Angina: Don't Ignore This Major Risk Factor for Heart Attack

You're walking up the stairs and feel some tightness in your chest.

You've just had a nice, big meal and start to feel an odd, squeezing sensation in -- this is weird -- your jaw.

You wake up in the middle of the night, and it feels like someone is sitting on your chest.

In all three scenarios, one of the first, scary thoughts is bound to be, "Am I having a heart attack?" You may be, and you should get medical attention right away.

But another possibility is that you're experiencing a bout of angina.

Heart attacks and angina have the same root cause: a pumping heart muscle that isn't getting the blood -- and therefore the oxygen -- it needs.

If it's a heart attack, the oxygen shortage causes the death of heart tissue. The medical term is myocardial infarction: The myocardium is the heart's muscle, and an infarct is an area of dead tissue resulting from low blood supply.

Angina, on the other hand, is just a symptom of the oxygen shortage -- or, to use some more medical terminology, myocardial ischemia (the term used for inadequate blood flow to any part of the body). This isn't to say that angina is unimportant: Angina is a major risk factor for having a heart attack in the future and is frequently the first sign that atherosclerosis has narrowed the coronary arteries that supply the heart. Doctors divide angina into two types, stable and unstable. Stable angina occurs when someone is active or excited. Unstable angina can occur even if someone is at rest and relaxed.

Many people have chest discomfort that feels very much like angina but turns out to be something completely unrelated to the heart. And many others with myocardial ischemia don't have classic, grip-your-chest angina or, indeed, any chest discomfort. These "anginal equivalents" include difficulty breathing (dyspnea), nausea, fatigue, sweating, and light-headedness, and they're more commonly experienced by women, people with diabetes, and older people.

FIRST DIBS

Your heart is located a little to the left of the center of your chest, behind the breast bone (sternum). In a reasonably fit adult, it beats about 70 times a minute and pumps out about 3 ounces of blood with each beat, which works out to over 2,000 gallons of blood a day.

To do all that work, the heart needs a reliable supply of blood, so it doesn't seem accidental that the blood vessels that deliver it, the right and left coronary arteries, branch off from the aorta right after it emerges from the heart's main pumping chamber, the left ventricle.

The heart may get first dibs on freshly oxygenated blood but it's not greedy: A resting heart needs about a cup of blood per minute. Blood courses through the coronary arteries in phases, with most of it surging in when the heart is relaxed, and the ventricles (there are two of them, right and left) are filling up with blood.

SUPPLY AND DEMAND

The myocardial ischemia that causes angina happens when the myocardium doesn't get the blood it needs to do the work that is being demanded of it. Exercise, anger, or fear cause a rush of the hormones epinephrine (formerly called adrenaline) and norepinephrine. The hormones make the heart pump harder and faster. To step up its game, the heart requires more energy in the form of oxygen, sugar, and fats, all of which the blood supplies. Normally, this is all remarkably well coordinated: If the heart needs more energy, signals are sent, arteries expand, and more blood comes rushing in.

But woe betide us: Our coronary arteries are prone to atherosclerosis, a process in which plaque accumulate on their smooth inner walls. Less blood can get through when that happens, so the myocardium ends up crying out for more oxygen and other provisions. Meanwhile, waste products, like lactic acid, build up because circulating blood can't sweep them away. The result is angina -- as well as those anginal equivalents.

The trouble really starts when those plaques erode or break open, spilling their cholesterol-rich insides into the bloodstream. Clots form, and what was a narrow passageway becomes a blocked one. The result: a more serious case of angina -- the unstable variety -- or, very possibly, a full-fledged heart attack.

THICK MUSCLE

Conditions other than atherosclerosis may cause myocardial ischemia. When the heart is constantly forced to work harder because of high blood pressure or diseased heart valves, the myocardium grows thicker. That has two effects. First, more muscle needs more blood, so the demand for blood increases. Second, an enlarged heart may slow down the flow of blood through the coronary arteries, so the supply of blood decreases. The reason: Once the myocardium has thickened up, the same volume of blood has to pass through many more little blood vessels. It's like what happens to your shower when someone else in the house runs the water at the same time.

Coronary arteries can also have a spasm that makes them narrower, even when there's no narrowing from atherosclerosis. A rush of epinephrine can trigger such a spasm.

SYMPTOMS: THE PRESSURE IS ON

Heaviness, pressure, and squeezing are the usual descriptions for what angina feels like. The discomfort often feels like it's coming from right behind the breastbone. It may then spread to either shoulder, the neck, the jaw -- even the teeth. The reason it seems to radiate out is that the sensory nerves for those parts of the body go to the same area of the spinal cord as the sensory nerves for the heart.

Stable and unstable

Stable angina might be better termed predictable angina because the defining characteristic is that a certain amount of exertion, or a particular level of emotion, predictably provokes an episode.

