What is a Heart Attack?

WHAT IS A HEART ATTACK?

The definition of heart attack is the slow or complete interruption of blood flow to the myocardium (cardiac muscle). A heart attack is technically known as myocardial infarction, or MI for short, (Myo means muscle; cardio means heart; infarction means death of the tissue).

Atherosclerosis

As described earlier, the cardiac muscle receives its nutrients and oxygen supply from two arteries, namely the left and right coronary arteries (see the chapter on anatomy). Each artery divides into several branches, and each branch supplies a specific area of the cardiac muscle. The main cause of myocardial infarction is atherosclerosis, or hardening of the arteries, which is responsible for about 95 percent of all heart attacks.

Atherosclerosis and arteriosclerosis—this terminology is used interchangeably, but the following definitions are more accurate: arteriosclerosis (ahr teer ee o’ skle ro’sis): the term used for the process and damage of the arteries in general. Arterio means (artery); sclerosis means (hardening or scarring).

Atherosclerosis is pronounced (ath”ur o”skle ro’sis).Atherosclerosis is the specific process of cholesterol and fat deposits on the inner side or inner wall of the artery known as plaque deposits. It is by far the most common form of artery damage (Figure 1).

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Figure 1Schematicdiagram of atherosclerosis formation in the coronary artery

Arteries are blood vessels that transfer blood away from the heart. Tissues and organs receive their supply of oxygen from oxygenated blood through arteries. If for any reason an artery occludes, its share of blood to the organ it supplies stops or significantly diminishes. That organ will eventually die if that artery remains blocked or suffers extensive damage.

Since arteries travel long distances under a certain amount of pressure generated by the heart, their anatomy differs from veins. The muscular layer of the artery is much more developed to withstand the higher pressure. An artery is made of three layers (Figure 2):

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Figure 2 Schematic illustration of the three layers of an artery. The intima, media and adventitia, the endothelium is the cells layer

  1. Intima (inner surface and closest to blood)
  2. Media (middle layer)
  3. Adventitia (outer cover)

Intima

The intima is the innermost layer of an artery or a vein and is the closest to the blood. This layer of specialized cells, called the endothelium, serves as a protective cover to the innermost structures. It is a very fine, transparent, colorless structure that is highly elastic. These cells release a substance into the blood stream, preventing it from clotting.

Media

This is the middle layer of the arterial wall; it contains smooth muscle fibers and elastic tissue. These muscle fibers protect the artery and withstand the pressure generated by the heart. It also can constrict if the organ or tissue it supplies requires more blood. This layer lies between the intima on the inside and the adventitia (outer layer) on the outside. This layer can be distinguished by its color and its muscular layer. Unlike an artery, this middle layer in a vein has fibrous elements in excess, and the elastic or muscular fibers are in much smaller proportions.

Adventitia

This is the outermost layer of the artery; it contains nerve endings and minute arterioles that supply blood to the artery itself. This outer layer consists of collagen fibers that serve to anchor the blood vessel to the surrounding tissues giving it stability.

No one knows exactly how atherosclerosis begins, or what mechanism is responsible for triggering the process. However, researchers believe that if the blood is saturated with fats (e.g. due to excessive intake of cholesterol and triglycerides), these fats tear the specialized layer of cells (endothelium), causing the process of atherosclerosis to start.

Another possible source for damage to the endothelial cells is high blood pressure. The strain exerted on the arterial wall over a long period causes these cells to deteriorate and rupture.

Atherosclerosis is a two-step process:

  1. The damage of the specialized cells;
  2. The fats circulating in the blood infiltrate into the muscular layer of the artery, the muscle fibers become highly irritated, causing further damage.

When the arteries are damaged, this may lead to the damage of the tiny blood vessels that supply oxygen to the artery itself; this disruption may cause the blood cells to gather and stick together, reducing the oxygen supply. Like any other injury, swelling of the arterial wall occurs enhancing further the formation of plaque.

Once the specialized layer of cells (endothelium) are damaged, they are dislodged, exposing the tissue of the middle layer (media) to the blood stream. The tissue of this layer has the affinity to attract cells from the blood that are responsible in the process of clotting. These cells are called platelets (platelets normally collect at the site of a wound, to help stop bleeding).

