William E. Golden, MD

Over 8 million people seek emergency department (ED) attention every year for assessment of chest pain. The American Heart Association recently issued a scientific statement to give guidance on rapid, effective approaches to the assessment of such patients.

Conclusions

Most patients who present with chest pain to ED settings do not have acute ischemia: Less than 5% have an ST segment elevation myocardial infarction, and up to 25% can have a non–ST segment elevation event. Up to 7% of patients with chest pain after cocaine exposure have infarctions.

At the same time, up to 2% of patients with acute coronary syndromes (ACS) are inadvertently discharged from EDs with potentially twice the risk-adjusted mortality of patients admitted for management of acute ischemia.

Symptom-limited treadmill stress testing is felt to be safe at 8-12 hours for low- and intermediate-risk chest pain patients who have normal baseline EKGs and capacity to exercise, and are not taking digoxin.

Ischemia induced during stress protocols for echocardiography or myocardial perfusion imaging (MPI) indicates impaired coronary perfusion in the face of increased oxygen demand. MPI also can be used to detect rest ischemia indicating impaired regional myocardial perfusion, a hallmark of the ACS.

Both stress echocardiography (sensitivity: 86%; specificity: 81%) and MPI (87%; 73%) are more effective in detecting coronary artery disease than exercise treadmill testing (70%; 75%). However, while MPI is an effective test, it is associated with considerable radiation exposure.

Use of pharmacologic agents can be substituted for exercise in patients unable to exercise according to modified Bruce protocols. Dobutamine increases myocardial demand. Vasodilators such as adenosine, dipyridamole, and regadenoson simulate exercise stress conditions by dilating coronary arteries and creating maldistribution of myocardial perfusion.

A major clinical trial is ongoing to assess the value of CT coronary arteriography, which has a very high negative predictive value, in assessing chest pain syndrome patients in the ED.

As many as 20%-25% of patients with negative chest pain unit evaluations present again for similar evaluations.

Implementation

The goal of ED evaluation of chest pain is the exclusion of ACS and other urgent conditions as appropriate diagnoses. Assessment of the presence of coronary artery disease is best handled in other settings. Experience with chest pain units and accelerated diagnostic protocols have provided effective evidence-based strategies for triaging these patients.

While classic anginal symptoms can aid in the evaluation of acute chest pain, ACS patients can present with atypical or confusing complaints and require care assessment by evaluating health professionals. Nausea and diaphoresis associated with severe chest pain are highly associated with acute ischemia, but elderly patients may have predominantly respiratory complaints.

Patients with sudden-onset, severe chest pain should be considered for pneumothorax, pulmonary embolus, or aortic dissection.

Patients at low risk for myocardial infarction (less than 5%) should be identified by current symptoms, past history, and a new electrocardiogram. These patients have normal EKGs, normal initial cardiac injury lab findings, and stable hemodynamics and cardiac rhythm. The Thrombolysis in Myocardial Infarction (TIMI) risk score is widely used, but has not performed consistently for low-risk populations.

Patients with acute ST segment elevation frequently have near-total or total coronary occlusion and are candidates for reperfusion interventions.

Patients who present during the first 6 hours of chest pain onset and who have negative cardiac markers should be retested after 8 hours to validate the negative results. Newer assays of troponin have good sensitivity and specificity, and are preferred over creatine kinase MB and myoglobin measurement. Laboratories should return results within an hour of specimen sampling or else point-of-service assessment should be considered. B-type natriuretic peptide, while useful for congestive heart failure evaluation, does not offer value in the assessment of acute ischemia.

For patients with indeterminant initial presentations, chest pain protocols can help structure observation. Exercise stress testing is optional in patients with cocaine-related chest pain after a negative period of observation and testing.

Patients who have no additional chest discomfort, undiagnostic initial and follow-up EKGs, and negative injury lab values can be discharged without stress testing for outpatient follow-up investigations.

Repeat treadmill stress testing has limited value in patients with a previous negative evaluation for chest pain in an emergency setting. These patients may eventually require coronary arteriography as negative cardiac caths, in comparison to noninvasive evaluation, reduce repeat ED chest pain evaluations by more than 50%.

Reference

Amsterdam EA et al. Testing of Low-Risk Patients Presenting to the Emergency Department with Chest Pain (Circulation 2010;122:756-76).

