Pathology of Myocardial infraction

(Photo Essay)
Medical Author: Michael C. Fishbein, M.D.
Medical Editor: Leslie J. Schoenfield, M.D., Ph.D.
Medical Reviewing Editor: Jay W. Marks, MD

•
•
• What is a Heart Attack?
• What are the structures and functions of a normal coronary artery?
• What happens to the coronary artery in atherosclerosis?
• Who gets coronary artery plaques and what happens to the plaques?
• What causes a Heart Attack?
• What happens to the heart muscle after a person survives a Heart Attack?
• Can a person have more than one Heart Attack?

What is a Heart Attack?

A heart attack is a layperson's term for a sudden blockage of a coronary artery.

This blockage, which doctors call a coronary artery occlusion, may be fatal, but most
patients survive it. Death can occur when the occlusion leads to an abnormal heartbeat
(severe arrhythmia) or death of heart muscle (extensive myocardial infarction). In both of
these situations, the heart can no longer pump blood adequately to supply the brain and
other organs of the body. Almost all heart attacks occur in people who have coronary
artery disease (coronary atherosclerosis). So, this photo essay will review the structure
(anatomy) of the normal coronary artery, the structural abnormalities (pathology) of the
coronary artery in atherosclerosis, and the effect of these abnormalities on the heart.

What are the structures and functions of a normal coronary artery?

The coronary arteries carry blood to the heart to supply oxygen and necessary
nutrients. As seen in Figure 1, the wall of a coronary artery has 3 distinct layers: the inner
(intima), middle (media), and outer (adventitia) layers. The wall of the artery surrounds
the lumen of the artery, which is the channel through which blood flows.
Figure 1: Normal Coronary Artery
Cross-sectional Microscopic View

In Figure 1, smooth muscle is red, and connective (supporting) tissue is black (elastic) or
blue (collagen).

The intima is best seen in the close-up view in Figure 1. It is composed of a

layer of so-called endothelial cells that covers the artery's inner (lumenal) surface,
connective (supporting) tissue (collagen and elastin), and a layer of compact elastic tissue
called the internal elastic lamina (IEL). In the past, the intima was thought to be simply a
passive layer whose major purpose was to serve as a barrier. Now, however, we know that
the endothelial cells actually keep track of the pressure, flow, and "health" of the artery.
Moreover, endothelial cells secrete chemicals that can adjust the function of the artery
(e.g., vasodilator chemicals to widen and vasoconstrictors to narrow it) and growth of the
artery wall (e.g., growth factors).

The media (M) is a layer made up primarily of smooth muscle cells (SMCs). The
muscle can contract and relax to control the blood pressure and flow in the artery. Elastic
tissue and collagen in the media, along with elastic tissue in the IEL, increase the
elasticity and strength of the wall of the artery, as the artery contracts and relaxes. The
adventitia is a layer of connective tissue and cells (e.g., SMCs) that produce this
connective tissue.

The adventitia contains potent factors, including one called tissue

thromboplastin, that promote blood clotting. The clots are useful when the artery
becomes injured because they can limit excessive bleeding from the injured artery.

What happens to the coronary artery in atherosclerosis?

In coronary artery disease (coronary atherosclerosis), injury to the intima of the

artery leads to the formation of plaques, which are regions of thickening on the inner
lining of the artery. How then do the plaques form? In response to the injury, the smooth
muscle cells (SMCs) from the media and perhaps from the adventitia move (migrate) into
the intima. In the intima, these SMCs reproduce themselves (divide) and make
(synthesize) connective tissue. These processes of migration, division, and synthesis,
which collectively are referred to as intimal proliferation (buildup), cause thickening of
the intima.

When cholesterol, other fats, and inflammatory cells, such as white blood cells,
enter the proliferating, thickened intima, the result is an atherosclerotic plaque. Then, as
these plaques grow, they accumulate scar (fibrous) tissue and abundant calcium.
(Calcium is the hard material in our teeth and bones.) Hence, the plaques are often hard,
which is why atherosclerosis is sometimes referred to as "hardening of the arteries."

Who gets coronary artery plaques and what happens to the plaques?

Most adults in industrialized nations have some plaques (atherosclerosis) on the

inner (lumenal) surface of their coronary arteries. Autopsy studies of young soldiers who
died in World War II, the KOrean War, and the Vietnam War showed that even young
adults in their 20s usually have coronary arteries that exhibit localized (focal) thickening
of the intima. This thickening is the beginning of intimal proliferation and plaque
formation. The distribution, severity (amount of plaque), and rate of growth of the
plaques in the coronary arteries vary greatly from person to person. Figure 2 shows a
coronary artery with an uneven (asymmetric), stable atherosclerotic plaque.

