Читать книгу Preventing and Reversing Heart Disease For Dummies - James M. Rippe - Страница 5

In This Chapter

▶ Understanding what causes atherosclerosis and coronary heart disease

▶ Determining the causes and effects of angina

▶ Exploring what causes heart attacks

▶ Learning about arrhythmias, heart failure, and other forms of heart disease

Your heart works harder than any other muscle in your body. Your life depends on this small but mighty pump never stopping. It’s about the size of your clenched fist and weighs less than a pound. Depending on your age and physical condition, a normal heart beats 60 to 90 times per minute when you are sitting and may get up to 150 to 200+ times per minute when you are maxing out aerobic physical activity. A healthy heart is equipped to sustain at this pace for 70 to 90 years and beyond. The key word here is healthy.

From the moment you are born (and even before), multiple factors related to your biology, behavior, and environment have an impact, for good or ill, on your heart and cardiovascular system. Heart disease is progressive: It starts stealthily in the coronary (and other) arteries and progresses silently for years before any detectable signs of disease emerge. Research over the last 25 years provided new insights into how heart disease begins, starting at the cellular and molecular levels. These new insights are helping to prevent heart disease in the first place and to halt or, in some aspects, even reverse its progress.

In this chapter, I first present a brief overview of the heart and cardiovascular system. Then, I discuss the silent precursors and early stages of heart disease. Next, I look at angina and unstable angina, two types of chest pain that are often the first signs of heart disease for many people. Finally, I discuss how disease progression may result in heart attacks, arrhythmia (heart rhythm problems), heart failure, and other acute problems.

Touring the Heart and Cardiovascular System

Understanding how your heart and cardiovascular system work provides a foundation for understanding heart disease and its many manifestations. Even if you begin snoozing at the mere idea of technical stuff, don’t forget that knowledge is power. These basics can help you do a better job of keeping your heart healthy.

Pumping for life: The heart’s anatomy and function

The heart is located in the center of the chest cavity, just to the left of the midline of the body. Figure 2-1 illustrates the exterior of a healthy heart and Figure 2-2 illustrates the interior. You need to understand the following important parts:

✔ The heart muscle: Called the myocardium (myo = muscle and cardium = heart; pronounced my-o-car-dee-um), this muscle contracts and relaxes to pump blood throughout the cardiovascular system.

✔ The coronary arteries: Three large coronary arteries and their many branches deliver a continuous supply of oxygenated blood to the heart. Narrowing of these arteries causes chest pain; blockage causes heart attack.

✔ The pumping chambers: The heart’s job is to pump blood to the lungs to get oxygen and to pump the oxygenated blood to the rest of the body. To fulfill these tasks, the heart has a left and a right side (shown in Figure 2-2), each with one main pumping chamber called a ventricle located in the lower part of it. Sitting above the left and right ventricles are two small booster pumps called atria (or atrium, when you’re talking about just one).

The right ventricle pumps deoxygenated blood from the body to the lungs to receive a new supply of oxygen and back to the heart, through the left atrium to the left ventricle. The left ventricle pumps oxygenated blood through the arterial system to the rest of the body where it feeds every single living cell. Various disease conditions can damage each of these structures.

✔ The valves: Four valves regulate the flow of blood in and out of the heart and from chamber to chamber. They act a bit like cardiac traffic cops by directing the way blood flows, how much of it flows, and when to stop it from flowing. Disease and injury can cause heart valves to leak, narrow, or otherwise malfunction, disrupting the heart’s ability to pump blood efficiently.

✔ The electrical system: This electrical system is controlled by a group of specialized cells that spontaneously discharge, sending electrical currents down specialized nerves and tissues, causing the heart to contract. When any of these electrical structures becomes diseased or disordered, arrhythmias (ay-rith-mee-uhz), or heart rhythm disturbances, occur.

✔ The pericardium: The entire heart is positioned in a thin sac called the pericardium (peri = around and cardium = heart; pronounced per-ry-car-dee-um). Fluid within the sac lubricates the constantly moving surfaces. Inflammation of the pericardium from an infection or other cause causes pericarditis. Build-up of excess fluid inside the pericardium can cause problems with how the heart functions, a condition called cardiac tamponade.