This column, "The Effective Physician," appears regularly in Internal Medicine News, an Elsevier publication. Dr. Golden is professor of medicine and public health and Dr. Hopkins is program director for the internal medicine/pediatrics combined residency program at the University of Arkansas, Little Rock.

Over 8 million people seek emergency department (ED) attention every year for assessment of chest pain. The American Heart Association recently issued a scientific statement to give guidance on rapid, effective approaches to the assessment of such patients.

Conclusions

Most patients who present with chest pain to ED settings do not have acute ischemia: Less than 5% have an ST segment elevation myocardial infarction, and up to 25% can have a non–ST segment elevation event. Up to 7% of patients with chest pain after cocaine exposure have infarctions.

At the same time, up to 2% of patients with acute coronary syndromes (ACS) are inadvertently discharged from EDs with potentially twice the risk-adjusted mortality of patients admitted for management of acute ischemia.

Symptom-limited treadmill stress testing is felt to be safe at 8-12 hours for low- and intermediate-risk chest pain patients who have normal baseline EKGs and capacity to exercise, and are not taking digoxin.

Ischemia induced during stress protocols for echocardiography or myocardial perfusion imaging (MPI) indicates impaired coronary perfusion in the face of increased oxygen demand. MPI also can be used to detect rest ischemia indicating impaired regional myocardial perfusion, a hallmark of the ACS.

Both stress echocardiography (sensitivity: 86%; specificity: 81%) and MPI (87%; 73%) are more effective in detecting coronary artery disease than exercise treadmill testing (70%; 75%). However, while MPI is an effective test, it is associated with considerable radiation exposure.

Use of pharmacologic agents can be substituted for exercise in patients unable to exercise according to modified Bruce protocols. Dobutamine increases myocardial demand. Vasodilators such as adenosine, dipyridamole, and regadenoson simulate exercise stress conditions by dilating coronary arteries and creating maldistribution of myocardial perfusion.

A major clinical trial is ongoing to assess the value of CT coronary arteriography, which has a very high negative predictive value, in assessing chest pain syndrome patients in the ED.

As many as 20%-25% of patients with negative chest pain unit evaluations present again for similar evaluations.

Implementation

The goal of ED evaluation of chest pain is the exclusion of ACS and other urgent conditions as appropriate diagnoses. Assessment of the presence of coronary artery disease is best handled in other settings. Experience with chest pain units and accelerated diagnostic protocols have provided effective evidence-based strategies for triaging these patients.

While classic anginal symptoms can aid in the evaluation of acute chest pain, ACS patients can present with atypical or confusing complaints and require care assessment by evaluating health professionals. Nausea and diaphoresis associated with severe chest pain are highly associated with acute ischemia, but elderly patients may have predominantly respiratory complaints.

Patients with sudden-onset, severe chest pain should be considered for pneumothorax, pulmonary embolus, or aortic dissection.

Patients at low risk for myocardial infarction (less than 5%) should be identified by current symptoms, past history, and a new electrocardiogram. These patients have normal EKGs, normal initial cardiac injury lab findings, and stable hemodynamics and cardiac rhythm. The Thrombolysis in Myocardial Infarction (TIMI) risk score is widely used, but has not performed consistently for low-risk populations.

Patients with acute ST segment elevation frequently have near-total or total coronary occlusion and are candidates for reperfusion interventions.

Patients who present during the first 6 hours of chest pain onset and who have negative cardiac markers should be retested after 8 hours to validate the negative results. Newer assays of troponin have good sensitivity and specificity, and are preferred over creatine kinase MB and myoglobin measurement. Laboratories should return results within an hour of specimen sampling or else point-of-service assessment should be considered. B-type natriuretic peptide, while useful for congestive heart failure evaluation, does not offer value in the assessment of acute ischemia.

For patients with indeterminant initial presentations, chest pain protocols can help structure observation. Exercise stress testing is optional in patients with cocaine-related chest pain after a negative period of observation and testing.

Patients who have no additional chest discomfort, undiagnostic initial and follow-up EKGs, and negative injury lab values can be discharged without stress testing for outpatient follow-up investigations.

