Define myocardial infarction.
What is the pathophysiology of myocardial infarction?
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Aug 31
Myocardial infarction, commonly known as a heart attack, occurs when there is a blockage in one or more of the coronary arteries that supply blood to the heart muscle. This blockage prevents oxygen-rich blood from reaching a section of the heart, leading to damage or death of the heart muscle tissue.
The pathophysiology of myocardial infarction involves a process called atherosclerosis, where plaque builds up in the arteries over time, narrowing the passageway for blood flow. This plaque can rupture, leading to the formation of a blood clot that completely blocks the artery. Without oxygen and nutrients, the heart muscle cells begin to die, causing the symptoms of a heart attack such as chest pain, shortness of breath, and sweating.
If the blockage is not quickly treated, the affected area of the heart muscle can become permanently damaged, leading to complications such as heart failure or arrhythmias. Treatment for myocardial infarction typically involves medications to dissolve the clot, procedures such as angioplasty or bypass surgery to restore blood flow, and lifestyle changes to reduce the risk of future heart attacks.
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Google Gemini AI
Aug 31
Definition of Myocardial Infarction (MI)
Myocardial infarction, commonly known as a heart attack, is a condition characterized by the death of cardiac muscle (myocardium) tissue due to prolonged ischemia (lack of blood supply).
Pathophysiology of Myocardial Infarction
The pathophysiology of myocardial infarction involves a combination of factors:
1. Atherosclerosis and Thrombosis:
- Atherosclerosis leads to the formation of plaques within the coronary arteries, narrowing their lumen and reducing blood flow to the myocardium. - Plaque rupture or erosion can trigger the formation of a blood clot (thrombus) within the coronary artery, which can completely block blood flow.
2. Ischemia and Hypoxia:
- Obstruction of a coronary artery by a thrombus deprives the downstream myocardium of oxygen and nutrients. - This leads to ischemia, where the cells become energy-deprived and start to die.
3. Cell Death:
- Prolonged ischemia results in the death of cardiac muscle cells (myocytes), which is irreversible. - The infarcted area becomes necrotic and ceases to function.
4. Inflammatory Response:
- The dead tissue triggers an inflammatory response, with the release of cytokines and inflammatory cells. - This response aims to remove the necrotic tissue and promote healing, but it can also contribute to further damage.
5. Scar Formation:
- Over time, the infarcted area is replaced by scar tissue, which is non-functional and cannot contract. - Scar formation can weaken the heart wall and lead to complications such as heart failure.
6. Reperfusion:
- If the blockage is removed within a short period of time (typically within hours), blood flow can be restored to the ischemic area. - However, reperfusion can also lead to additional injury called "reperfusion injury," which can exacerbate damage and extend the infarct size.