What is Heart Disease?
When people speak of heart disease, they usually mean the condition more accurately described as coronary artery disease — a narrowing of the coronary arteries that reduces blood flow to the heart muscle. Chest pain (angina) and heart attack (myocardial infarction) are the most common manifestations. In the United States, coronary artery disease is by far the most prevalent type of life-threatening cardiovascular disease. It’s also the most preventable.
The coronary arteries play a vital role by supplying the heart with oxygen-rich blood. The heart muscle depends on two main arteries, the right and left coronary arteries, for its entire supply of blood and oxygen. Like the branches of a tree, each main artery divides into progressively smaller channels that carry blood to the heart muscle cells (see Figure 1). Either of these arteries or any of their branches can be narrowed by a buildup of fatty plaque, known medically as atherosclerosis. This term combines two Greek words, athere (porridge) and sclerosis (hardening). The name is accurate: in atherosclerosis, the artery walls become filled with soft, mushy deposits that eventually make the artery hard, stiff, and narrow. Inflammation — the process by which the body responds to injury or infection — triggers a release of chemicals and cells thought to contribute to the development and rupture of plaques.
Figure 1: Supplying the heart
It’s often said that the heart is the size of your fist, but it’s actually closer to the size of two fists. The aorta, the body’s largest blood vessel, is almost the diameter of a garden hose. A network of coronary arteries, each about as thick as a strand of spaghetti, emerges from the aorta. These arteries branch into smaller and smaller vessels that eventually penetrate the heart muscle, supplying it with oxygen and nutrients. This illustration shows the main coronary arteries (for simplicity’s sake, the veins are not pictured). The lighter-shaded vessels represent those that wrap around the back of the heart.
These deposits can restrict blood flow, resulting in ischemia, or oxygen deprivation. Ischemia can impair the heart’s ability to pump blood, interrupt its normal pumping rhythm, or even cause a heart attack. A partial or temporary interruption in blood supply, causing mild ischemia, injures the heart muscle and can produce angina. A heart attack results from complete or prolonged interruption of blood flow from plaque — or more precisely, from the interplay between plaque rupture, cholesterol buildup, blood clotting, and inflammation, which causes severe or prolonged ischemia that leads to the death of heart muscle cells (see Figure 2).
Figure 2: From healthy artery to heart attack
Heart attacks aren’t just the result of a buildup of fatty plaque in the arteries. Inflammation triggered by damage or stress in the inner lining of an artery sets off the steady growth of atherosclerotic plaque, which can suddenly erupt, causing a heart attack.
Stage 1: Excess LDL passes through the artery
Cholesterol travels in the bloodstream within 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.
Coronary artery disease can also independently lead to heart failure, abnormal heart rhythms (arrhythmias), or cardiac arrest. Heart failure occurs when the heart can’t pump sufficient blood, producing shortness of breath, fatigue, and fluid accumulation. Arrhythmias can cause palpitations, shortness of breath, and fainting. Cardiac arrest — when the heart suddenly stops, usually due to an electrical disturbance in the heart — suspends both consciousness and breathing and is fatal without immediate, appropriate medical care.