Repeat treadmill stress testing has limited value in patients with a previous negative evaluation for chest pain in an emergency setting. These patients may eventually require coronary arteriography as negative cardiac caths, in comparison to noninvasive evaluation, reduce repeat ED chest pain evaluations by more than 50%.

Reference

Amsterdam EA et al. Testing of Low-Risk Patients Presenting to the Emergency Department with Chest Pain (Circulation 2010;122:756-76).

This column, "The Effective Physician," appears regularly in Internal Medicine News, an Elsevier publication. Dr. Golden is professor of medicine and public health and Dr. Hopkins is program director for the internal medicine/pediatrics combined residency program at the University of Arkansas, Little Rock.

Over 8 million people seek emergency department (ED) attention every year for assessment of chest pain. The American Heart Association recently issued a scientific statement to give guidance on rapid, effective approaches to the assessment of such patients.

Conclusions

Most patients who present with chest pain to ED settings do not have acute ischemia: Less than 5% have an ST segment elevation myocardial infarction, and up to 25% can have a non–ST segment elevation event. Up to 7% of patients with chest pain after cocaine exposure have infarctions.

At the same time, up to 2% of patients with acute coronary syndromes (ACS) are inadvertently discharged from EDs with potentially twice the risk-adjusted mortality of patients admitted for management of acute ischemia.

Symptom-limited treadmill stress testing is felt to be safe at 8-12 hours for low- and intermediate-risk chest pain patients who have normal baseline EKGs and capacity to exercise, and are not taking digoxin.

Ischemia induced during stress protocols for echocardiography or myocardial perfusion imaging (MPI) indicates impaired coronary perfusion in the face of increased oxygen demand. MPI also can be used to detect rest ischemia indicating impaired regional myocardial perfusion, a hallmark of the ACS.

Both stress echocardiography (sensitivity: 86%; specificity: 81%) and MPI (87%; 73%) are more effective in detecting coronary artery disease than exercise treadmill testing (70%; 75%). However, while MPI is an effective test, it is associated with considerable radiation exposure.

Use of pharmacologic agents can be substituted for exercise in patients unable to exercise according to modified Bruce protocols. Dobutamine increases myocardial demand. Vasodilators such as adenosine, dipyridamole, and regadenoson simulate exercise stress conditions by dilating coronary arteries and creating maldistribution of myocardial perfusion.

A major clinical trial is ongoing to assess the value of CT coronary arteriography, which has a very high negative predictive value, in assessing chest pain syndrome patients in the ED.

As many as 20%-25% of patients with negative chest pain unit evaluations present again for similar evaluations.

Implementation

The goal of ED evaluation of chest pain is the exclusion of ACS and other urgent conditions as appropriate diagnoses. Assessment of the presence of coronary artery disease is best handled in other settings. Experience with chest pain units and accelerated diagnostic protocols have provided effective evidence-based strategies for triaging these patients.

While classic anginal symptoms can aid in the evaluation of acute chest pain, ACS patients can present with atypical or confusing complaints and require care assessment by evaluating health professionals. Nausea and diaphoresis associated with severe chest pain are highly associated with acute ischemia, but elderly patients may have predominantly respiratory complaints.

Patients with sudden-onset, severe chest pain should be considered for pneumothorax, pulmonary embolus, or aortic dissection.

Patients at low risk for myocardial infarction (less than 5%) should be identified by current symptoms, past history, and a new electrocardiogram. These patients have normal EKGs, normal initial cardiac injury lab findings, and stable hemodynamics and cardiac rhythm. The Thrombolysis in Myocardial Infarction (TIMI) risk score is widely used, but has not performed consistently for low-risk populations.

Patients with acute ST segment elevation frequently have near-total or total coronary occlusion and are candidates for reperfusion interventions.

Patients who present during the first 6 hours of chest pain onset and who have negative cardiac markers should be retested after 8 hours to validate the negative results. Newer assays of troponin have good sensitivity and specificity, and are preferred over creatine kinase MB and myoglobin measurement. Laboratories should return results within an hour of specimen sampling or else point-of-service assessment should be considered. B-type natriuretic peptide, while useful for congestive heart failure evaluation, does not offer value in the assessment of acute ischemia.

For patients with indeterminant initial presentations, chest pain protocols can help structure observation. Exercise stress testing is optional in patients with cocaine-related chest pain after a negative period of observation and testing.