Illustration by Kathryn Born

Figure 2-1: A typical healthy heart.

Illustration by Kathryn Born

Figure 2-2: The interior of a normal heart.

Connecting every cell in your body: The cardiovascular system

A pump is useless without the rest of the plumbing, which in your body is called the cardiovascular system. Here’s a quick look at how it all fits together and functions.

✔ The lungs: The lungs are composed of an intricate series of air sacs surrounded by a complex, highly branching network of blood vessels. Their sole purpose is to receive the deoxygenated blood from the heart, fill the red corpuscles full of fresh oxygen, and send them back to the heart for delivery to the body. The red blood cells give off waste products such as carbon dioxide at the same time they take on oxygen; the lungs then expel the carbon dioxide. This low-pressure system facilitates the rapid flow and reoxygenation of enormous amounts of blood.

✔ The arteries: As oxygenated blood returns to the left side of the heart, it is pumped out to the body through the aorta, the main artery of the body, and into the rest of the arterial system to feed the entire body with oxygenated blood. Although the heart exerts enough force to push oxygenated blood throughout the body, the arteries also have muscular walls that help push the blood along. The force exerted against resistance of the artery walls creates a high-pressure system that is very elastic to allow the arteries to expand or contract to meet the needs of various organs and muscles. Your blood pressure reading results from measuring the pressure in these arteries when contracting and at rest. (Read more about high blood pressure in Chapter 8.)

✔ The capillaries: The arterial system divides and redivides into a system of ever smaller branches to distribute nourishing blood to each individual cell, ultimately ending up in a network of microscopic vessels called capillaries, which deliver oxygenated blood to the working cells of every organ and muscle in the body.

✔ The veins: After oxygen leaves the capillary system, the deoxygenated blood and waste products from the cells are carried back through the body in the veins. The veins ultimately come together in two very large veins, called the inferior vena cava (vee-nuh cay-vuh) and the superior vena cava. The inferior vena cava drains blood from the lower part of the body and superior vena cava drains blood from the upper part of the body. These veins discharge blood into the right atrium of the heart to be pumped into the right ventricle and out to the lungs again to start the whole process over again.

✔ The blood: Although blood is not considered part of the cardiovascular system, circulating blood to every cell of the body is the reason the cardiovascular system exists. This red fluid transports oxygen and fuel to the cells and removes waste products. It’s also the delivery vehicle for many specialized cells and biochemicals, including those that contribute to the development of heart disease.

Keeping the beat: How the nervous system controls heart rate

In addition to its internal electrical system, the heart has profound linkages to the nervous system that provide additional control of the heart rate. Two main branches of the involuntary nervous system interact with the heart – the sympathetic nervous system and the parasympathetic nervous system. In simple terms, the sympathetic nervous system helps the heart speed up, and the parasympathetic nervous system helps the heart slow down. They act through direct nerve links to the heart and through the release of chemical substances that reach the heart through the bloodstream.

Understanding How Heart Disease Begins and Develops

The human cardiovascular system is wondrously complex. If every element is in balance and working as it should, a state called homeostasis, then the whole system, including the heart and blood vessels, would remain healthy. Unfortunately, multiple factors related to your biology and lifestyle can tip the system out of balance and trigger the development of heart disease. The earliest changes typically start in childhood or adolescence and then silently progress for years before producing changes that can be seen in diagnostic tests or symptoms that you experience. The most common type of cardiovascular disease is atherosclerosis.

Defining atherosclerosis – the most common form of cardiovascular disease

Atherosclerosis results from the gradual buildup of fatty deposits called plaque, or lesions, in the interior walls of large and medium-sized arteries. The disease process starts with small changes in the artery wall and takes years to develop to a point where the narrowing arteries may produce symptoms or negatively affect your health.

