Cholesterol travels in the blood plasma mainly in the form of particles consisting of thousands of cholesterol molecules and other lipids bound to a protein. One type of particle—low–density lipoproteins (LDLs), often called the “bad cholesterol”—is associated with the deposition of cholesterol in arterial plaques, growths that develop on the inner walls of arteries. Another type—high–density lipoproteins (HDLs), or “good cholesterol”—appears to reduce the deposition of cholesterol. Exercise increases HDL concentration, whereas smoking has the opposite effect on the LDL/HDL ratio.
Hypertension (high blood pressure) promotes atherosclerosis and increases the risk of heart attack and stroke. Atherosclerosis tends to raise blood pressure by narrowing the vessels and reducing their elasticity. According to one hypothesis, chronic high blood pressure damages the endothelium that lines arteries, promoting plaque formation. Fortunately, hypertension is simple to diagnose and can usually be controlled by diet, exercise, medication, or a combination of these. A diastolic pressure above 90 may be cause for concern, and living with extreme hypertension—say, 200/120—is courting disaster.
As atherosclerosis progresses, arteries become narrower, and the threat of heart attack or stroke increases. There may be warning signs. For example, if a coronary artery is only partially blocked, the person may feel occasional chest pain, a condition known as angina pectoris. The pain is most likely to appear when the heart is laboring hard as a result of physical or emotional stress, and it signals that part of the heart is not receiving enough O2. However, many people with atherosclerosis are completely unaware of their condition until catastrophe strikes.
The final blow is usually a heart attack or a stroke. A heart attack is the death of cardiac muscle tissue resulting from prolonged blockage of one or more coronary arteries, the vessels that supply oxygen–rich blood to the heart. Because they are small in diameter to begin with, the coronary arteries are particularly vulnerable. Such blockage can destroy cardiac muscle quickly, since the constantly beating heart muscle cannot survive long without oxygen. A stroke is the death of nervous tissue in the brain, usually resulting from rupture or blockage of arteries in the head.
Heart attacks and strokes frequently result from a thrombus, or blood clot, that clogs an artery. A key process leading to the clogging of an artery by a thrombus is an inflammatory response triggered by the accumulation of LDLs in the artery′s inner lining. Such an inflammation, which is analogous to the body′s response to a cut infected by bacteria, can cause plaques to rupture, releasing fragments that form a thrombus. The thrombus may originate in a coronary artery or an artery in the brain, or it may develop elsewhere in the circulatory system and reach the heart or brain via the bloodstream. The transported clot, called an embolus, is swept along until it lodges in an artery too small for the clot to pass. An embolus is more likely to become trapped in a vessel that has been narrowed by plaques. The embolus blocks blood flow, and cardiac or brain tissue downstream from the obstruction may die from O2 deprivation. If damage in the heart interrupts the conduction of electrical impulses through cardiac muscle, heart rate may change drastically or the heart may stop beating altogether. Still, the victim may survive if a heartbeat is restored by cardiopulmonary resuscitation (CPR) or some other emergency procedure within a few minutes of the attack. The effects of a stroke and the individual′s chance of survival depend on the extent and location of the damaged brain tissue.