Patients who have no additional chest discomfort, undiagnostic initial and follow-up EKGs, and negative injury lab values can be discharged without stress testing for outpatient follow-up investigations.

Repeat treadmill stress testing has limited value in patients with a previous negative evaluation for chest pain in an emergency setting. These patients may eventually require coronary arteriography as negative cardiac caths, in comparison to noninvasive evaluation, reduce repeat ED chest pain evaluations by more than 50%.

Reference

Amsterdam EA et al. Testing of Low-Risk Patients Presenting to the Emergency Department with Chest Pain (Circulation 2010;122:756-76).

This column, "The Effective Physician," appears regularly in Internal Medicine News, an Elsevier publication. Dr. Golden is professor of medicine and public health and Dr. Hopkins is program director for the internal medicine/pediatrics combined residency program at the University of Arkansas, Little Rock.

Over 8 million people seek emergency department (ED) attention every year for assessment of chest pain. The American Heart Association recently issued a scientific statement to give guidance on rapid, effective approaches to the assessment of such patients.

Conclusions

Most patients who present with chest pain to ED settings do not have acute ischemia: Less than 5% have an ST segment elevation myocardial infarction, and up to 25% can have a non–ST segment elevation event. Up to 7% of patients with chest pain after cocaine exposure have infarctions.

At the same time, up to 2% of patients with acute coronary syndromes (ACS) are inadvertently discharged from EDs with potentially twice the risk-adjusted mortality of patients admitted for management of acute ischemia.

Symptom-limited treadmill stress testing is felt to be safe at 8-12 hours for low- and intermediate-risk chest pain patients who have normal baseline EKGs and capacity to exercise, and are not taking digoxin.

Ischemia induced during stress protocols for echocardiography or myocardial perfusion imaging (MPI) indicates impaired coronary perfusion in the face of increased oxygen demand. MPI also can be used to detect rest ischemia indicating impaired regional myocardial perfusion, a hallmark of the ACS.

Both stress echocardiography (sensitivity: 86%; specificity: 81%) and MPI (87%; 73%) are more effective in detecting coronary artery disease than exercise treadmill testing (70%; 75%). However, while MPI is an effective test, it is associated with considerable radiation exposure.

Use of pharmacologic agents can be substituted for exercise in patients unable to exercise according to modified Bruce protocols. Dobutamine increases myocardial demand. Vasodilators such as adenosine, dipyridamole, and regadenoson simulate exercise stress conditions by dilating coronary arteries and creating maldistribution of myocardial perfusion.

A major clinical trial is ongoing to assess the value of CT coronary arteriography, which has a very high negative predictive value, in assessing chest pain syndrome patients in the ED.

As many as 20%-25% of patients with negative chest pain unit evaluations present again for similar evaluations.

Implementation

The goal of ED evaluation of chest pain is the exclusion of ACS and other urgent conditions as appropriate diagnoses. Assessment of the presence of coronary artery disease is best handled in other settings. Experience with chest pain units and accelerated diagnostic protocols have provided effective evidence-based strategies for triaging these patients.

While classic anginal symptoms can aid in the evaluation of acute chest pain, ACS patients can present with atypical or confusing complaints and require care assessment by evaluating health professionals. Nausea and diaphoresis associated with severe chest pain are highly associated with acute ischemia, but elderly patients may have predominantly respiratory complaints.

Patients with sudden-onset, severe chest pain should be considered for pneumothorax, pulmonary embolus, or aortic dissection.

Patients at low risk for myocardial infarction (less than 5%) should be identified by current symptoms, past history, and a new electrocardiogram. These patients have normal EKGs, normal initial cardiac injury lab findings, and stable hemodynamics and cardiac rhythm. The Thrombolysis in Myocardial Infarction (TIMI) risk score is widely used, but has not performed consistently for low-risk populations.

Patients with acute ST segment elevation frequently have near-total or total coronary occlusion and are candidates for reperfusion interventions.

Patients who present during the first 6 hours of chest pain onset and who have negative cardiac markers should be retested after 8 hours to validate the negative results. Newer assays of troponin have good sensitivity and specificity, and are preferred over creatine kinase MB and myoglobin measurement. Laboratories should return results within an hour of specimen sampling or else point-of-service assessment should be considered. B-type natriuretic peptide, while useful for congestive heart failure evaluation, does not offer value in the assessment of acute ischemia.