Platelets are very sticky cells; therefore, they collect at the site of injury within the artery. This leads to the formation of a clot(s) that may block the artery entirely. A portion of that clot may also dislodge, travel with the bloodstream, and may end up in the brain, blocking a small artery and/or causing a stroke (Figure 3).

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Figure 3The arterial wall, A = damage to the endothelial cells, B = the exposed tissue attracts platelets from the blood, C = a large numbers of platelets, collect in the injured area, blood clots form, and may dislodge, and travel in the blood stream, eventually blocking smaller arteries causing a heart attack or a stroke, Pl = platelets, En = endothelial cells, D = site of damage, BC = blood clots

Like hypertension, atherosclerosis is also known as a silent killer. When it starts, you cannot stop it because you do not see it and you do not feel it. As you load your system with fats and triglycerides, you are causing more and more damage to the inner layers of the arteries. This destructive process continues all the time, throughout the circulation affecting the arterial system.

Angina Pectoris

The first sign of coronary arteries involvement by atherosclerosis is certain warning signals that manifest themselves in the form of chest pain known as angina pectoris. Angina is aching of the cardiac muscle itself due to lack of nutrients and oxygen. Angina pectoris happens when the coronary arteries are becoming narrower. Usually, angina starts during some sort of physical activity such as climbing stairs, or manual labor, as well as emotional excitement. Normally, the pain will subside shortly after the activity or excitement has stopped.

Anginal pain is usually a dull or pressing pain just beneath the sternum or breastbone. Some patients describe the pain as a “burning” or “squeezing” sensation, tightness, or crushing pain. It is very common to see that the sufferer of anginal pain clenches his fist against his chest while describing the pain. The location of angina cannot be pointed out with one finger because it is diffuse in nature and is never a localized pain (Figure 4).

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Figure 4 Sites of anginal pain, 1 = Dull diffuse pain in the upper chest, 2 = beneath the sternum, neck and mandible, 3 = beneath the sternum, left shoulder and arm, 4 = Epigastric, 5 = Neck and mandible, 6 = Left  shoulder and both arms

Anginal pain is not affected by body position nor by deep respiration; it is usually a dull ache, seldom sharp. It continues steadily with gradual changes. Anginal pain manifests itself in many different forms:

  1. A dull, diffuse pain presents itself in the upper chest region and may seem to remain within that area.
  2. A dull pain that is located just beneath the sternum. It radiates to the base of the neck and the lower border of the mandible.
  3. A dull pain just beneath the sternum, it radiates to the left shoulder and the inner area of the left arm down to the little finger.
  4. A dull sensation, or more likely, patients complain of an upset stomach.
  5. The feeling of a dull, uncomfortable pain at the base of the neck and the lower border of the mandible.
  6. A dull, diffuse pain in the left shoulder and the inner area of both arms.

Although the above six different sites of anginal pain are typical, a combination of these may very well happen. Some people describe to have pain in the back in between both shoulder blades as well.

Anginal pain usually disappears with rest, but is better relieved with medication such as nitroglycerine. However, if pain persists, and/or increase in intensity this might indicate that a heart attack might be eminent, and the individual should seek immediate medical help by going to the nearest emergency room. Certain people might be prone to angina in extreme hot or cold temperatures or after a heavy meal. If this is the case, try to cut down on your work or exercise, in winter, dress warmly, and reduce the portions of your meals.

In summer, engage in your activity in the early morning or late afternoon to avoid the heat of the day. Your physician might prescribe a mild exercise program, depending upon your condition. (Nutrition, rehabilitation, and exercise are discussed in separate chapters.)

Angina pectoris and myocardial infarction are two different conditions; however, both have the same underlying cause, atherosclerosis. Angina pectoris is the reduction of oxygen to the cardiac muscle causing pain. A myocardial infarction is the complete interruption of oxygen to the cardiac muscle. If this deficiency of oxygen is not reversed, the cardiac muscle will die (Figure 5).

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Figure 5 Schematic illustration of left coronary artery showing areas of narrowing, a complete interruption of oxygen may lead to a heart attack, 1 = partially occluded coronary arteries, 2 = totally occluded coronary artery, 3 = distal to a totally occluded artery 2 will slowlyfade away and eventually disappear

Depending upon the severity of the blockage, you will learn how to avoid those activities that bring about angina; bear in mind that it is how strenuously you do these activities rather than how long that causes angina. You might be able to walk a mile or more without any pain if you pace yourself but will have severe pain if you walked rapidly and vigorously for only half a block. If certain activity prompts anginal pains such as mowing the lawn, housework, or sexual intercourse, discuss the matter with your physician—he might prescribe or change the dosage of your medication.