Narrowing in the heart’s arteries leads to coronary heart disease (CHD), also called coronary artery disease (CAD). CHD gradually starves the heart muscle of the high level of oxygenated blood that it needs to function properly. A lack of adequate blood supply to the heart typically produces symptoms that range from angina and unstable angina (see “Recognizing angina, or chest pain” and “Defining Unstable Angina” later in this chapter) to heart attack or sudden death. Narrowing of the carotid arteries that carry blood to the brain increases your risk of stroke. Narrowed arteries in your legs or arms results in peripheral artery disease (PAD).

The term atherosclerosis comes from two Greek words – athero (paste, gruel) and sclerosis (hardness) – that may give you a graphic image of hardened sludge. Not a pretty picture, is it? But it’s an apt image for these deposits of cholesterol, other fats, cellular wastes, platelets, calcium, and other substances. These deposits typically start with fatty streaks and grow to large bumps that distort the artery and block its interior where the blood must flow. Some plaques are stable and others are unstable or vulnerable to cracking or rupturing, which often leads to an artery-blocking blood clot and subsequent heart attack. The sections that follow profile that development process.

During the last 15 to 20 years, evidence from extensive population studies and clinical research has increased doctors’ understanding of the many factors and pathways that contribute to the beginnings and progress of atherosclerosis. The next sections provide an overview of medical science’s best understanding right now; however, you need to remember that new studies continually add to the knowledge of this complex, multifaceted disease.

Triggering the precursors of atherosclerosis

Biological factors that contribute to the development of cardiovascular disease are present from birth and perform vital functions that enable the human body to grow and resist infection. As a consequence, all human beings are born with the potential to develop heart disease. The early precursors of atherosclerosis frequently occur in children, teens, and young adults. Fortunately, adopting a heart-healthy lifestyle can usually reverse these early manifestations. The sooner you start, the better, but it’s never too late.

Current biomedical evidence has led to a consensus that atherosclerosis is a multifactorial chronic inflammatory disease that starts with the dysfunction of and/or injury to the endothelium, which is the inner lining of artery walls. Although only a single-cell-deep layer, the endothelium regulates the normal functioning of the arterial vessel walls. It acts as the traffic cop responding to the many blood-borne influences and biochemical signals that can modify the arterial walls. When any factor stresses or injures the endothelium, it triggers the inflammatory response that activates a variety of immune system signals and cells that rush to repair the damage.

If this process is triggered just occasionally, then this immune response repairs the damaged cells and shuts down until additional injury occurs. Unfortunately, the damage produced by most risk factors is constant and chronic. Risk factors such as elevated levels of LDL cholesterol and other lipids (fats), high blood pressure, smoking, and insulin resistance and diabetes cause chronic endothelial dysfunction and inflammation, and keep the immune response stuck in the “on” position.

Inflammation serves as a mediator in the disease progression by recruiting various immune system fighter and repair cells. The exact pathways by which inflammation exerts its influence are emerging from current research. Scientists are looking especially for inflammation markers that may help physicians diagnose and treat people at high risk of CHD in its early stages before symptoms arise, when lifestyle and medical therapies may halt or even reverse the disease.

Progressing to fatty streaks

Among the factors causing endothelial dysfunction to progress to atherosclerotic plaque, elevated levels of the certain types of cholesterol, particularly low-density lipoprotein (LDL) cholesterol, and other lipids play a major roll.

Here’s an overview of what happens:

1. Excess LDL cholesterol is deposited on the artery walls.

As a basic building block for every cell, cholesterol constantly circulates in the blood along with other substances that are vital for life. When blood levels of cholesterol, particularly LDL cholesterol, are too high, excess LDL cholesterol is deposited on the endothelial lining of arteries where special receptor cells latch on to the LDL molecules.

2. Trapped LDL damages the cells, triggering the body’s immune system into action.

This trapped LDL can damage the cells by a process called oxidation. The oxidation attracts protective substances related to the immune system. Cells such as macrophages already in artery walls engulf the oxidized excess lipid. (Risk factors also function to create more dangerous LDL particles such as small dense LDL that pass more easily through the endothelial into the first layer of the artery wall, called the intima.)

3. As the immune system tries to remove excess lipids and repair the damage, yellow fatty streaks appear on the artery walls.

