What Is Acute Myocardial Infarction?

Highlights
1. Acute myocardial infarction is the medical name for a heart attack. Heart attacks occur
when the flow of blood to the heart becomes blocked. They can cause tissue damage and
can even be life-threatening.

What Causes Acute Myocardial Infarction?

Your heart is the main organ in your cardiovascular system, which also includes different types
of blood vessels. Some of the most important vessels are the coronary arteries. They take
oxygen-rich blood to all of the organs in your body, including your heart. When these arteries
become blocked or narrowed due to a buildup of plaque, the blood flow to your heart can
decrease significantly or stop completely. This can cause a heart attack. Several factors may lead
to a blockage in the coronary arteries.

Bad Cholesterol

Bad cholesterol, also called low-density lipoprotein (LDL), is one of the leading causes of a
blockage in the arteries. Cholesterol is a colorless substance thats found in the food you eat.
Your body also makes it naturally. Not all cholesterol is bad, but LDL cholesterol can stick to the
walls of your arteries and produce plaque. Plaque is a hard substance that blocks blood flow in
the arteries. Blood platelets, which help the blood to clot, may stick to the plaque and build up
over time.

Saturated Fats

Saturated fats may also contribute to the buildup of plaque in the coronary arteries. Saturated fats
are found mostly in meat and dairy products, including beef, butter, and cheese. These fats may
lead to an arterial blockage by increasing the amount of bad cholesterol in your blood system and
reducing the amount of good cholesterol.

Trans Fat

Another type of fat that contributes to clogged arteries is trans fat, or hydrogenated fat. Trans fat
is usually artificially produced and can be found in a variety of processed foods. Trans fat is
typically listed on food labels as hydrogenated oil or partially hydrogenated oil.

Who Is at Risk for Acute Myocardial Infarction?

Certain factors may increase your risk of having a heart attack.
High Blood Pressure

Youre at greater risk for heart attack if you have high blood pressure. Normal blood pressure is
below 120/80 mm Hg (millimeters of mercury) depending on your age. As the numbers increase,
so does your risk of developing heart problems. Having high blood pressure damages your
arteries and accelerates the buildup of plaque.

High Cholesterol Levels

Having high levels of cholesterol in your blood puts you at risk for acute myocardial infarction.
You may be able to lower your cholesterol by making changes to your diet or by taking certain
medications called statins.

High Triglyceride Levels

High triglyceride levels also increase your risk for having a heart attack. Triglycerides are a type
of fat that clog up your arteries. Triglycerides from the food you eat travel through your blood
until theyre stored in your body, typically in your fat cells. However, some triglycerides may
remain in your arteries and contribute to the buildup of plaque.

Diabetes and High Blood Sugar Levels

Diabetes is a condition that causes blood sugar, or glucose, levels to rise. High blood sugar levels
can damage blood vessels and eventually lead to coronary artery disease. This is a serious health
condition that can trigger heart attacks in some people.

Obesity

Your chances of having a heart attack are higher if youre very overweight. Obesity is associated
with various conditions that increase the risk of heart attack, including:

diabetes
high blood pressure
high cholesterol levels
high triglyceride levels

Smoking

Smoking tobacco products increases your risk for heart attack. It may also lead to other
cardiovascular conditions and diseases.

Age

The risk of having a heart attack increases with age. Men are at a higher risk of a heart attack
after age 45, and women are at a higher risk of a heart attack after age 55.
Family History

Youre more likely to have a heart attack if you have a family history of early heart disease.
Your risk is especially high if you have male family members who developed heart disease
before age 55 or if you have female family members who developed heart disease before age 65.

Other factors that can increase your risk for heart attack include:

stress
a lack of exercise
the use of certain illegal drugs, including cocaine and amphetamines
a history of preeclampsia, or high blood pressure during pregnancy

How Is Acute Myocardial Infarction Treated?

Heart attacks require immediate treatment, so most treatments begin in the emergency room. A
surgical procedure called angioplasty may be used to unblock the arteries that supply blood to
the heart. During an angioplasty, your surgeon will insert a long, thin tube called a catheter
through your artery to reach the blockage. They will then inflate a small balloon attached to the
catheter in order to reopen the artery, allowing blood flow to resume. Your surgeon may also
place a small, mesh tube called a stent at the site of the blockage. The stent can prevent the artery
from closing again.

Your doctor may also want to perform a coronary artery bypass graft (CABG) in some cases. In
this procedure, your surgeon will reroute your veins and arteries so the blood can flow around
the blockage. A CABG is sometimes done immediately after a heart attack. In most cases,
however, its performed several days after the incident so your heart has time to heal.

A number of different medications can also be used to treat a heart attack:

Blood thinners, such as aspirin, are often used to break up blood clots and improve blood
flow through narrowed arteries.
Thrombolytics are often used to dissolve clots.
Antiplatelet drugs, such as clopidogrel, can be used to prevent new clots from forming
and existing clots from growing.
Nitroglycerin can be used to widen your blood vessels.
Beta-blockers lower your blood pressure and relax your heart muscle. This can help limit
the severity of damage to your heart.
ACE inhibitors can also be used to lower blood pressure and decrease stress on the heart.
Pain relievers may be used to reduce any discomfort you may feel.

How Can Acute Myocardial Infarction Be Prevented?

There are many steps you can take to prevent a heart attack, even if youve had one before.
One way to lower your risk is to eat a heart-healthy diet. This diet should largely consist of:

whole grains
vegetables
fruits
lean protein

You should also reduce the amount of the following in your diet:

sugar
saturated fat
trans fat
cholesterol

This is especially important for people with diabetes, high blood pressure, and high cholesterol.