Avoid emotional upsets such as outbursts of temper. Control your excitement or anxiety since they could trigger angina. Some kinds of recurring emotional problems can be very difficult to handle; seek professional advice and help. Long-standing tensions will aggravate your angina; discuss them with your physician or clergyman. Do not do things all by yourself; ask someone to help. Breathing exercises can relieve these tensions.

Angina pectoris may take one of three forms:

  1. Stable or chronic angina
  2. Unstable angina
  3. Variant angina

Stable or Chronic Angina

Stable angina is predictable; it occurs during some level of physical activity and/or emotional stress. It builds up gradually until it reaches maximum. Rest and nitroglycerine diminish the pain very effectively. 

The pain is a dull, crushing, tight, squeezing sensation just beneath the sternum and is not in one area. Shortness of breath, fainting, anxiety, and nausea may accompany the pain.

Diagnosing stable angina is easily achieved with the help of an electrocardiogram, physical examination, and diagnostic testing. Although an electrocardiogram is very effective in the diagnosis of anginal pain, a resting electrocardiogram may not reveal any changes. In these cases, a stress test (described later) may be important since it will reveal any underlying causes. Moreover, a Holter monitor (the electrocardiogram is recorded for twenty-four hours while the patient wears a special recorder) may prove to be very beneficial.

Unstable Angina

It is more severe in nature than stable angina and usually precedes a myocardial infarction (heart attack). It is also known as pre-infarction angina. Unstable angina is severe and prolonged; it occurs at rest and during minimal exertion. It is intense and may last thirty minutes or more. All attacks happen at night, and patients wake from their sleep. The first symptom is shortness of breath, accompanied by nausea and/or vomiting. Nitroglycerine may not be very effective

Variant Angina

Variant angina is also known as prinzmetal angina. It occurs at rest, and the cause is usually  coronary artery spasm. Variant angina is caused by spasm whereas the smooth muscular layer of the artery contracts or constricts. Therefore, a diminished amount of blood flow occurs causing severe chest pain. Most of the time spasm is the result of exertion or stress. By contrast to unstable angina, the pain is caused by an obstruction or a narrowing of the artery. If a spasm occurs in an area of obstruction or disease, the pain may be quite severe. The attacks usually occur always at the same time between midnight and the early-morning hours. The quality of pain resembles those of unstable angina, severe diffuse pain beneath the sternum with sensation of tightness and crushing discomfort.

Patients with variant angina may experience arrhythmia and conduction system abnormalities; the pain is quickly relieved with nitroglycerine. Nitroglycerine dilates the artery hence, allowing more blood to flow.

Myocardial Infarction

Myocardial infarction (heart attack or death of the cardiac muscle) is an injury to the myocardium (heart muscle) because of blood supply interruption to the heart. Myocardial infarction is the main cause that leads to death. Almost half of a myocardial infarction sufferers die within one hour after the onset of the symptoms. Those that seek treatment stand a good chance at overcoming death.

As described in chapter two, myocardial infarction (death of the cardiac muscle) starts by build-up of atherosclerosis. However, the cause is triggered by a condition in which the cardiac muscle suffers when the oxygen supply is interrupted; for example, in severe coronary spasm, or in coronary thrombosis (blood clot in the coronary artery) in which the myocardium suffers gradually leading to injury and infarction.

The left ventricle is mostly affected because of its thicker wall, its size, abundant blood circulation, and greater workload.

Acute coronary syndrome (ACS) is another term that refers to a spectrum of clinical presentations ranging from those for ST-segment elevation myocardial infarction (STEMI) to presentations found in non–ST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. In terms of pathology, ACS is almost always associated with rupture of an atherosclerotic plaque and partial or complete clotting of that artery.

Myocardial infarction also triggers the release of the hormone epinephrine and norepinephrine that are secreted by the adrenal medulla (the innermost layers of the suprarenal glands) in response to the infarction. This is the most powerful vasopressor (an agent who contracts the muscular tissue of the arteries) substance known, increasing blood pressure, stimulating the cardiac muscle, accelerating the heart rate, and increasing the cardiac output.

