The human heart is a wonderful pump, just a little smaller than a man's clinched fist, that moves about 4,000 gallons of blood per day through your body each day without a rest. A healthy heart will beat more than 2.5 billion times in the average person's lifetime -- unless something goes wrong.
And things go wrong frequently: More than one third of American men and ten percent of American woman can expect to have cardiovascular disease by the age of 60.
What most often goes wrong appears, at first glance, to be a plumbing problem: clogged coronary arteries are unable to supply blood to the heart itself. On a deeper level, the problem is biochemical: the clogs come from an excess of cholesterol.
But on the most basic level, it's usually a lifestyle problem. What we eat and drink, what we choose not to inhale (like tobacco), how we deal with stress and how we exercise all affect the cholesterol which affects the coronary plumbing.
As you'll learn in the next few chapters, the medical treatments that deal with heart disease like a plumbing job for the Roto- Rooter truck are usually doomed to failure without lifestyle changes. Prevention is so much more important than intervention because damaged heart muscle never heals completely. Portions of heart muscles that die form scar tissue that is incapable of contributing to the heart's pumping. Once gone, gone forever.
Most heart problems are caused by ischemia, insufficient oxygen to the heart, and known as "Ischemic Heart Disease (IHD)" to physicians and researchers. IHD begins when deposits of cholesterol ("plaque") build up in one, or all, of the three coronary arteries that deliver blood to the heart muscle, the myocardium. This narrowing of the arteries is known as atherosclerosis or arteriosclerosis.
If the coronary artery blockage is not complete, but is severe enough to cause pain during stress or exercise, the IHD is known as angina pectoris, literally "strangling" or "choking in the chest." If the angina episode does not last for very long, the heart muscle may not be damaged. However, if it continues, portions of the muscle could die.
Angina is treated with vasodilators, drugs which relax the muscle layer of arteries thereby increasing their diameter and blood flow. The most common vasodilator is nitroglycerin, taken orally or by transdermal skin patch.
Alcohol is also a vasodilator. This property may contribute to the lower coronary death rate among moderate drinkers, although further research is needed.
It's also hypothesized that moderate alcohol consumption may provide some protection against a more dangerous arterial condition which is closely related to angina: spasms.
The coronary artery, like all arteries, has a muscle layer that can contract or relax. This allows your body to regulate blood flow during times of exertion, sending more blood to the working muscles and restricting it to parts of the body (like the digestive organs) which need it less at that time. The muscle walls also affect blood pressure. In fact, without muscle tension in the arteries, your blood pressure would drop to zero and you would die. (This is what happens in anaphylactic shock when sensitive people are exposed to bee stings, penicillin or other allergens).
The down side to coronary artery muscles is that they can twitch or spasm just like other muscles. If a healthy artery spasms, little harm may occur. But when they spasm along a section of coronary artery already narrowed by cholesterol plaque, the result could be a complete -- or nearly complete -- cutoff of the blood supply. If the spasms last too long, the heart muscle could be damaged.
More serious still is an acute myocardial infarction (MI), the classic heart attack which stops its victims in their tracks. The MI is a complete blocking of the coronary artery by a blood clot.
Usually the clot lodges at the point of an existing build-up of cholesterol which has already narrowed the artery. The clot is also called a thrombus which is why this kind of heart attack is sometimes called a coronary thrombosis.
Sometimes the clot and blockage are caused by part of the cholesterol plaque coming loose from the artery wall and causing the blockage itself. Medical researchers think the process is usually far more complex, involving a combination of other factors.
The process may be caused partly by the tendency of clots to form near artery blockages. This may happen because the blood -- which usually flows smoothly -- becomes turbulent near the cholesterol build-ups. This turbulence (like the eddies that swirl around an obstruction in a stream) may cause damage, to blood platelets or perhaps to the artery walls, which can accelerate clotting. And just as sand and silt tend to accumulate downstream of a river's obstruction, the turbulence may also create the physical condition for a clot to form and grow.
Platelets are very small cells in the blood, smaller than a red blood cell, which play many key roles in the body, including one in the clotting process. When you receive a cut, many life-saving biochemical processes swing into action to keep you from losing blood. Among these processes, platelets become more "sticky" and begin to clump together to staunch the blood flow. At the same time, a long, stringy protein called fibrinogen is produced, tangling itself through the clumping platelets, like reinforcing rods in a concrete dam, making the clot hold together better.
Two other key contributors to fast and efficient clotting are adrenalin and noradrenalin, hormones produced in times of stress. These hormones evolved as life-saving mechanisms because a person wounded by a saber-tooth tiger or by another person in battle would bleed less and be more likely to survive. These hormones also act as vasoconstrictors which narrow the arteries, again preserving blood if wounded.
These defense mechanisms become life-threatening when they happen at the wrong place and time, such as in your coronary arteries.
The actual process may involve turbulence which could help to dislodge part of the plaque; then, the area from which the plaque is dislodged releases chemical messengers that initiate the clotting process. A clot forms completing the blockage started by the dislodged plaque, and a full-blown myocardial infarction puts the victim just heartbeats away from death and disability.
Research has confirmed that both aspirin and moderate alcohol consumption decrease the stickiness of platelets and their tendency to clot. There are also indications that moderate alcohol consumption may decrease the production of fibrinogen and help dissolve clots once they have formed, a process
known as fibrinolysis.
While all this tells us what goes wrong in the plumbing, and goes some way towards explaining "Why do heart attacks happen?" it just shoves the cause down the line to another question: "Why does cholesterol block arteries?" Read on.