Wednesday, May 28, 2008

chest pain an alarming symptom

Chest pain occur due to many reason.Among them unstable angina is very alarming.
unstable angina
What is unstable angina?

Stable angina, unstable angina and myocardial infarctions ultimately are all caused by the same process – coronary artery disease.

A myocardial infarction, or heart attack, occurs when a plaque ruptures in a coronary artery, leading to the sudden formation of a blood clot superimposed on the plaque. The blood clot often totally occludes the artery, leading to death of the heart muscle being supplied by that artery. And a myocardial infarction is the death of heart muscle.

Unstable angina occurs when a blood clot forms on a plaque, suddenly increasing the degree of blockage in a coronary artery. By definition, in unstable angina the clot does not completely occlude the artery, but merely increases the degree of blockage. Because blood flow across the blockage suddenly becomes more sluggish, angina occurs even at rest.

Indeed, the blood flow can become so sluggish, and the angina can persist for so long, that some of the heart muscle cells being supplied by the partially occluded artery can actually die in patients with unstable angina. Since the death of heart cells is the definition of a myocardial infarction, once some of the cells die, the patient has “officially” had a heart attack.
Our ability to detect cell death in patients with unstable angina has greatly improved over the past few years, mainly by the development of more sensitive assays for the enzyme, troponin. Troponin is a heart muscle protein that is released into the bloodstream when heart muscle cell death occurs. As our ability to measure troponin increases, more and more patients with unstable angina are being diagnosed with heart attacks.

This is what happened in Mr. Cheney’s case. His troponin level was found to be elevated a few hours after he was admitted, and this tipped off his doctors that his coronary artery blockage was severe enough to be causing cell death – albeit a very tiny amount of cell death.

How is unstable angina diagnosed?

Anybody with a history of coronary artery disease should suspect unstable angina if their angina occurs at a markedly lower-than-normal level of exercise, if it occurs at rest, if it persists longer than usual or is more difficult to relieve with nitroglycerin, or especially if it wakes them up at night. Any of these symptoms can indicate a suddenly “narrower” coronary artery, implying that a blood clot has superimposed itself on an atherosclerotic plaque.

People without any history of coronary artery disease can also develop unstable angina, but these individuals seem to be at higher risk because they often don’t recognize the symptoms.

The classic symptoms of angina include chest pressure or pain, sometimes squeezing or “heavy” in character, often radiating to the jaw or left arm.
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Unfortunately, many patients with angina do not have classic symptoms. Their discomfort may be very mild, and may be localized to the back, abdomen, shoulders, or either or both arms. Nausea or merely a feeling of heartburn may be the only symptom. What this means, essentially, is that anyone middle aged or older, especially anyone with one or more risk factors for coronary artery disease, should be alert to symptoms that might represent angina.

Not surprisingly, most people presenting with unstable angina have a history of known coronary artery disease. This is likely because they know what these symptoms mean, and they get themselves to the hospital before cardiac damage becomes irreversible. People without known coronary artery disease, on the other hand, tend to stay at home, explaining away their disturbing symptoms as something they ate or something they lifted – and they most often either die there, or finally come to the hospital once they’ve had a completed heart attack. Unstable angina is largely a condition of experience.

How is unstable angina diagnosed?

Unstable angina is usually diagnosed by the medical history and by the ECG. Patients complaining of symptoms consistent with angina, occurring at rest or with minimal exertion, especially when they have a history of coronary artery disease, should be presumed to have unstable angina.

Especially if the patient’s pain has been relatively prolonged, the doctor checks cardiac enzymes to determine whether heart muscle damage (i.e., a heart attack) has occurred. Until a few years ago, the chief cardiac enzyme that was measured was CPK. Rises in heart –muscle-specific CPK levels were unusual with unstable angina, so most of these patients were felt not to have muscle damage. However, in the past few years, since the enzyme troponin has been commonly measured, it has become apparent that a substantial proportion of patients presenting with typical unstable angina actually do have death of cardiac cells.

How should unstable angina be treated?

Until a few years ago, unstable angina was generally considered as basically an exacerbation of typical angina – that is, the pattern of angina changed for the worse, but because (it was thought) no heart cell damage occurred, the goal of therapy was simply to “quiet down” the angina with drugs, and send the patient home. If this could be accomplished, it was assumed, the patient was no worse off than before the angina became unstable.