For some, stable angina means only very slight limitations on physical activity: they can't bound up the stairs like they used to, for example. But for others it can make almost any kind of physical activity trying. Stable angina may also vary quite a bit with the time of day, probably because vascular tone -- how easily arteries expand and contract -- changes.

Stable angina is usually caused by atherosclerosis that has narrowed the arteries. The symptoms are stable because atherosclerotic plaque is, too. People can live with stable angina for years. Rest, calming down, or popping a nitroglycerin tablet (more on that below) usually relieves an individual episode.

Unstable angina often comes on suddenly and seemingly out of the blue. A formerly unobtrusive atherosclerotic plaque may have ruptured, causing a complete blockage. A coronary artery may have spasmed shut. The basic symptoms are the same as stable angina, but unstable angina may occur with little if any exertion, happen more often, and be far more severe, so the uncomfortable sensations of pressure and squeezing are painful.

Stable angina is often a manage-and-monitor situation. The unstable version is a medical emergency that almost invariably involves a trip to the hospital and a battery of tests. Indeed, unstable angina is sometimes referred to as preinfarction angina to drive home the point that the risk of heart attack is high.

DIAGNOSIS

Doctors often begin by asking about risk factors for atherosclerosis (smoking, diabetes, high blood pressure, family history of heart attack). They will listen to the heart for sounds that might indicate valve problems or heart failure.

Almost every angina patient will get an electrocardiogram (ECG), which senses the electrical activity of the heart. An ECG can detect myocardial ischemia even when it isn't producing angina. It can also help a doctor discover an irregular heart that might be caused by ischemia or a myocardium thickened by chronic overwork.

Often ECGs are done when people are walking on a treadmill or riding a stationary bike. These stress tests -- banking regulators appropriated the term from medicine -- are a way to see how someone's heart responds to exertion, but under safe, controlled conditions. Ischemia that wasn't apparent on an ECG when the person was at rest may become apparent with a stress test.

Some patients go on to have echocardiograms, which use ultrasound waves to produce images of the heart. Others may get tests designed to show whether a coronary artery is blocked. High-speed CT scanners are increasingly used for this purpose, but the coronary angiogram, which involves injecting a dye into the arteries with a catheter so they show up better on an x-ray, remains the definitive exam for coronary artery blockage.

Experts have come up with elaborate "if this, then that" pathways for angina diagnosis. It's beyond the scope of this article to delineate the many branches of those flowcharts: there are just too many contingencies. Suffice it to say that if the angina is unstable, many more tests will be ordered, and that the overriding purpose of the tests is to find out if a heart attack has started -- or is about to start. In either case, immediate treatment is needed.

TREATMENT

Mild to moderate stable angina will almost always be treated with medications.

Nitroglycerin is the iconic drug, and it remains the mainstay for quick relief from an anginal episode, although there are also long-acting nitrate drugs that can be taken on a regular, preventive basis.

Nitroglycerin is a potent vasodilator: it widens and relaxes arteries and veins, although its main effect seems to be on the veins. Wider veins decrease blood return to the heart, lessening its workload. Most often taken as a pill that dissolves on the tongue, nitroglycerin starts working in just a few minutes.

People with stable angina are also usually prescribed a beta blocker. By interfering with the action of epinephrine and norepinephrine, beta blockers slow down the heart so its need for blood is a little less urgent. If beta blockers are ineffective or the side effects are intolerable, calcium channel blockers are an alternative. They dilate the coronary arteries and also reduce the heart's energy demands. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs) also make demand-side adjustments, lowering blood pressure and relaxing arteries throughout the body.

Antiplatelet therapy is another prong in the angina treatment strategy.

Platelets are cell-like particles in the blood that help it clot. Antiplatelet therapy makes platelets less "sticky," reducing the risk that the clots that cause heart attacks (and strokes) will form. Tried-and-true aspirin is the antiplatelet workhorse, but clopidogrel (Plavix) has come on strong as an alternative, especially for people who don't respond to aspirin. An increasing number of angina patients are prescribed both drugs.

Angioplasty and coronary bypass are the two main "revascularization" procedures.

Angioplasty, which involves using a catheter to open up the artery and then inserting a stent to keep it open, is less invasive than coronary bypass and is usually seen as the first choice if the atherosclerosis isn't too severe. Coronary bypass, which uses arteries from other parts of the body to reroute coronary circulation, is a major operation and, as a rule, reserved for the treatment of more complicated or widespread atherosclerosis.

But there's a lot of debate about the relative merits of angioplasty and coronary bypass. A study published in 2008 in The New England Journal of Medicine gave a slight nod to coronary bypass as the treatment for patients with multiple blockages, but it was hardly the final word. Several studies are under way that may make the choice between angioplasty and coronary bypass clearer. - Harvard Health Letter

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Health - Angina: Don't Ignore This Major Risk Factor for Heart Attack