For patients with indeterminant initial presentations, chest pain protocols can help structure observation. Exercise stress testing is optional in patients with cocaine-related chest pain after a negative period of observation and testing.

Patients who have no additional chest discomfort, undiagnostic initial and follow-up EKGs, and negative injury lab values can be discharged without stress testing for outpatient follow-up investigations.

Repeat treadmill stress testing has limited value in patients with a previous negative evaluation for chest pain in an emergency setting. These patients may eventually require coronary arteriography as negative cardiac caths, in comparison to noninvasive evaluation, reduce repeat ED chest pain evaluations by more than 50%.

Reference

Amsterdam EA et al. Testing of Low-Risk Patients Presenting to the Emergency Department with Chest Pain (Circulation 2010;122:756-76).

This column, "The Effective Physician," appears regularly in Internal Medicine News, an Elsevier publication. Dr. Golden is professor of medicine and public health and Dr. Hopkins is program director for the internal medicine/pediatrics combined residency program at the University of Arkansas, Little Rock.

Over 8 million people seek emergency department (ED) attention every year for assessment of chest pain. The American Heart Association recently issued a scientific statement to give guidance on rapid, effective approaches to the assessment of such patients.

Conclusions

Most patients who present with chest pain to ED settings do not have acute ischemia: Less than 5% have an ST segment elevation myocardial infarction, and up to 25% can have a non–ST segment elevation event. Up to 7% of patients with chest pain after cocaine exposure have infarctions.

At the same time, up to 2% of patients with acute coronary syndromes (ACS) are inadvertently discharged from EDs with potentially twice the risk-adjusted mortality of patients admitted for management of acute ischemia.

Symptom-limited treadmill stress testing is felt to be safe at 8-12 hours for low- and intermediate-risk chest pain patients who have normal baseline EKGs and capacity to exercise, and are not taking digoxin.

Ischemia induced during stress protocols for echocardiography or myocardial perfusion imaging (MPI) indicates impaired coronary perfusion in the face of increased oxygen demand. MPI also can be used to detect rest ischemia indicating impaired regional myocardial perfusion, a hallmark of the ACS.

Both stress echocardiography (sensitivity: 86%; specificity: 81%) and MPI (87%; 73%) are more effective in detecting coronary artery disease than exercise treadmill testing (70%; 75%). However, while MPI is an effective test, it is associated with considerable radiation exposure.

Use of pharmacologic agents can be substituted for exercise in patients unable to exercise according to modified Bruce protocols. Dobutamine increases myocardial demand. Vasodilators such as adenosine, dipyridamole, and regadenoson simulate exercise stress conditions by dilating coronary arteries and creating maldistribution of myocardial perfusion.

A major clinical trial is ongoing to assess the value of CT coronary arteriography, which has a very high negative predictive value, in assessing chest pain syndrome patients in the ED.

As many as 20%-25% of patients with negative chest pain unit evaluations present again for similar evaluations.

Implementation

The goal of ED evaluation of chest pain is the exclusion of ACS and other urgent conditions as appropriate diagnoses. Assessment of the presence of coronary artery disease is best handled in other settings. Experience with chest pain units and accelerated diagnostic protocols have provided effective evidence-based strategies for triaging these patients.

While classic anginal symptoms can aid in the evaluation of acute chest pain, ACS patients can present with atypical or confusing complaints and require care assessment by evaluating health professionals. Nausea and diaphoresis associated with severe chest pain are highly associated with acute ischemia, but elderly patients may have predominantly respiratory complaints.

Patients with sudden-onset, severe chest pain should be considered for pneumothorax, pulmonary embolus, or aortic dissection.

Patients at low risk for myocardial infarction (less than 5%) should be identified by current symptoms, past history, and a new electrocardiogram. These patients have normal EKGs, normal initial cardiac injury lab findings, and stable hemodynamics and cardiac rhythm. The Thrombolysis in Myocardial Infarction (TIMI) risk score is widely used, but has not performed consistently for low-risk populations.

Patients with acute ST segment elevation frequently have near-total or total coronary occlusion and are candidates for reperfusion interventions.