A stable plaque may grow slowly, but has an intact inner (lumenal) surface with
no clot (thrombus) on this surface.

Figure 2: Coronary Artery with Stable Atherosclerotic Plaque

Cross-sectional Microscopic View
What causes a Heart Attack?

Rupture of a stable plaque in a coronary artery is the initial pathological event

leading to a heart attack. When the rupture occurs, a clot suddenly forms in the lumen
(channel) of the artery at the site of the rupture. Bleeding into the plaque often
accompanies the rupture.

The clot then blocks (occludes) the artery and thereby decreases the blood flow to
the heart. This sequence of events in the coronary arteries is the basic problem in over
75% of people who suffer a heart attack. In some patients, more often women, there is
just an erosion or ulceration of the plaque surface, rather than a full rupture that leads to
clot formation in the coronary artery. Figure 3 shows an atherosclerotic plaque rupture
and a clot in a coronary artery.

Figure 3: Rupture of Atherosclerotic Plaque in Coronary Artery

Cross-sectional Microscopic View
What happens to the heart muscle after a person survives a Heart
Attack?

According to medical studies, 50% to 75% of people survive their first heart
attack The others die during the heart attack because the decreased coronary blood flow
causes a severe abnormal heart rhythm or extensive death of heart muscle. Figure 4
shows the heart of a patient who died 5 days after a heart attack.

The photos show his myocardial infarction as it appears on the surface of the left
ventricle and when the heart is sliced to view the muscle wall. About 90% of myocardial
infarctions involve only the left ventricle (LV), which pumps oxygen-rich blood that
comes from the lungs to the entire body. The other 10% also involve the right ventricle
(RV), which pumps the blood to the lungs.

Figure 4: Myocardial Infarction Caused by Heart Attack

Views of Heart Surface and Slice Across Heart

If a person survives a heart attack, the heart muscle may return to normal or
become a region of dead heart muscle (the myocardial infarction). The amount and health
of the remaining heart muscle is the major determinant of the future quality of life and
longevity for a patient after a heart attack.

A heart attack can interrupt the normal electrical wiring of the heart, leading to
abnormal heart rhythms. The heart attack can also weaken the pumping action of the
heart causing shortness of breath due to heart failure. Each of these complications of a
heart attack can occur at any time during the recovery period as a result of dead, dying, or
scarring heart muscle.
Can a person have more than one Heart Attack?

Yes. Not uncommonly, people with coronary artery disease have more than one
heart attack over the years. In fact, by looking at the heart tissue at autopsy, pathologists
can tell when myocardial infarctions occurred. Thus, very recent (acute, hours old)
infarctions may appear as a pale brown region, infarctions days old (subacute) appear
yellow, and healed (weeks to years old) infarctions appear as white scars in the heart
muscle. Figure 5 shows three myocardial infarctions of different ages in the muscle of a
left ventricle.

Figure 5: Three Myocardial Infarctions of Different Ages

Slice Across Heart Ventricles

A heart attack is a layperson's term for a sudden blockage of a coronary artery. This photo
essay inlcudes graphics, pictures, and illustrations of diseased heart tissue and the
mechanisms that lead to coronary artery disease, and possible heart attack.

Medications

• Aspirin and Antiplatelet Medications

•
• MISOPROSTOL-ORAL, Cytotec
•
• DICLOFENAC W/MISOPROSTOL-ORAL TABLET, Arthrotec
• mifepristone-oral, Mifeprex
Doctor's & Expert's Views

• Heart Disease Prevention in Women

•
• Heart Bypass Surgery -Audio Medical Podcast
•
• Heart Disease Risk and C-reactive Protein (CRP)
•
• Cox-2 Inhibitors Dilemma: What Patients Should Do

Procedures & Tests

• Coronary Artery Bypass Graft

•
• Electrocardiogram (ECG or EKG)
•
• Coronary Artery Disease Screening Tests
•
• Angioplasty and Stents (Percutaneous Coronary Intervention, PCI)
 PATHOLOGY OF SMOKER’S LUNG

Medical Author: Michael C. Fishbein, M.D.

