Myocardial infarction

Acute myocardial infarction (AMI or MI), commonly known as a heart attack, is a serious, sudden heart condition usually characterized by varying degrees of chest pain or discomfort, weakness, sweating, nausea, vomiting, and arrhythmias, sometimes causing loss of consciousness. It occurs when a part of the heart muscle is injured, and this part may die because of sudden total interruption of blood flow to the area. It is often a life-threatening medical emergency which demands both immediate attention and activation of the emergency medical services.

Pathophysiology

Ischemia and infarction

The underlying mechanism of a heart attack is the destruction of heart muscle cells due to a lack of oxygen. If these cells are not supplied with sufficient oxygen by the coronary arteries to meet their metabolic demands, they die by a process called infarction.

Related Topics:
Oxygen - Coronary arteries - Metabolic - Infarction

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The decrease in blood supply has the following consequences:

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• Heart muscle which has lost blood flow long enough, e.g. 10-15 minutes, ends up dying (necrosis) and does not grow back. Thus the heart ends up permanently weaker as a pump for the remainder of the individual's life;
• Injured, but still living, heart muscle conducts the electrical impulses which initiate each heart beat much more slowly. The speed can end up so slow that the spreading impulse is preserved long enough for the uninjured muscle to complete contraction; now the slowed electrical signal, still traveling within the injured area, can re-enter and trigger the healthy muscle (termed re-entry) to beat again too soon for the heart to relax long enough and receive any blood return from the veins. If this re-entry process results in sustained heart rates in the >200 to over 400 beats per minute range called ventricular tachycardia (V-Tach) or ventricular fibrillation (V-Fib), then the rapid heart rate effectively stops heart pumping. Heart output and blood pressure falls to near zero and the individual quickly dies. This is the most common mechanism of the sudden death that can result from a myocardial infarction. The cardiac defibrillator device was specifically designed for stopping these too rapid heart rates. If used properly, it stimulates the entire heart muscle to contract all at once, in synchrony; hopefully stopping continuation of the re-entry process. If used within one minute of onset of V-Tach or V-Fib, the defibrillator has a high success rate in stopping these often fatal arrhythmias allowing a functional heart rhythm to return.

Histopathological examination of the heart shows that there is a circumscribed area of ischemic necrosis (coagulative necrosis). In the first 12-48 hours, myocardial fibers are still well delineated, with intense eosinophilic (pink) cytoplasm, but lose their transversal striations and the nucleus. The interstitial space may be infiltrated with red blood cells.

Related Topics:
Histopathological - Eosinophilic - Nucleus

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When the healing has commenced (e.g. after 5 -10 days) the area of coagulative ischemic necrosis shows myocardial fibers with preservation of their contour, but the cytoplasm is intensely eosinophilic and transversal striations and nuclei are completely lost. The interstitium of the infarcted area is initially infiltrated with neutrophils, then with lymphocytes and macrophages, in order to phagocytose the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue, which will replace the infarct with a fibrous (collagenous) scar.

Related Topics:
Neutrophil - Lymphocyte - Macrophage

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Atherosclerosis

The most common cause of heart attack by far is atherosclerosis, a gradual buildup of cholesterol and fibrous tissue in plaques in the arterial wall, typically over decades. However plaques can become unstable, rupture, and additionally promote a thrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium).

Related Topics:
Atherosclerosis - Plaque - Arterial - Thrombus - Myocardium

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All risk factors for atherosclerosis are also (modifiable) risk factors for ischemic heart disease: older age, smoking, hypercholesterolemia (more accurately hyperlipoproteinemia, especially high low density lipoprotein (LDL) and low high density lipoprotein (HDL), diabetes (with or without insulin resistance) and obesity.

Related Topics:
Smoking - Hypercholesterolemia - Hyperlipoproteinemia - Low density lipoprotein - High density lipoprotein - Diabetes - Insulin resistance - Obesity

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The blood flow problem is nearly always a result of exposure of atheroma tissue within the wall of the artery to the blood flow inside the artery, atheroma being the primary lesion of the atherosclerotic process. The many blood stream column irregularities, visible in the single frame angiogram image to the right, reflects artery lumen changes as a result of decades of advancing atherosclerosis.

Related Topics:
Atheroma - Artery - Angiogram - Lumen

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Heart attacks rates are higher in association with intense exertion, be it stress or physical exertion, especially if the exertion is unusually more intense than the individual usually performs. Quantitatively, the period of intense exercise and subsequent recovery is associated with about a 6-fold higher myocardial infarction rate (compared with other more relaxed times frames) for people who are physically very fit. For those in poor physical condition, the rate differential is over 35-fold higher. One observed mechanism for this phenomenon is the increased arterial pulse pressure stretching and relaxation of arteries with each heart beat which, as has been observed with IVUS, increases mechanical "shear stress" on atheromas and the likelihood of plaque rupture.

Related Topics:
Stress - IVUS - Atheroma

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Increased spasm/contraction of coronary arteries in association with cocaine abuse can also precipitate myocardial infarction.

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