Patients who present during the first 6 hours of chest pain onset and who have negative cardiac markers should be retested after 8 hours to validate the negative results. Newer assays of troponin have good sensitivity and specificity, and are preferred over creatine kinase MB and myoglobin measurement. Laboratories should return results within an hour of specimen sampling or else point-of-service assessment should be considered. B-type natriuretic peptide, while useful for congestive heart failure evaluation, does not offer value in the assessment of acute ischemia.

For patients with indeterminant initial presentations, chest pain protocols can help structure observation. Exercise stress testing is optional in patients with cocaine-related chest pain after a negative period of observation and testing.

Patients who have no additional chest discomfort, undiagnostic initial and follow-up EKGs, and negative injury lab values can be discharged without stress testing for outpatient follow-up investigations.

Repeat treadmill stress testing has limited value in patients with a previous negative evaluation for chest pain in an emergency setting. These patients may eventually require coronary arteriography as negative cardiac caths, in comparison to noninvasive evaluation, reduce repeat ED chest pain evaluations by more than 50%.

Reference

Amsterdam EA et al. Testing of Low-Risk Patients Presenting to the Emergency Department with Chest Pain (Circulation 2010;122:756-76).

This column, "The Effective Physician," appears regularly in Internal Medicine News, an Elsevier publication. Dr. Golden is professor of medicine and public health and Dr. Hopkins is program director for the internal medicine/pediatrics combined residency program at the University of Arkansas, Little Rock.

Over 8 million people seek emergency department (ED) attention every year for assessment of chest pain. The American Heart Association recently issued a scientific statement to give guidance on rapid, effective approaches to the assessment of such patients.

Conclusions

Most patients who present with chest pain to ED settings do not have acute ischemia: Less than 5% have an ST segment elevation myocardial infarction, and up to 25% can have a non–ST segment elevation event. Up to 7% of patients with chest pain after cocaine exposure have infarctions.

At the same time, up to 2% of patients with acute coronary syndromes (ACS) are inadvertently discharged from EDs with potentially twice the risk-adjusted mortality of patients admitted for management of acute ischemia.

Symptom-limited treadmill stress testing is felt to be safe at 8-12 hours for low- and intermediate-risk chest pain patients who have normal baseline EKGs and capacity to exercise, and are not taking digoxin.

Ischemia induced during stress protocols for echocardiography or myocardial perfusion imaging (MPI) indicates impaired coronary perfusion in the face of increased oxygen demand. MPI also can be used to detect rest ischemia indicating impaired regional myocardial perfusion, a hallmark of the ACS.

Both stress echocardiography (sensitivity: 86%; specificity: 81%) and MPI (87%; 73%) are more effective in detecting coronary artery disease than exercise treadmill testing (70%; 75%). However, while MPI is an effective test, it is associated with considerable radiation exposure.

Use of pharmacologic agents can be substituted for exercise in patients unable to exercise according to modified Bruce protocols. Dobutamine increases myocardial demand. Vasodilators such as adenosine, dipyridamole, and regadenoson simulate exercise stress conditions by dilating coronary arteries and creating maldistribution of myocardial perfusion.

A major clinical trial is ongoing to assess the value of CT coronary arteriography, which has a very high negative predictive value, in assessing chest pain syndrome patients in the ED.

As many as 20%-25% of patients with negative chest pain unit evaluations present again for similar evaluations.

Implementation

The goal of ED evaluation of chest pain is the exclusion of ACS and other urgent conditions as appropriate diagnoses. Assessment of the presence of coronary artery disease is best handled in other settings. Experience with chest pain units and accelerated diagnostic protocols have provided effective evidence-based strategies for triaging these patients.

While classic anginal symptoms can aid in the evaluation of acute chest pain, ACS patients can present with atypical or confusing complaints and require care assessment by evaluating health professionals. Nausea and diaphoresis associated with severe chest pain are highly associated with acute ischemia, but elderly patients may have predominantly respiratory complaints.

Patients with sudden-onset, severe chest pain should be considered for pneumothorax, pulmonary embolus, or aortic dissection.

Patients at low risk for myocardial infarction (less than 5%) should be identified by current symptoms, past history, and a new electrocardiogram. These patients have normal EKGs, normal initial cardiac injury lab findings, and stable hemodynamics and cardiac rhythm. The Thrombolysis in Myocardial Infarction (TIMI) risk score is widely used, but has not performed consistently for low-risk populations.