Medical Revising Editor: Jay W. Marks, MD

Cigarette smoking is associated with a wide variety of abnormalities throughout

the body that cause not only illness, but also, all too often, death. Indeed, if all deaths
from diseases related to smoking (lung disease, heart disease, and cancers of many
different organs) were considered, a case could be made for cigarette smoking as the
leading cause of death in industrialized countries. Ironically, it is also the most
preventable cause of death in our society!

This photo essay will focus on smoker's lung. The term "smoker's lung" refers to
the structural and functional abnormalities (diseases) in the lung caused by cigarette
smoking. First, the normal structure and function of the lung will be described and
illustrated. Then, the structural and functional abnormalities caused by smoking will be
described and illustrated.

Table of Contents
• What is the structure of the normal lung?
• What processes determine normal function of the lung?
• What are the abnormalities (diseases) in smoker's lung?
• What happens to the lung in emphysema?
• How does emphysema come about?
• Why does smoker's lung look black?
• What happens to the airways in chronic bronchitis?
• Are smokers with COPD predisposed to developing pneumonia?
• What about lung cancer in smokers?
• Are any of the pulmonary consequences of smoking reversible?
• From what do smokers die?
What is the structure of the normal lung?

We have a right lung and a left lung that reside in the chest cavity and surround
the heart. A thin membrane called the pleura covers the outer surface of the lung. The air
we breathe gets into the lung through an airway (path for air).

Figure 1 is a diagram showing the main parts of the airway and lung.

Figure 1: NORMAL AIRWAY AND LUNG

The airway consists of the oral and nasal cavities, which connect to the voice box
(larynx), which connects to the windpipe (trachea). Note in the diagram that the windpipe
splits into two air passages called bronchi, one going to each lung (right and left main
bronchi). The trachea and larger bronchi contain C-shaped rigid bars of cartilage in their
walls. The cartilage helps to keep the airway from collapsing when there is negative
pressure in the airway, as occurs when we breathe in (inhale or inspire). The right lung
has three separate sections (upper, middle, and lower lobes), while the left lung has just
an upper and a lower lobe. Each lobe has its own bronchi and blood supply.

Further along in the airway, within the lung, the bronchi continue to divide into
ever-smaller (narrower) tubes, much like the branches of a tree. (Hence, the term
tracheobronchial tree.) The walls of the bronchi contain muscles that can cause the
airway to expand (widen) or contract (narrow). For example, during exercise, the airway
expands to increase airflow (ventilation).

Conversely, when exposed to polluted or very cold air, the airway contracts to
protect the downstream tissues from injury. The smaller branches of the bronchial tree,
called bronchioles, also contain muscle, but they lack cartilage. Notice in Figure 1 that
the very smallest bronchioles (respiratory bronchioles) connect directly to tiny air sacs in
the lung, called alveoli.
Figure 2 shows a microscopic section of a normal bronchial wall.

Figure 2: NORMAL BRONCHIAL WALL

In this picture, you can see that the bronchial wall contains cartilage and muscle,
as described above. Also, note that different types of cells make up the lining (epithelium)
of the bronchi (as well as of the trachea and bronchioles). One type of cell is called a
goblet cell because of its shape.

The goblet cells produce mucus, which lubricates the airways and traps inhaled
foreign material (e.g., bacteria, viruses, and pollutants). Other cells in the epithelium are
called ciliated cells, which are discussed in the next paragraph. Beneath the surface of the
airway, the goblet cells and other epithelial cells are clustered into structures called
bronchial glands. These glands secrete additional mucus and other lubricating fluids.

Inflammatory cells are also in the normal bronchial wall. Look again at Figure 2
and observe that they are scattered beneath the lining of the airway. These inflammatory
cells, also known as white blood cells, include neutrophils, lymphocytes, and
macrophages. Their job (in this situation) is to destroy and/or engulf any inhaled foreign
material that becomes trapped in the mucus.

In doing so, however, inflammatory cells create debris. To help dispose of the
debris, most of the cells that line the airway have hair-like processes called cilia. These
ciliated cells sweep and push the foreign material and debris up into the larger airways
where they can be coughed up or spit out.

The lung resembles a sponge and is composed of millions of alveoli. This

structure provides a huge surface for gas exchange that has been estimated to be equal to
the size of a tennis court. (These tiny air sacs can be seen with a magnifying glass.)
Figure 3 is a microscopic section of a normal lung, showing the alveoli.

