How does a heart attack happen?

Let's say that you nick your arm. The platelets in your bloodstream race to your wound and then clump together and harden. A bumpy scab soon appears - from the platelets, fibrin and plasma that keep you bleeding to death.

The same thing happens inside your body when you have a heart attack. A piece of plaque, perhaps 40 years in the making, gets knocked about by materials in the bloodstream whizzing by - and the jostling causes the plaque to rupture.

The platelets rush to the rescue, piling on the damaged plaque - forming a clot. In minutes the clot does what plaque and cholesterol could not accomplish for decades: The clot blocks your artery, depriving the heart muscle of oxygen and killing heart tissue. That, in short, is how a heart attack happens.

Next, your nervous system freaks out and you begin sweating, your heart rate increases and your skin feels clammy. You begin to feel weak and nauseated. While these side effects do not seem helpful, they may actually save your life.

Research has shown that people who sweat profusely while they are having a heart attack are more likely to seek immediate treatment - which gives them a better chance of survival.

A heart attack happens when an artery in your heart becomes blocked.  This means that oxygen cannot get to your heart muscle and a part of your heart dies.  This usually happens because your arteries become blocked by fat and cholesterol.  This is called coronary artery disease.

The following describes how a heart attack occurs:

• Stage 1: Excess LDL passes through the artery. Cholesterol travels in the bloodstream inside spherical particles called lipoproteins. About two-thirds of blood cholesterol is in the form of low-density lipoprotein (LDL), often called "bad" cholesterol, because excess LDL leaves the blood and lodges in the artery walls. The higher your LDL, the greater your risk for atherosclerosis. So-called "good cholesterol," or high-density lipoprotein (HDL), carries cholesterol away from the arteries to the liver, where it's eventually eliminated from the body via the digestive tract. HDL also helps keep blood vessels dilated and fights inflammation, minimizing blood vessel injury caused by LDL.
• Stage 2: Plaque builds up and the artery narrows. LDL cholesterol lodges in the artery wall, where it triggers a harmful sequence of events. Any injury to the inner layer of cells lining the artery (caused by high blood pressure, smoking, or diabetes, for example) speeds this process. White blood cells arrive on the scene and engulf LDL cholesterol in the artery wall. These cells then enlarge and transform into fat-laden foam cells.
• Stage 3: A fibrous cap tops the plaque. As foam cells die, they release soft, fatty gruel that provokes further inflammation. Smooth muscle cells in the artery wall enlarge and multiply, forming a cap over the whole mess and adding to the bulk of the plaque.
• Stage 4: The plaque ruptures. Large plaques block blood flow more than small plaques, but they tend to be covered by thick, fibrous caps that can resist breaking apart. Smaller plaques may be too small to block blood flow, but still can be dangerous, as they are active, dynamic lesions teeming with inflammatory cells. And they sometimes have very thin, underdeveloped caps that rupture easily. About three of every four heart attacks occur because of plaque rupture.
• Stage 5: A clot blocks the artery. Once a plaque ruptures, a protein called tissue factor is released into the bloodstream, where it attracts platelets. The platelets stick to the disrupted plaque, triggering proteins in the blood to start clotting. The result is a thrombus -- a clot of red blood cells, platelets, and other material -- that completes the blockage and prevents blood from reaching the heart cells downstream. Deprived of blood and oxygen, a portion of the heart muscle dies.