Patients with acute ST segment elevation frequently have near-total or total coronary occlusion and are candidates for reperfusion interventions.

Patients who present during the first 6 hours of chest pain onset and who have negative cardiac markers should be retested after 8 hours to validate the negative results. Newer assays of troponin have good sensitivity and specificity, and are preferred over creatine kinase MB and myoglobin measurement. Laboratories should return results within an hour of specimen sampling or else point-of-service assessment should be considered. B-type natriuretic peptide, while useful for congestive heart failure evaluation, does not offer value in the assessment of acute ischemia.

For patients with indeterminant initial presentations, chest pain protocols can help structure observation. Exercise stress testing is optional in patients with cocaine-related chest pain after a negative period of observation and testing.

Patients who have no additional chest discomfort, undiagnostic initial and follow-up EKGs, and negative injury lab values can be discharged without stress testing for outpatient follow-up investigations.

Repeat treadmill stress testing has limited value in patients with a previous negative evaluation for chest pain in an emergency setting. These patients may eventually require coronary arteriography as negative cardiac caths, in comparison to noninvasive evaluation, reduce repeat ED chest pain evaluations by more than 50%.

Reference

Amsterdam EA et al. Testing of Low-Risk Patients Presenting to the Emergency Department with Chest Pain (Circulation 2010;122:756-76).

This column, "The Effective Physician," appears regularly in Internal Medicine News, an Elsevier publication. Dr. Golden is professor of medicine and public health and Dr. Hopkins is program director for the internal medicine/pediatrics combined residency program at the University of Arkansas, Little Rock.

Background

Testosterone deficiency is a poorly understood entity among many physicians and patients. In order to provide an evidence-based foundation for diagnosis and management, the Endocrine Society published an updated guideline on this condition early this year.

Conclusions

The symptoms of androgen deficiency in men vary with the age of onset and degree of testosterone deficiency.

The signs and symptoms most consistent with testosterone deficiency include decreased libido, erectile dysfunction, gynecomastia, loss of body hair, hot flushes/sweats, bone loss and/or low-impact fractures, azoospermia/infertility, and incomplete sexual development. A variety of less-specific symptoms also may be attributable to testosterone deficiency: decreased energy or mood, sleep disturbance, poor concentration, modest anemia, and increased body fat with decreased muscle bulk/mass.

Testosterone deficiency can result from defects in testicular production of androgens (primary testicular failure), at the hypothalamic-pituitary level (secondary failure), or from combined mechanisms. The distinction is important because combined and secondary defects might be caused by specific diseases that may require treatment; and the potential to restore fertility in some patients with secondary testicular failure with correct hormone stimulation. Testosterone levels decline by 1%-2% per year in older men, and the circadian variability of levels present in younger men is also commonly lost with aging.

Randomized trials of testosterone replacement in men with testosterone deficiency have shown consistent improvement in bone density, lean body mass with concomitant reduction in fat mass, and sense of physical well-being; the trials were less consistent in effects on muscle strength, libido, erectile function, quality of life, depression, cognition, and muscle strength. Testosterone replacement has not been demonstrated to reduce fractures. Many of the trials are limited by small sample size and short follow-up.

Implementation

Androgen deficiency should not be diagnosed without the presence of both symptoms and low testosterone levels.

Screening is not indicated in the general population or in men who are being evaluated for unrelated health issues. There is not a consensus case definition for androgen deficiency; there are few data on the performance of screening criteria; and the long-term implications of replacement is unclear in the most commonly affected populations: older men and men with chronic illness.

Patients should not be evaluated for androgen deficiency during an acute illness because illness can suppress testosterone levels.

High-dose glucocorticoids, opiates (particularly methadone and long-acting opiates), eating disorders, and excessive exercise can affect testosterone levels and should be asked about in the evaluation of a patient who is potentially androgen deficient.

A morning total testosterone level is the recommended initial test for androgen deficiency; this should be repeated to confirm deficiency.

Patients who have total testosterone levels near the lower limit of normal and in whom protein binding may be abnormal, such as those who have concomitant obesity, diabetes, chronic illness, or thyroid disease, might require measurement of free testosterone levels in their evaluation.