Myocardial infarction affects both right and left ventricles but more often it happens in the left ventricle in four different locations (Figure 6):

  1. Subendocardial infarction is the inner most area of the myocardium and is closest to the cavity of the ventricle.
  2. Intramural infarction is an infarct that usually involves the middle area of the myocardium.
  3. Transmural infarctionthe infarct usually involves the entire thickness of the myocardium, known as anterior, inferior, posterior, or lateral wall infarction. Anterior wall myocardial infarction is the most severe; it affects large areas and may trigger arrhythmias.
  4. Subepicardial infarction—the infarct usually involves the outermost area of the myocardium.

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Figure 6 Different sites of myocardial infarct, 1 = subendocardial infarction, 2 = intramural infarction, 3 = transmural infarction, 4 = subepicardial infarction, MV = mitral valve, TV = tricuspid valve, LV = left ventricle, RV = right ventricle, S = septum, P = papillary muscle

Pathologic Changes

Myocardium changes do not appear until after six hours from the onset of the infarction. The changes that occur are as follows:

  1.  After the first six hours, swelling occurs in the injured area. It  becomes bluish pale in color.
  2. Within eighteen to thirty-six hours, the myocardium turns reddish purple.
  3. Two to three days after, the injured site turns grayish yellow  and covers the entire damaged region.
  4. Three to four weeks later, phagocyte cells (specialized cells that devour dead tissue) start cleaning the damaged site, reducing the thickness of the infarcted area.
  5.  Within four to six weeks, the infarct region becomes somewhat jellylike in consistency, grayish in color, and starts forming scar tissue.

Silent Ischemia

It has been documented that myocardial ischemia does not always make its presence known. Studies reveal that many patients are completely unaware of any indications of extensive coronary artery obstruction. It is only when routine electrocardiogram is required that evidence of an old infarct is revealed.

One should then ask why some individuals experience pain while others do not. Those that were asymptomatic may have a higher pain threshold or smaller ischemic area. Others may completely deny their symptoms.

Arrhythmias

Arrhythmia is defined as “an irregular heartbeat.” The heartbeat is controlled by a group of cells known as the pacemaker (turn to chapter one on anatomy of the heart). During a heart attack when part of the heart muscle is injured, some of the fibers that form the conduction system are also affected, causing a change in the normal rhythm. The heartbeat can become faster, slower, or irregular. Frequent electrocardiograms are important to determine whether any of the conduction system is severely affected.

Not all arrhythmias are caused by myocardial infarction. There are many conditions that trigger arrhythmias, it is not the intention of this book to discuss them, suffice to say that your physician can determine the exact reason and cause of an arrhythmia.

Because of the disruptive action of the cardiac muscle, certain manifestations occur in the form of symptoms:

  1. Palpitation
  2. Shortness of breath
  3. Weakness
  4. Chest pain
  5. Anxiety
  6. Syncope
  7. Fainting

Once arrhythmia is diagnosed, certain drugs are administered that would control these irregularities until the cardiacmuscle has healed from the myocardial infarction or from the trigger that caused it. If the damage to the fibers of the conduction system were permanent, it would become necessary to implant a pacemaker to regulate the contraction of the heart.

A pacemaker is an electronic device specifically designed and implanted in cardiac patients who suffer from various forms of arrhythmia. It is a device that senses the disturbance of the conduction system and, therefore, delivers an electric shock to the cardiac muscle. A complete pacemaker system has two basic components:

1)        The electrode is a specially designed catheter that has one or two electrodes at one end. The other end of the catheter is an occasions, two such electrodes are used.

2)        Pulse generator is the power source; it houses an intricate electronic circuitry that senses any changes to the cardiac rhythm. If the heart skips one or more contractions, the pulse    generator will immediately sense the disturbance in the rhythm; it will   generate an electric current that travels through the catheter electrode, which in turn stimulates or shocks the cardiac muscle to contract, therefore, maintaining a normal heart rate.

What to Expect after a Heart Attack

After a heart attack, the healing period may seem to pass very slowly because you are to cut down on a number of activities. Patients feel depressed, particularly if they are free of any symptoms, since they feel they can achieve a lot more. This process might take several months with regular trips to your doctor. Lifestyles of patients will totally change.

Once the healing process is completed, most people resume their normal activities very regularly, including returning to their jobs. Some patients may never have another heart attack, and this is the goal of a slow recovery period. Another very important aspect in recovering after a heart attack is rehabilitation (see chapter four).

