineers have developed an electrical defibrillator that can be permanently implanted in the chests of patients deemed likely to have ventricular fibrillation. The device can be programmed to activate the moment a patient has an attack. The problem is that ventricular fibrillation is so unpredictable that it is difficult to tell who might need such an apparatus. Because the devices are expensive (approximately forty thousand dollars) and surgery is required for implantation in the chest, it is impractical to use them in all patients thought to be at risk.
Stroke is the name for brain damage caused by artery blockage. The word “stroke” reflects the abrupt and seemingly random manner in which damage can occur, as if something struck, or hit, the brain. Strokes can cause paralysis, loss of speech, dementia, coma or death. In the weeks or months afterward, some function usually returns, but the improvement is usually partial. While significant recovery can occur, in most cases, some disability remains.
Strokes cause irreversible damage within minutes, and until recently, little could be done to ameliorate it. Recently, doctors have started giving “clot busting” drugs to patients seen soon after the onset of stroke in an attempt to dissolve the blood clots that cause it. If such clots can be dissolved within roughly three hours of onset, damage can sometimes be lessened. Unfortunately, clot-dissolving drugs can sometimes cause bleeding in the brain, which causes more damage, so treatment is reserved for a select few judged to be at low risk of bleeding.
A stroke can be a tragic and life-changing event. While they might not kill, strokes often cause severe disability. Active, robust individuals can be rendered completely dependent by severe paralysis or loss of speech. In the United States, strokes are the third most common cause of death behind heart disease and cancer but the number one cause of disability
Disease of the heart arteries does not directly cause strokes. Recall, however, that the left ventricle is directly upstream from the brain. Damage to this part of the heart, stagnation of blood caused by congestive heart failure or attempts to operate on the heart can trigger blood clots that float to the brain and cause strokes. There is, then, a strong relationship between coronary heart disease and strokes.
The central role of the left ventricle
It should be apparent to you by now that what causes most death and disability from coronary disease is damage of the left ventricle. The more injury there is to it, the higher the chances of mechanical failure, electrical failure or stroke. The importance of the left ventricle creates a difference in perspective between patients and doctors. While you might be focused on how much angina or shortness of breath you're having, your doctors might be more concerned with protecting your left ventricle. They might recommend medication or surgery to prevent damage or improve its function--even though you might not be particularly bothered by symptoms.
Of course, if injury to the left ventricle were predictable or could be easily reversed, preventing and treating heart disease would be a much simpler proposition than it is. But doctors can't accurately predict such damage. The need for treatment to prevent damage is based on guesswork. Such judgements are subject to bias, which one reason treatment of coronary artery disease varies so much from doctor to doctor.
If you've read this far, you're knowledgeable about how arteries work, how atherosclerosis leads to narrowing and blockage and how coronary disease affects the heart. You're now ready for the exciting part, how atherosclerosis and coronary artery disease can not only be treated but prevented in the first place.