Unstable Angina (Part II)
From Richard N. Fogoros, M.D.
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. 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 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.)
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. 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 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.)
posted by Heart Scan @ 12:58 AM
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