Soon more circulating fighter cells, known as monocytes, enter the artery lining and transform into macrophages to gobble up more excess lipids. Other protective mechanisms such as platelets, T-cells, and growth factors for smooth muscle cells arrive and work hard to restore the damage from excess lipids. As these macrophages engulf the cholesterol, they transform into macrophage foam cells, which usually appear as yellow fatty streaks visible on the interior artery walls.

4. The fatty streaks continue to grow and form scar tissue.

When blood cholesterol levels are lower and plenty of HDL cholesterol (the good guys) is present to carry away LDL, then these fatty streaks can be halted or reversed. (For more on cholesterol and controlling it, see Chapter 9.) But when excess cholesterol and/or other risk factors such as the circulating platelets and other clotting factors and excess smooth muscles are present, the deposits typically continue growing. Through pathways not yet clear, risk factors can also help modify HDL lipoproteins so that they no longer act protectively but instead contribute to the atherosclerotic process.

As the process seals off the excess lipids, it actually creates cholesterol-rich pockets covered with scar tissue. These lesions narrow the arteries and typically deform artery walls as they grow larger.

Growing from fatty streaks to large plaques

Decades of time and the presence of various risk factors are required for the fatty streaks to develop into intermediate (moderate-sized, symptomless) and advanced (larger, symptom-producing) plaques. Figure 2-3 illustrates the typical but gradual development and progression of coronary heart disease.

Illustration by Kathryn Born

Figure 2-3: The process of coronary artery disease.

Growing to moderate, intermediate types of plaque

In the presence of normal mechanical forces, such as the impact of flowing blood against artery walls, and risk factors that can injure artery walls, many fatty streaks begin growing into larger deposits. More cholesterol and other lipid (fat) particles migrate into the artery walls. This happens particularly in areas where the intima of the artery has thickened, probably to adapt to mechanical forces exerted on the arteries.

More and more fatty substances aren’t taken into macrophages or the smooth muscle cells; instead, they begin pooling between them. Some cells die and release their lipids into this core. At that point, a thin layer of intimal tissue has begun forming a cap to contain this lipid pool. Other substances such as cytokines (various small proteins active in the immune system) and growth factors may also play a role in forming the cap and helping it continue to grow. The formation and growth of the cap mark the transition from intermediate lesions to what medspeak terms advanced (and typically more dangerous) lesions.

Becoming advanced atherosclerotic plaques

As plaques continue to grow, they reach a condition and size that may produce symptoms such as angina, unstable angina, or even heart attack or stroke. The various advanced types of atherosclerotic plaques are characterized by a well-defined lipid core that is contained by a cap composed of layers of smooth muscle cells and other substances.

At first this cap appears to be nearly normal intimal layers. But as the plaque grows larger, the composition of the cap’s layers changes, becoming more fibrous, or scarlike, as substances such as collagen and calcium enter the mix.

Some advanced plaques are stable, but others are vulnerable to cracking or rupture. When a crack or tear occurs, the lipid core is exposed to arterial blood from which sticky platelets may trigger the formation of a blood clot intended to repair the break. The clot, however, enlarges the size of the plaque. Some plaques grow larger by a cyclical process of cracking and clotting, which gradually narrows the artery. Fewer plaques may grow by a process of cap erosion rather than rupture.

The plaques that are more vulnerable to cracking are more likely to form a clot that totally blocks the artery and causes a sudden event such as a heart attack or stroke. So looking briefly at the difference between plaques is important – and the topic of the next section.

Differentiating between stable and unstable plaques

As individual plaques grow to moderate size and begin exhibiting the rich lipid core and thin fibrous cap associated with the first level of advanced lesions, they appear to be more vulnerable to rupture and dangerous clot formation than larger, older, thicker plaques. Bigger doesn’t necessarily mean more vulnerable, either. The most vulnerable plaques, which can give rise to the deadliest heart attacks, typically block the vessel by only about 40 percent to 50 percent.

Medical scientists and physicians are particularly interested in ways to accurately identify these types of vulnerable plaques, because they seem to be responsible for the majority of sudden acute cardiovascular events, including heart attack, cardiac arrest, and stroke. Figure 2-4 illustrates the way in which such a process suddenly blocks an artery and causes an acute event.