Figure 3: NORMAL LUNG ALVEOLI

The wall (alveolar septum) of each alveolus contains a very small blood vessel
called a capillary. Blood flows slowly through each capillary to allow time for the lung to
perform its main function, which is the exchange of gas (oxygen and carbon dioxide).
The actual site for gas exchange is pictured in the high magnification section on the right
side of figure 3. Thus, the capillary blood picks up oxygen (O2) from the inhaled air in
the alveoli. At the same time, the capillary blood releases the body's waste gases, most
importantly carbon dioxide (CO2), into the alveoli. (Waste gases are by-products of the
body's metabolism.)

What processes determine normal function of the lung?

As just indicated, the main function of the lung is the exchange of the gases
oxygen and carbon dioxide. So, the blood in the alveolar capillaries takes oxygen from
inhaled air that is in the alveoli. Then, the oxygenated blood circulates through the body
to deliver the oxygen to the tissues. In the exchange of gases, the blood in the alveolar
capillaries releases carbon dioxide to the alveoli. Then, when we breathe out (exhale or
expire), the carbon dioxide is removed from the alveoli through the airway and
eliminated from body. Accordingly, three processes determine normal lung function:

1. Ventilation
2. Diffusion
3. Blood supply
Ventilation:

The moving of air into and out of the lung. This process requires an open
(unobstructed) airway. Increasing and decreasing the size of the chest cavity is what
accomplishes the movement of air. You see, as the chest cavity enlarges, a vacuum is
created in the airway and air rushes in. Then, with breathing out, the chest cavity
becomes smaller and air is pushed out. The muscles in the chest wall (intercostal muscles
between the ribs), and the muscles in the diaphragm work together to change the size of
the chest cavity. (The diaphragm is a flat muscular membrane that separates the chest
from the abdomen.) In addition, when we breathe really hard, we even use muscles in the
neck (referred to as accessory muscles for breathing) to help expand the chest.

Diffusion:

The process that accomplishes the actual gas exchange across the alveolar walls.
This process requires normal alveolar septae (the walls of the air sacs) that contain intact
capillaries. Finally, a normal blood supply depends on normal capillaries, normal red
blood cells (no anemia), and normal pumping of blood by the heart. Any disease that
interferes with ventilation, diffusion, or blood supply to the lung will impair lung
(pulmonary) function and decrease delivery of oxygen to the tissues of the body.

What are the abnormalities (diseases) in smoker's lung?

The major abnormalities in smoker's lung are grouped under the label of Chronic
Obstructive Pulmonary Disease (COPD). It is estimated that 40 million people
worldwide suffer from COPD. COPD is the 4th leading cause of death in the USA. Even
more disturbing is the fact that COPD is the only one of the "top 5" causes of death to
increase in the past decade.

While COPD has been thought of as a disease of men, it is estimated that by the
year 2010 there will be more women than men affected by COPD. These statistics are
especially sad because COPD is preventable disease by stopping smoking; unfortunately,
this is easier said than done. About 70% of smokers want to quit, but only 7% who try are
smoke free after one year; however, one should not give up. Numerous tries, sometimes
more than 10, and professional help often are needed, but the health benefits of smoking
cessation make it worth the effort.

COPD is made up of two major, related diseases. One, emphysema, involves the
lung alveoli, and the other, chronic bronchitis, involves the bronchial airway. (Both
conditions are discussed below.) In this essay, I will use the term chronic bronchitis to
include chronic bronchiolitis and chronic respiratory bronchiolitis. I do this because these
three conditions have the same pathology (structural abnormalities), cause the same
symptoms, and differ only in their location in the airway. At any rate, some smokers
primarily have emphysema and some primarily have chronic bronchitis. Most, however,
have a combination of these two diseases.
What happens to the lung in emphysema?

In emphysema, the walls of the air sacs (alveolar septae) are destroyed.
Consequently, the individual air spaces (alveoli) become larger but irregular and
decreased in number. These larger spaces are less efficient than normal sized alveoli for
gas exchange. Thus, emphysema impairs diffusion of oxygen and carbon dioxide (gas
exchange). The more extensive the emphysema, the poorer the gas exchange becomes.
Also, in emphysema, the capillaries are destroyed with the rest of the alveolar wall. As a
result, emphysema also disrupts the normal blood supply.

Figure 4 contrasts the nasty appearance of a smoker's emphysematous lung with a

normal lung.

Figure 4: SMOKER'S AND NON-SMOKER'S LUNGS

Emphysema usually starts in the upper lobes of the lung and, as depicted in this
photo, is more severe in the upper lobes for complex reasons. That is, the abnormal
(enlarged and irregular) air sacs (alveoli) are more prominent in the upper lobes. (The
blood vessels in the lungs should not be mistaken for the abnormal air sacs.)

