Unstable Angina (Part I)
From Richard N. Fogoros, M.D.,
In this article we will review unstable angina – what causes it, how it differs from a classic heart attack, how it is diagnosed, and how it ought to be treated.
As recently as the mid-1990s, it is likely that a heart patient would have been sent home from most emergency rooms with the diagnosis of a “simple angina,” or even “chest pain of non-cardiac origin.” And until a few months ago, even with the correct diagnosis, it is likely he would have been managed much more conservatively, with outpatient drug therapy only.
What has changed? Two things: our understanding of the cause of unstable angina, and our understanding of the best way of diagnosing and treating it.
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.
In this article we will review unstable angina – what causes it, how it differs from a classic heart attack, how it is diagnosed, and how it ought to be treated.
As recently as the mid-1990s, it is likely that a heart patient would have been sent home from most emergency rooms with the diagnosis of a “simple angina,” or even “chest pain of non-cardiac origin.” And until a few months ago, even with the correct diagnosis, it is likely he would have been managed much more conservatively, with outpatient drug therapy only.
What has changed? Two things: our understanding of the cause of unstable angina, and our understanding of the best way of diagnosing and treating it.
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.
posted by Heart Scan @ 1:12 AM
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