However, it has now become clear that many patients presenting with unstable angina have a greatly increased risk, over the next few weeks to months, of having a full-blown heart attack, and even death. This, along with a better understanding of what causes unstable angina (that is, a blood clot forming at the site of an atherosclerotic plaque that slows but does not totally occlude blood flow) has led to the notion that much more aggressive management is needed.

Two general approaches to therapy have evolved: a) treat aggressively with drugs to stabilize the ischemia, then evaluate non-invasively (the Wait and See approach,) or b) treat aggressively with drugs to stabilize the ischemia, while at the same time planning for early invasive intervention (the Aggressive approach.)

What drugs are used to “stabilize” unstable angina?
Both the Wait and See and the Aggressive approaches involve the intensive use of medication to stabilize or eliminate the cardiac ischemia. These medications are generally aimed at either protecting the jeopardized heart muscle, or preventing further progression of the blood clot.

In the former category are beta blockers and intravenous nitroglycerin, both of which are started immediately. Beta blockers reduce the effect of adrenalin on the heart muscle, and nitroglycerin reduces the cardiac workload by lowering cardiac muscle tension. Both of these effects reduce the amount of blood flow needed by the cardiac muscle. In “clot stabilizing” category are either heparin or enoxaparin (drugs that inhibit the thrombin clotting system) and aspirin and/or IIb/IIIa inhibitors (drugs that inhibit platelets).
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What is the Wait and See approach?

Using this approach, patients are carefully observed in the coronary care unit for signs of continuing ischemia. Such signs include more chest discomfort, further changes in the ECG, or continuing rises in cardiac enzymes.

If there are no further signs of ischemia, then patients are converted to an all-oral drug regimen they can continue at home. Before discharge from the hospital, a stress and thallium study is done to assess the patient’s potential for developing further ischemia. If the stress test is favorable, they are discharged to home. If, on the other hand, signs of early ischemia are seen on the treadmill test, they are sent for catheterization and angiography, in order to be evaluated for possible revascularization (angioplasty and/or stent, or bypass surgery.)

Using the Wait and See approach, approximately half the patients are discharged from the hospital without receiving catheterization.
What is the aggressive approach?
The aggressive approach begins the same way as the Wait and See approach, that is, with intensive drug therapy to stabilize the ischemia. But while this is being done, arrangements are being made to perform catheterization and angiography, with the clear goal in mind of doing angioplasty and/or stent. This procedure is performed as soon as it can be done practically.
Which approach is better?
This has been a very controversial question. Many patients do very well with the more conservative Wait and See approach to unstable angina.

But as noted, when Mr. Cheney was admitted to the hospital there was little hesitation in going quickly to an aggressive treatment regimen, and most medical commentators agreed that this was indeed the correct approach in his case.

What can we say about the appropriateness of the conservative approach vs. the aggressive approach?
Thanks to data accumulated over the past year or two, we can say the following regarding therapy given to patients with unstable angina:
In patients with ECG changes and elevated troponin levels early interventional therapy yields a significantly reduced incidence of full-blown myocardial infarction, and of death. In these patients, the Aggressive approach should now be considered as standard.
In patients with no ECG changes and with normal troponin levels, there is no evidence to date that aggressive early catheterization yields better results. In these patients, the Wait and See approach is entirely appropriate.

Summary

We now know that in most patients, unstable angina represents an acute deterioration in a previously stable atherosclerotic plaque. Indeed, the essential difference between unstable angina and a classic myocardial infarction is simply that in unstable angina, the acute blood clot only partially occludes the coronary artery instead of completely occluding it. For this reason, and because patients who are “stabilized” using medical therapy are now known to have a high incidence of having a classic heart attack in the near future, unstable angina probably is best thought of as being an “incomplete myocardial infarction.” This fact justifies an aggressive early approach in many patients with unstable angina.

At this point in time, many doctors in many emergency rooms have not yet gotten “up to speed” in the appropriate treatment of unstable angina. They still think of unstable angina in terms of being somewhat-worse-than-usual angina, instead of being a somewhat-milder-than-usual heart attack. This is a problem. Even the Wait and See approach to unstable angina is far more aggressive than the treatment used for routine angina. Patients whose doctors who do not treat unstable angina with sufficient respect are at extremely high risk for a poor outcome.

Mr. Cheney was fortunate to have up-to-date doctors. But in the end he did not receive exotic or unusually aggressive treatment. He just received excellent, but standard, medical care. There’s no reason we shouldn’t all expect exactly the same treatment.

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