Illustration by Kathryn Born

Figure 2-4: When the plaque narrowing a coronary artery cracks open or ruptures, a clot forms, which can block the artery entirely, causing a heart attack.

Current evidence suggests that stable plaques typically have thicker, more fibrous caps with few inflammatory cells and more calcification, which make the cap tougher. Stable plaques also appear to have fewer lipids within. Although stable plaques often are large, the edges or shoulders of the lesion usually are smooth and tapered.

Unstable plaques, by contrast, are smaller in size but are very rich in cholesterol and incorporate many more inflammatory cells, which release chemicals that degrade the fibrous cap. Unstable plaques often appear structurally weak. In addition, the thinner cap may be easily ruptured or torn by a number of forces, ranging from the normal flow of blood at high stress points in the arterial system to sudden pressures such as suddenly increased blood pressure from exertion.

Researchers continue to look for tests and techniques that accurately identify and assess unstable plaque. Such tools would enable physicians to better identify individuals at greater risk of acute events and begin preventive measures.

Understanding a different type of coronary disease: Microvascular disease

Some people who experience reduced flow of blood to the heart do not have narrowings of the larger coronary arteries caused by atherosclerotic plaque. Instead, they have coronary microvascular disease (MVD). MVD occurs much more often in women than men, particularly in premenopausal or younger women. In MVD, smaller blood vessels in the heart, which range from 100 micrometers (about the size of a human hair) to 200 micrometers constrict, preventing adequate oxygenated blood from reaching the heart muscle. As a result, people with MVD may have clear larger coronary arteries but still experience the symptoms of chest pain, although the discomfort is usually more diffuse and may last longer than with angina in CHD.

The causes of MVD are not yet clear, but chronic inflammation appears to play an important role. And the risks factors for CHD, such as high blood pressure (particularly before menopause), unhealthy cholesterol levels, smoking, and diabetes appear to contribute. Current research is also looking for possible risk factors unique to MVD as well as for more effective diagnostic techniques.

If you have symptoms of heart disease (see the next section) but have clear coronary arteries, ask your physician about MVD, particularly if you are a woman.

Knowing when chest pain is an emergency

People with coronary artery disease and angina typically live with this problem for many years and discover how to manage it effectively with appropriate medicines and advice from their physicians. When angina pain changes in character, however, it can signal unstable angina or even heart attack. If you experience any of the following characteristics of chest discomfort, you need to call 911 and be taken to a hospital immediately:

✔ Pain or discomfort that is worse than you have ever experienced before

✔ Pain or discomfort that is not relieved by three nitroglycerin tablets in succession, each taken five minutes apart

✔ Pain or discomfort that is accompanied by fainting or lightheadedness, nausea, and/or cool clammy skin

✔ Pain or discomfort lasting longer than 20 minutes

If any of these symptoms occur, you need to call an ambulance and be taken immediately to a hospital. Under no circumstances should you drive yourself to the hospital.

Recognizing the Symptoms and Manifestations of Coronary Heart Disease

Because every person is an individual, physical responses to progressive coronary artery disease vary. Not every individual with heart disease has every manifestation and symptom of the condition. Individuals likewise experience specific symptoms in different ways. But these manifestations are typical:

✔ Nothing: Many people can have significant coronary atherosclerosis but experience no discomfort or other sign of the disease. That’s why this condition is known in medicine as silent ischemia. Ischemia means lack of blood flow. People with diabetes are particularly susceptible to silent ischemia, but others can have it, too.

✔ Angina: More formally known as angina pectoris, angina is typified by temporary chest pain, usually during exertion. This pain usually is felt as a tightness or uncomfortable feeling across the chest or up to the neck and jaw, not as a sharp stab. Angina also may have other manifestations.

✔ Unstable angina: Chest pain that is new, occurs when you’re at rest, or suddenly grows more severe is called unstable angina. It’s a medical emergency.

✔ Heart attack: Completely cutting off blood flow to a coronary artery causes an acute heart attack, or myocardial infarction (MI), the most severe result of coronary heart disease. The closure can be gradual or the result of a blood clot. A spasm in a coronary artery, particularly in the area of a narrowing, may also result in heart attack.

