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Acute Myocardial Infarction and Its Causes

그레이스성형외과의원 · 아이홀지방이식·가슴성형 읽어주는 최문섭 원장 · February 25, 2019

Acute Myocardial Infarction and Its Causes The heart begins beating when we are still in our mother’s womb and works continuously for our entire lives without a single moment of re...

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This page is an English translation of a Korean Naver Blog archive entry. For exact wording and source context, verify against the Korean archive original and the original Naver post.

Clinic: 그레이스성형외과의원

Original post date: February 25, 2019

Translated at: April 24, 2026 at 4:39 AM

Medical note: This translation does not guarantee medical accuracy or suitability for treatment decisions.

Acute Myocardial Infarction and Its Causes image 1

The heart begins beating when we are still in our mother’s womb and works continuously for our entire lives without a single moment of rest. An adult heart is a 250-300 g muscular pouch that pumps about 5 liters of fresh blood throughout the body at a rate of about 70 beats per minute—about 30 million liters a year, and about 1.5 billion liters over 60 years. The heart muscle, which works this hard without stopping, must receive enough energy and oxygen, and the coronary arteries play that role.

Acute myocardial infarction is a disease in which the coronary arteries that supply blood to the heart muscle suddenly become blocked for various reasons, causing necrosis in the myocardium.

Acute myocardial infarction is not only one of the most common causes of hospital admission in Korea as well as in developed countries, but also one of the most common causes of death. The initial mortality rate of myocardial infarction reaches about 30%, and more than 50% of fatal cases are known to die before even reaching the hospital. Medications and treatment methods for acute myocardial infarction have advanced rapidly and have reduced the mortality rate by more than 30%, but it remains a frightening disease in which 1 out of every 25 patients dies within one year after discharge.

Causes and Risk Factors

  1. Causes
  1. Plaque rupture and thrombus formation

The most fundamental cause of acute myocardial infarction is atherosclerosis, and the most common mechanism is that the coronary artery becomes completely blocked by a thrombus (blood clot) formed when an atherosclerotic plaque in a coronary artery ruptures or cracks, leading to necrosis of the myocardium.

  1. Others

Coronary artery spasm, coronary artery embolism, and coronary artery dissection (tear) can also cause acute myocardial infarction.

  1. Atherosclerosis

Atherosclerosis is a vascular disease in which cholesterol is deposited in the walls of blood vessels, narrowing the inside diameter (lumen) of the vessels and causing impaired blood flow through the narrowed vessels. When atherosclerosis develops in the coronary arteries that supply blood to the heart muscle and gradually becomes more severe, the blood vessels narrow and cause blood flow obstruction, leading to angina; if they become completely blocked, myocardial infarction occurs.

  1. Stages of atherosclerosis

In the progression of atherosclerosis, the first stage is called an early lesion, in which cholesterol is deposited in a normal blood vessel and the intima becomes thickened. As it progresses further, lipids form foam within macrophages, and the intima accumulates and becomes significantly thickened; this stage is called a fatty streak lesion.

A more advanced stage of atherosclerosis is called a fibrous atheroma. At this stage, lipids gather and accumulate in the center of the deposited lesion, forming a large lipid core, and vascular smooth muscle cells proliferate around the lipids to form a fibrous cap; this is called a fibrous atheroma.

After that, highly complex lesion features appear, and the fibrous cap cracks or ruptures, forming a thrombus within the vessel. If the condition progresses severely, complete occlusion leads to acute myocardial infarction, and if the vessel is partially blocked, it is called unstable angina.

At this point, if treatment is performed to remove the thrombus and heal the fibrous cap, the lesion enters the recovery stage and becomes a fibrous atheroma again.

  1. Risk factors for atherosclerosis

(1) Non-modifiable risk factors

· Age: men ≥45 years, women ≥55 years

· Sex: men > women

· Race: white > yellow race

· Family history: family history of premature heart disease (first-degree relatives, men <55 years, women <65 years)

(2) Modifiable risk factors

· Smoking · Hyperlipidemia: high LDL cholesterol, low HDL cholesterol · Hypertension · Diabetes · Obesity

· Lack of exercise · Gout · Menopause and oral contraceptives · Personality type (type A) · Alcohol consumption · Others: patients with chronic renal failure, etc.

In addition to the risk factors described above, many factors that we do not know are thought to be involved in the development of atherosclerosis and myocardial infarction. However, among the risk factors we do know, even the modifiable ones—especially smoking, hyperlipidemia, hypertension, and diabetes—must be thoroughly managed as major risk factors, because preventing the occurrence of myocardial infarction in advance is of utmost importance.

  1. Progression of myocardial necrosis after coronary artery occlusion

When atherosclerosis becomes very severe and the coronary artery becomes occluded, myocardial infarction occurs and necrosis progresses. When the coronary artery is blocked, ischemia first occurs due to lack of blood, and within 2 to 3 hours after that, necrosis progresses from the center of the subendocardium toward the outer layers. Once 24 hours have passed after coronary artery occlusion, the entire myocardium progresses to necrosis and enters an irreversible state.

If treatment is provided within 20 minutes after the onset of myocardial infarction and blood flow is restored, it will not progress to myocardial necrosis, so the duration of coronary artery occlusion and the progression of myocardial necrosis can be said to correspond. Once myocardial infarction occurs due to atherosclerosis, restoring blood flow as quickly as possible is what prevents the least amount of damage.

  1. Left ventricular remodeling after acute myocardial infarction

If acute myocardial infarction has already occurred, even if the blood vessel is reopened, the size, shape, and thickness of the ventricle change, creating a risk of future complications. In particular, the size of the myocardial infarction, pressure, and the location and extent of the blockage have a major impact on later treatment and care.

An apartment can be improved through remodeling, but our heart, in the shape inherited from our mother, is best able to pump blood throughout the body effectively as it is. Therefore, after myocardial infarction, minimizing left ventricular remodeling through rapid reperfusion therapy and active drug treatment is the most important way to preserve heart function and prevent complications caused by myocardial infarction.

So far, I have explained acute myocardial infarction and its causes.

In the next part, we will look at the symptoms and complications of acute myocardial infarction.

Source: Korea Disease Control and Prevention Agency, National Health Information Portal

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