The underlying cause of nearly all heart attacks is atherosclerosis, the buildup of plaques within the walls of the coronary arteries. Some plaques are unstable and can rupture. When this occurs, a cascade of fast-moving events culminates in the formation of a blood clot at the site of the plaque. Together, the plaque and blood clot can completely block the coronary artery, starving the heart tissue of oxygen and nutrients and ultimately leading to death of portions of the heart muscle.

A heart attack may seem to happen in an instant. However, the accumulation of plaque that sets the stage for this life-threatening event occurs over nearly a lifetime, beginning in childhood and taking many decades to develop. A number of factors play key roles in the stages leading up to a heart attack. They include cholesterol, triglycerides, inflammation, blood clots, and, sometimes, a spasm of a coronary artery.

Cholesterol and Heart Attack

Cholesterol is a waxy, fat-like substance present in the tissues of every human, even the healthiest among us. Cholesterol is found in all animals and thus in all foods from animal sources, including beef, poultry, fish, cheese, and dairy products.

Cholesterol is necessary for the body to function properly. It is needed to manufacture certain hormones, is an essential component of cell membranes, is required for the formation of bile salts that help absorb dietary fat from the intestine, and is a part of the outer covering around nerve fibers that enables communication between nerves. But despite cholesterol’s importance to life, you may have more of it than you need. In fact, the liver can manufacture all the cholesterol that your body requires, which means that your diet does not need to contain any cholesterol at all.

Particles called lipoproteins, formed in the liver, transport cholesterol and other fats through the bloodstream to where they are needed in the body. There are three major lipoproteins: very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL).

The liver secretes VLDL, which is converted to LDL in the bloodstream. Most cholesterol is transported on LDL and enters cells, where it’s used for essential functions. However, problems occur when high blood levels of LDL cholesterol lead to deposits of cholesterol in the artery walls, initiating the formation of plaques that narrow the arteries and slow the flow of blood. For this reason, LDL cholesterol is known as “bad” cholesterol.

HDL also carries cholesterol in the blood but, unlike LDL, it plays a positive role. It serves as a scavenger, removing cholesterol from cells and plaques and carrying it back to the liver for reprocessing into new VLDL or for excretion from the body in stool. Thus, HDL cholesterol is often referred to as “good” cholesterol, because it clears cholesterol from the arteries.

Because elevated cholesterol levels contribute to the development of atherosclerosis, reducing your cholesterol levels can help prevent heart attacks. However, when your doctor encourages you to lower your cholesterol level, he or she is talking about reducing your LDL cholesterol, not your HDL cholesterol level. In fact, the higher your HDL cholesterol, the better.

Triglycerides and Heart Attack

With all the attention on cholesterol, triglycerides are sometimes overlooked, even though they are the body’s most common type of lipid (fat) and its storage form of fat. Like cholesterol, triglycerides are present in the foods you eat and produced by your body in the liver. They are also transported in the blood by lipoproteins, mostly VLDL.

The body requires a certain level of triglycerides to function properly, but if triglyceride levels in the blood are elevated, they pose a risk of a heart attack. In addition, elevations in triglycerides are commonly associated with low HDL cholesterol levels. High triglyceride levels also alter the size, density, and composition of LDL particles, which may in turn promote atherosclerosis. No matter how elevated triglycerides increase your risk of a heart attack, a high level should motivate you to work with your doctor to lower it.

Inflammation and Heart Attack

About half of all heart attacks occur in individuals with normal or even low cholesterol levels. In fact, a small number of people who have a heart attack have no major risk factors at all—they do not smoke or have diabetes, they are not overweight, and their LDL cholesterol, HDL cholesterol, triglyceride, and blood pressure levels are normal. This fact has led researchers to look for other factors involved in the cause of heart attacks. One of these is inflammation.

Chronic inflammation within the artery walls is associated with atherosclerosis development and an increased risk of heart attacks. C-reactive protein (CRP), which is produced by the liver, is a byproduct of chronic inflammation in the body. High levels of CRP in the blood may indicate excessive inflammation within the walls of the arteries, where inflammation appears to cause plaque instability. These unstable plaques are more likely to rupture, initiating the formation of a blood clot that can trigger a heart attack.

Blood Clots and Heart Attack

When a plaque ruptures, clot-producing blood cells (called platelets) rush to the area and attach themselves to the inner lining of the artery (endothelium). As these platelets aggregate, they activate proteins that promote blood clot formation. If a blood clot completely blocks blood flow within a coronary artery, a heart attack will occur.

Spasm of a Coronary Artery and Heart Attack

In some cases, a heart attack is triggered by a severe contraction, or spasm, of a coronary artery. When this happens, the affected artery becomes narrowed and blood flow to the heart is decreased or halted. A spasm can occur in a coronary artery that shows signs of atherosclerosis or in one that appears normal. The cause of spasms is often unknown, but possible triggers include extreme emotional stress, cigarette smoking, and cocaine use.

Publication Review By: Roger S. Blumenthal, M.D. and Simeon Margolis, M.D., Ph.D.

Published: 08 Mar 2011

Last Modified: 15 Jan 2015