In someone with severe emphysema, the entire chest actually can enlarge. What
probably happens is that the patient's extra (compensatory) efforts to suck in as much air
as possible (to increase ventilation) contribute to enlarging the lungs and the chest. Thus,
a person with severe emphysema often develops what has been described as a barrel-
chest.
How does emphysema come about?

Simply put, the cigarette smoke attracts inflammatory cells (white blood cells,
including neutrophils, lymphocytes, and macrophages) into the lung. Then, the
inflammatory cells release substances called proteases. The proteases dissolve the
proteins in the alveolar walls (septae) and thereby destroy the septae. As a result, the
alveoli join together (coalesce) to form the larger, irregular, inefficient air sacs.

It turns out that about half of all smokers develop emphysema. Mild emphysema
is seen occasionally in non-smokers and may be due to passive smoking (exposure to
other people smoking) and industrial air pollution. Severe emphysema, however, is seen
only in smokers or in some people with rare inherited diseases (e.g., alpha-1-antitrypsin
deficiency). Still, it takes about 30 years of smoking to develop fatal emphysema. This is
because people usually don't die from emphysema until more than 60% of the lung tissue
is affected.

Why does smoker's lung look black?

The lung is connected and exposed by the airways to a potentially noxious outside
world. Accordingly, the alveolar spaces normally contain specialized scavenger cells,
called alveolar macrophages. The job of these macrophages is to engulf (phagocytize)
any possibly harmful foreign material that enters the lung through the airways.

As you can imagine, cigarette smoke contains many impurities that are inhaled in
great numbers directly into the lung. For this reason, the alveolar spaces of the smoker
contain numerous scavenger cells (macrophages) that are filled with engulfed
(phagocytized) particles of impurities and debris, as illustrated in

Figure 5: SCAVENGER CELLS IN SMOKER'S ALVEOLUS

 Under the microscope, with this high magnification, you can actually see the
black and brown engulfed particles in the alveolar scavenger cells. Indeed, smoker's lung
may have so much of this particulate material that the lung looks gray-black to the naked
eye. So, most of the time, you don't need a microscope to tell if someone is or was a
heavy smoker. A naked eye examination of a smoker's lung usually will reveal an
enlarged gray-black lung with enlarged air spaces (the emphysema, as you saw in Figure
4 and will see again in Figure 8).

What happens to the airways in chronic bronchitis?

In chronic bronchitis, smoke damages the cells that line the airway (epithelial
cells). Nicotine is one of the many components of cigarette smoke that is directly toxic to
the lining cells of the airway. (Of course, the nicotine is also addictive.) The tissue
damage attracts inflammatory cells. These cells then release enzymes that further damage
the lining cells of the airway and stimulate goblet cells to increase in number and to
increase mucus production.

Figure 6 is a microscopic section of a bronchial wall in a smoker with chronic

bronchitis.

Figure 6: BRONCHIAL WALL IN CHRONIC BRONCHITIS

The major consequence of chronic bronchitis is airway obstruction. In fact, this

figure demonstrates mucus and debris blocking the bronchial airway. Indeed, the most
important cause of airway obstruction in chronic bronchitis is blockage by mucus,
inflammation, progressive scarring (fibrosis), and/or narrowing (constriction) of the
airways. As a result of the bronchial blockage, gases cannot get to and from the alveoli.
In other words, chronic bronchitis interferes with ventilation.
 It is important to know that people with asthma likewise have chronic bronchitis
with airway obstruction. In asthma, however, the cause of obstruction is somewhat
different and the obstruction usually occurs in attacks that are reversible. In any case,
both smokers and asthmatics with bronchitis may cough, wheeze, and spit up thick mucus
(sputum) from the lung.

Are smokers with COPD predisposed to developing pneumonia?

The answer is yes. As previously mentioned, smoking increases mucus production

and impairs the clearing action of the cilia in the airway. Also, the addition of bacteria,
inflammatory cells, and damaged lung cells to the secretions in the airway and lung make
the secretions especially thick, tenacious, and difficult to clear.

Therefore, in such a stagnant and nutritious (the mucus) environment, bacteria can
flourish and cause infection of the lung (pneumonia). Furthermore, even the
inflammatory cells are damaged by tobacco smoke so that their ability to fight infection is
diminished.