At Home after a Heart Attack

  • If you develop angina, shortness of breath, arm or hand                                     discomfort, you should stop what you are doing immediately, take some of your prescribed nitroglycerin, and rest for a few minutes. When the symptoms disappear, resume your activity at a slower pace
  • You should notify your physician or go to the nearest  emergency facility

i) Heavy pressure or chest pain radiating to your shoulder, arm, neck, and jaw is   not being relieved with medication
ii) Increased shortness of breath
iii) Fainting

iv)  Slow or rapid heart rate

  • Space your activities to allow your heart to rest

i.     Plan your work, spread harder tasks, and alternate with easier ones
ii.     If you feel tired, stop and take a fifteen-to-twenty-minute rest. Do not push yourself
iii.     Do not do all of your activities at one time. Rest in between
v.     Plan to rest twenty to thirty minutes twice a day
vi.     You should get at least five to eight hours of sleep every night

  •  If you do housework, follow these suggestions:

i.     Eliminate unnecessary tasks, such as drying dishes
ii.     Clean one room at a time; take a rest before going to the next
iii.     Do not move any furniture or heavy appliances
iv.     Make one side of the bed completely before going to the other side to cut down on the number of times you have to walk around the bed
v.     Try to sit down when ironing or when preparing food; try to keep everything at your level rather than getting up often to reach for the items you need
vi.     Do not do anything that requires using your arms above your shoulder level
vii.     Avoid washing windows or cars

  • Avoid tensing your body

i.     Do not strain when you have a bowel movement; ask your physician for laxatives
ii.     Do not lift any heavy objects, children, groceries, or suitcases; do not do any pushing   or pulling
iii.     Do not strain in opening stuck objects, such as boxes, jars, etc.,

  •  Walk dailyas much as you were waking at the hospital before your discharge. You maywalk outside when the weather is nice. Walkon level grounds; avoid any steps and hills. Avoid walking against the wind or in extreme cold weather. These conditions make your heart work harder. Take your walks after a period of rest, and while walking, if you experience any chest pain or discomfort, you should immediately sit down and rest. Take your nitroglycerin until the pain is completely gone. When you start your walking or exercise program, always start moderately and increase as you go along.
  • When climbing stairs,like anything else, start slowly. If you have to climb stairs, climb them once a day and go slow. Avoid too many stairs at one time. Increase as you go along.
  • With cold or warm temperatures, during winter, avoid going out on windy days. If you must, cover your mouth and nose with a handkerchief; try to complete your exercise program indoors. In summertime, go out early or late in the day so you can avoid the heat. Do not stay out for long periods.
  •  Sex should be treated like any other exercise. Rest for a while before engaging in sex, and avoid sex if you:

i.     Are tired
ii.     Have just eaten a heavy meal
iii.     Have been drinking
iv.     Are angry with your mate
v.     Experience any chest pain or discomfort. When you experience pain or discomfort, stop and take your nitroglycerine. The next time, take your nitro before engaging in sexual relations since your heartbeat will be faster

  •  Long trips—check with your physician prior to taking a long trip, particularly if you will be driving. Stop every hour and do some walking. This will stimulate your circulation to avoid any clot formation in your lower legs.
  •  Check with your physician prior to going to the mountains or very hot places. Avoid argumentative situations. You should stay away from conversations that might become upsetting since your heart will have to work very hard.

i.     After a meal, you should take a rest for about an hour since your heart is already working harder to compensate for digestion
ii.     You should stop smoking
iii.     Pace yourself for your daily chores

Conclusion

After hospitalization from of a heart attack, patients often become depressed. They associateheart attack with some disabling disease and think they are becoming invalid. This particularly happens to those who had been very active prior to their heart attack. They become anxious about whether they will be able to resume full physical, social, professional, and sexual activities.

Usually, there should be no worry if, of course, the patient follows the prescribed protocol of treatment that is essential to full recovery. Like any other injury, it takes time for the healing process, and unless this period is followed carefully, recurrent heart attacks might follow. On the other hand, if the recovery period is followed normally, many patients never experience another heart attack again.

Learn more in my new book available for ordering. In addition, an eBook is available also as a download. Follow the link at;

http://www.tatepublishing.com/bookstore/book.php?w=9781613468449