✔ Sudden death: The cause of sudden death from coronary heart disease often is a rhythm problem such as ventricular tachycardia or ventricular fibrillation. These rhythm problems sometimes occur in the setting of an acute heart attack. I’ve highlighted it here to make the point that the first indication or symptom for some people that they have CHD is a fatal cardiac arrest or heart attack. Many of these deaths happen to people in their 50s, 40s, or younger.

Recognizing angina, or chest pain

Angina typically is a discomfort felt in the chest, often beneath the breastbone (or sternum) or in nearby areas such as the neck, jaw, back, or arms.

✔ Individuals often describe the chest discomfort as a “squeezing sensation,” “vicelike,” “constricting,” or “ a heavy pressure on the chest.” (In fact, the term angina comes from a Greek word that means “strangling” – a strangling pain.)

✔ Angina often is brought on by physical exertion or strong emotions and typically is relieved within several minutes by resting or using nitroglycerin.

✔ Some individuals, particularly women, may experience angina as a symptom different from chest discomfort or in addition to it. Shortness of breath, nausea, faintness, abdominal pain, indigestion, or extreme fatigue may also be manifestations of angina.

✔ When chest pain occurs at rest, it usually is classified as unstable angina.

And just how do you pronounce the word? Some people say “an-jī-nuh” and others say “an-juh-nuh.” Either is correct. Some cardiologists may be a little snobby about their preference (who, us?), but pay them no mind.

Understanding the causes of angina

You know how your muscles begin to scream when you run faster than your blood can carry adequate oxygen to them. The same thing may happen when the coronary arteries become so narrowed by atherosclerotic plaques that blood flow to the heart is inadequate to supply the heart muscle with the oxygen it needs. The temporary chest discomfort known as angina is your heart’s way of getting your attention. It occurs when you ask your heart to work harder, and it therefore demands more blood – for instance, when you’re walking briskly or running, climbing a hill or stairs, having sex, or doing housework or yardwork. Strong emotions such as fear or anger also can trigger an episode.

Considering angina’s effect on the heart

Angina usually does not damage the heart. It is a temporary condition – the usual episode lasts only 5 to 10 minutes. (In MVD, the episodes can last longer, about 10 minutes up to 30 minutes.) Chest discomfort makes you stop and rest, slowing the heart and lessening its demand for blood. Alternatively, most people with angina know to take a nitroglycerin tablet under the tongue when they have an angina attack. The nitroglycerin dilates the coronary arteries, enabling blood flow to the heart to increase.

Any discomfort that doesn’t stop with rest or that lasts more than 5 to 10 minutes may be a heart attack and needs to be treated as an emergency.

Diagnosing angina

An individual’s own description of the discomfort he or she experiences provides the most important information leading to the diagnosis of angina. However, your physician will typically order appropriate tests based on your symptoms and signs. These may range from an electrocardiogram, exercise stress test, or stress echocardiogram to nuclear stress testing and cardiac catheterization (see Chapter 13). Some of these tests can be conducted in your physician’s office, but others require the resources of a hospital.

Distinguishing other causes of chest pain

All chest pain is not angina and does not involve the heart. Various conditions involving other structures in the chest can occasionally cause chest discomfort; these include spasm of the esophagus, acid reflux, hiatal hernia, and muscular pain.

Treating angina

People who have angina typically can live comfortably for many years with this condition by finding out how to manage the symptoms and lower their risk factors for complications.

Developing angina can be a big blow emotionally. So big that patients often adopt an unrealistically gloomy perception of their prognosis. Actually, there’s much you can do to adapt. Start with an open, frank discussion with your physician about the following lifestyle modifications:

✔ Adjusting your approach to physical activity, leisure-time pursuits, eating habits, and other practices to reduce risk factors and control and even reduce the symptoms of angina.

✔ Modifying strenuous activities that consistently and repeatedly produce angina, by taking simple measures such as slowing your walking pace, strolling (not sprinting) to the car through the rain, vacuuming or raking more slowly, and so on.