For all of these reasons, pneumonia is not only more common, but it is often also
more severe in smokers with COPD (chronic obstructive pulmonary disease, that is,
emphysema and/or chronic bronchitis) than in non-smokers without COPD. Moreover,
the inflammatory cells that accumulate in the lung to fight off the infection can fill the
alveolar spaces and thereby further limit diffusion of oxygen and carbon dioxide.

Therefore, smokers with COPD, who already have impaired breathing

(pulmonary function), often become much worse when there is a superimposed infection
of the lung (pneumonia).

Figure 7 is a microscopic section of a lung with pneumonia in a patient with

COPD.

Figure 7: PNEUMONIA IN COPD

 Notice that most of the alveoli are filled with inflammatory cells. Some alveoli,
however, are unaffected and empty because the involvement of this lung with pneumonia
is patchy.

What about lung cancer in smokers?

Smoke contains more than 60 carcinogens (chemicals that cause cancer) and
about 200 known toxic substances. Scientists are still learning about how carcinogens
work and why only some people who smoke get lung cancer. Genes are the hereditary
units in chromosomes and appear to have a lot to do with a person's susceptibility to
cancer.

The genes are made up of DNA (deoxyribose nucleic acid), which controls how
cells divide and reproduce (proliferate). Damage to DNA from cigarette smoke can lead
to uncontrolled cell proliferation and growth, which is what cancer is finally all about.

It is of interest that some smokers develop COPD, some develop lung cancer,
some get neither, and some get both. We really don't know the reason for these different
susceptibilities. Besides that, lung cancer from smoking can take a number of different
forms. For example, the cancer cells can resemble cells of the skin (squamous cell
carcinoma), cells of the bronchial glands (adenocarcinoma), or specialized cells of the
nervous system (neuroendocrine carcinoma).

Figure 8 shows an adenocarcinoma in a smoker's lung with severe emphysema.

Figure 8: SMOKER'S LUNG WITH EMPHYSEMA AND CANCER

 What do you think the outcome (prognosis) is for this patient with lung cancer?
Well, almost all types of lung cancer are particularly deadly. Thus, if a lung cancer is
more than an inch or so in diameter (as in this patient) or has spread outside of the lung,
fewer than 50% of affected individuals will survive another 5 years. And that is so even
with the best of therapy.

What's more, consider a cancer that is less than an inch in size (or not large
enough to be seen on a chest x-ray) and is confined to the lung. Unfortunately, even if
such a cancer is completely removed by surgery, about 25% of individuals will still die
from the cancer in less than 5 years from the time of diagnosis. The reason for this poor
outcome (prognosis) is that lung cancers tend to spread (metastasize) early in the course
of disease to other organs, most often the brain, liver, and bone.

Are any of the pulmonary consequences of smoking reversible?

First, the bad news is that emphysema is not reversible. But now, the good news!
If a person stops smoking, the inflammatory changes (chronic bronchitis) in the airways
probably will go away. Furthermore, when a person stops smoking, the risk of developing
lung cancer decreases, although it never goes back to normal. In other words, the risk of
cancer in ex-smokers is less than in smokers, but remains greater than in non-smokers.

From what do smokers die?

Remarkably, despite a wealth of information on death rates (mortality) from

cigarette smoking, little information is available on the specific causes of death in
smokers. Smokers with COPD can die from lack of oxygen (hypoxia) in the tissues of the
body. The hypoxia occurs because there is so little functioning lung left and/or the effort
of breathing is so great that affected individuals just stop breathing from exhaustion.

Other important causes of death in smokers include lung infection (pneumonia),

lung cancer, cancers of the digestive, urinary, and genital systems, and leukemia. Indeed,
because smoking can cause cancer in so many organs, 30% of all cancer deaths can be
related to cigarette smoking.

Nevertheless, because smoking is such a powerful risk factor for the development
of coronary atherosclerosis (hardening and blockage of the arteries of the heart), heart
disease is by far the most common cause of death in smokers. (See the article: Heart
Attack Pathology: Photo Essay.)

Moreover, since autopsies are done in less than 10% of patients who die in
hospitals and less than 1% of patients who die in nursing homes, we really can't prove
why most smokers die. You see, even though a clinician is often correct about the cause
of a person's death, only an autopsy can be definitive. (Please see the article on Autopsy.)
Medications

• nicotine-oral inhalation, Nicotrol

Procedures & Tests

• Chest X-ray
•
• Autopsy (Post Mortem Examination)

Presented By:

R. BALASUNDARAM

II MBBS

VMKVMC