Exercising several times a week will also improve your cardiovascular health. If youve had a
heart attack recently, you should speak with your doctor before starting a new exercise plan.

Its also important to stop smoking if you smoke. Quitting smoking will significantly lower your
risk of a heart attack and improve both your heart and lung health. You should also avoid being
around secondhand smoke.

Pathophysiology
Acute myocardial infarction (MI) generally refers to segmental (regional) myocardial necrosis,
typically endocardium-based, secondary to occlusion of an epicardial artery. In contrast,
concentric subendocardial necrosis may result from global ischemia and reperfusion in cases of
prolonged cardiac arrest with resuscitation. Areas of myocardial infarction may be subepicardial
if there is occlusion of smaller vessels by thromboemboli originating from coronary thrombi. In
the majority of patients, there is obstructive coronary disease at angiography.

The area of infarct occurs in the distribution of the occluded vessel. Left main coronary artery
occlusion generally results in a large anterolateral infarct, whereas occlusion of the left anterior
descending coronary artery causes necrosis limited to the anterior wall. There is often extension
to the anterior portion of the ventricular septum with proximal left coronary occlusions.

In hearts with a right coronary dominance (with the right artery supplying the posterior
descending branch), a right coronary artery occlusion causes a posterior (inferior) infarct. With a
left coronary dominance (about 15% of the population), a proximal circumflex occlusion will
infarct the posterior wall; in the right dominant pattern, a proximal obtuse marginal thrombus
will cause a lateral wall infarct only, and the distal circumflex is a small vessel.

The anatomic variation due to microscopic collateral circulation, which is not evident at autopsy,
plays a large factor in the size of necrosis and distribution. Unusual patterns of supply to the
posterior wall, such as wraparound left anterior descending or posterior descending artery
supplied by the obtuse marginal artery, may also result in unexpected areas of infarct in relation
to the occluded proximal segment.

A proximal occlusion at the level of an epicardial artery results in a typical distribution that starts
at the subendocardium and progresses towards the epicardium (the so-called wavefront
phenomenon). [1] Therefore, an area of necrosis or scarring is considered to have an "ischemic
pattern" if it is largest at the endocardium, with a wedge-shaped extension up to the epicardial
surface.

Ischemic injury, however, may be located in the mid myocardium or even the subepicardium if
the level of the coronary occlusion is distal within the myocardium. Therefore, in cases of
thromboemboli from epicardial thrombi (especially plaque erosions), there may be patchy
infarction, often associated with visible thrombi within the myocardial vessels, not centered in
the endocardium but occurring anywhere in the myocardium, including midepicardial and
subepicardial locations.

Infark miokard akut (MI) umumnya mengacu pada nekrosis miokard segmentasional (regional), biasanya
berbasis endokardium, sekunder akibat oklusi arteri epikardial. Sebaliknya, nekrosis subendoksi
konsentris dapat terjadi akibat iskemia global dan reperfusi dalam kasus henti jantung berkepanjangan
dengan resusitasi. Area infark miokard mungkin subepicardial jika terjadi oklusi pembuluh darah yang
lebih kecil dengan tromboemboli yang berasal dari trombi koroner. Pada sebagian besar pasien, ada
penyakit koroner obstruktif pada angiografi.
Area infark terjadi pada distribusi bejana yang tersumbat. Oklusi arteri koroner utama pada umumnya
menghasilkan infark anterolateral besar, sedangkan oklusi arteri koroner anterior kiri mengarah
menyebabkan nekrosis terbatas pada dinding anterior. Sering terjadi perpanjangan ke bagian anterior
septum ventrikular dengan oklusi koroner kiri proksimal.
Dalam hati dengan dominasi koroner kanan (dengan arteri kanan yang memasok cabang turun
temurun), oklusi arteri koroner yang tepat menyebabkan infark posterior (inferior). Dengan dominasi
koroner kiri (sekitar 15% dari populasi), oklusi circumflex proksimal akan terjadi pada dinding posterior;
Dalam pola dominan yang tepat, trombus marjinal proksimal tumpul akan menyebabkan dinding infark
lateral saja, dan sirkumfleks distal adalah bejana kecil.
Variasi anatomis karena sirkulasi kolateral mikroskopis, yang tidak terbukti pada otopsi, memainkan
faktor besar dalam ukuran nekrosis dan distribusi. Pola pasokan yang tidak biasa ke dinding posterior,
seperti sampul kiri anterior descending atau arteri turun posterior yang dipasok oleh arteri marjinal
tumpul, juga dapat menyebabkan area infark yang tidak terduga sehubungan dengan segmen proksimal
yang tersumbat.
Oklusi proksimal pada tingkat arteri epikardial menghasilkan distribusi tipikal yang dimulai pada
subendokardium dan berlanjut menuju epikardium (fenomena wavefront yang disebut). Oleh karena itu,
area nekrosis atau jaringan parut dianggap memiliki "pola iskemik" jika terbesar pada endokardium,
dengan ekstensi berbentuk baji sampai ke permukaan epikardial.
Cedera iskemik, bagaimanapun, mungkin terletak di pertengahan miokardium atau bahkan
subepicardium jika tingkat oklusi koroner distal di dalam miokardium. Oleh karena itu, dalam kasus
tromboemboli dari trombi epikardial (terutama erosi plak), mungkin ada infark yang merata, sering
dikaitkan dengan trombi yang terlihat di dalam pembuluh miokard, yang tidak berpusat pada
endokardium namun terjadi di mana saja di miokardium, termasuk di daerah midepicardial dan
subepicardial.