✔ Avoiding strenuous activities that require heavy lifting, such as snow shoveling (unless you discuss it with your physician).

✔ Adding slowly progressive exercise training, under your physician’s supervision, which can dramatically increase your ability to perform enjoyable activities of daily living.

✔ Considering with your physician other interventions such as medication or surgery if your angina causes unacceptably severe modifications of your lifestyle because quality of life is important!

Defining Unstable Angina

As the name suggests, unstable angina results when angina gets out of control. In unstable angina, the lack of blood flow and oxygen to the heart becomes acute and, therefore, very dangerous because the risk of complications such as heart attack is much greater.

Where stable angina has typical characteristics and predictable triggers, such as exertion or strong emotion, unstable angina is characterized by one or more of the following symptoms:

✔ Anginal discomfort at rest or when awakening from sleep

✔ A significant change in the pattern of the angina where it occurs with less exertion or is more severe than before

✔ A significant increase in the severity or frequency of angina

✔ New onset, or first experience, of anginal chest pain

If you experience any one of these characteristics, you must seek immediate medical attention.

Defining a Heart Attack

A heart attack, known medically as a myocardial infarction (MI), occurs when one of the three coronary arteries that supply oxygen-rich blood to the heart muscle (myocardium) becomes severely or totally blocked, usually by a blood clot. When the heart muscle doesn’t receive enough oxygenated blood, it begins to die. The severity of the heart attack depends on how much of the heart is injured or dies when the attack occurs.

When you think you’re having a heart attack it’s critical to go immediately to a hospital by ambulance where therapy can be initiated to save your heart muscle from dying. New clot-busting medicines, as well as procedures such as angioplasty, often can dissolve a clot that causes the heart attack, open the blood vessel, and save some or all of the heart muscle at risk. Although some of the heart muscle usually dies during a heart attack, the remaining heart muscle continues to function and often can compensate, to a very large degree, for the heart muscle that has died.

Understanding the causes of a heart attack

Heart attack almost always is caused when a blood clot forms at the site of an existing fatty plaque that has narrowed the coronary artery. Thus, individuals are at much higher risk for heart attack if they

✔ Have a history of coronary heart disease

✔ Have experienced previous bouts of angina

✔ Have suffered a previous heart attack

The blockage that triggers a heart attack usually is caused by an acute blood clot. Most acute blood clots occur when one of the plaques or fatty deposits on the artery walls cracks or ruptures. Other, much more rare causes of acute blockages in arteries, such as a severe coronary artery spasm, can also cause heart attack.

Recognizing the symptoms of a heart attack

Different people experience the symptoms of a heart attack in different ways. However, typical symptoms include some or all of the following symptoms (as described by the American Heart Association):

✔ Uncomfortable pressure, fullness, squeezing, or pain in the center of the chest lasting more than a few minutes

✔ Pain spreading to the shoulders, neck, or arms

✔ Chest discomfort with lightheadedness, fainting, sweating, nausea, or shortness of breath

In an individual who has angina, symptoms may be particularly difficult to differentiate from the chest discomfort of angina. However, when a heart attack is occurring, chest discomfort usually is more severe and may occur while the individual is at rest or less active than usual.

The signs of a heart attack often are subtle, particularly with individuals who have diabetes. People with diabetes may not have the classic symptoms of chest, shoulder, or arm discomfort. Chest pain experienced by many women likewise may not present the classic symptoms.

Coronary heart disease (CHD) is extremely common in men and women in the United States and particularly in men in their 40s and older and postmenopausal women. Even if you’ve never had a single sign of trouble, you need to call 911 and go straight to the hospital for prompt evaluation whenever you experience any of the preceding warning signs. Do not take a meeting. Do not put it off for an hour … just call 911 and go!

About two-thirds of the individuals who experience an acute heart attack also experience some warning symptoms in the weeks or days preceding the acute event. They often don’t realize what the warning signs were until after the event – with keen hindsight. So work on your foresight. That way you’ll know the warning signs of heart attack and take them seriously.

Differentiating between heart attack and sudden cardiac arrest