Luteinizing hormone and follicle-stimulating hormone levels should be measured in patients found to be testosterone deficient in order to distinguish primary from secondary testicular failure. Those men found to have secondary androgen deficiency should be evaluated further to assess for systemic disease (for example, hyperprolactinemia or hemochromatosis) and/or pituitary tumor.

Testosterone replacement is recommended to maintain secondary sex characteristics, improve sexual function and sense of well being, and improve bone density in patients who have androgen deficiency and who do not have identified contraindications. The choice of replacement medication and delivery system will depend on individual patient factors and preference.

Testosterone treatment is not recommended in men with breast or prostate cancer, elevated PSA, and/or unevaluated prostate abnormality, those at high risk for prostate cancer, those with severe lower urinary tract symptoms, or in men with hematocrit greater than 50 %, untreated sleep apnea or poorly controlled heart failure.

Men treated with testosterone replacement should be evaluated 3-6 months after it is initiated, and then annually thereafter. This follow-up should include measurement of testosterone, hematocrit and PSA levels, and a prostate exam. Bone density should be measured 1-2 years after initiation of testosterone replacement in patients with low bone density or fragility fracture; the subsequent interval of remeasurement of bone density remains controversial.

Urologic consultation is recommended when prostate abnormalities or rising PSA is detected while a man is taking testosterone.

Dr. Golden is professor of medicine and public health and Dr. Hopkins is program director for the internal medicine/pediatrics combined residency program at the University of Arkansas, Little Rock.

Reference

Testosterone Therapy in Men With Androgen Deficiency Syndromes: An Endocrine Society Clinical Practice Guideline (J. Clin. Endo. Metab. 2010;95:2536-59).

Background

Testosterone deficiency is a poorly understood entity among many physicians and patients. In order to provide an evidence-based foundation for diagnosis and management, the Endocrine Society published an updated guideline on this condition early this year.

Conclusions

The symptoms of androgen deficiency in men vary with the age of onset and degree of testosterone deficiency.

The signs and symptoms most consistent with testosterone deficiency include decreased libido, erectile dysfunction, gynecomastia, loss of body hair, hot flushes/sweats, bone loss and/or low-impact fractures, azoospermia/infertility, and incomplete sexual development. A variety of less-specific symptoms also may be attributable to testosterone deficiency: decreased energy or mood, sleep disturbance, poor concentration, modest anemia, and increased body fat with decreased muscle bulk/mass.

Testosterone deficiency can result from defects in testicular production of androgens (primary testicular failure), at the hypothalamic-pituitary level (secondary failure), or from combined mechanisms. The distinction is important because combined and secondary defects might be caused by specific diseases that may require treatment; and the potential to restore fertility in some patients with secondary testicular failure with correct hormone stimulation. Testosterone levels decline by 1%-2% per year in older men, and the circadian variability of levels present in younger men is also commonly lost with aging.

Randomized trials of testosterone replacement in men with testosterone deficiency have shown consistent improvement in bone density, lean body mass with concomitant reduction in fat mass, and sense of physical well-being; the trials were less consistent in effects on muscle strength, libido, erectile function, quality of life, depression, cognition, and muscle strength. Testosterone replacement has not been demonstrated to reduce fractures. Many of the trials are limited by small sample size and short follow-up.

Implementation

Androgen deficiency should not be diagnosed without the presence of both symptoms and low testosterone levels.

Screening is not indicated in the general population or in men who are being evaluated for unrelated health issues. There is not a consensus case definition for androgen deficiency; there are few data on the performance of screening criteria; and the long-term implications of replacement is unclear in the most commonly affected populations: older men and men with chronic illness.

Patients should not be evaluated for androgen deficiency during an acute illness because illness can suppress testosterone levels.

High-dose glucocorticoids, opiates (particularly methadone and long-acting opiates), eating disorders, and excessive exercise can affect testosterone levels and should be asked about in the evaluation of a patient who is potentially androgen deficient.

A morning total testosterone level is the recommended initial test for androgen deficiency; this should be repeated to confirm deficiency.

Patients who have total testosterone levels near the lower limit of normal and in whom protein binding may be abnormal, such as those who have concomitant obesity, diabetes, chronic illness, or thyroid disease, might require measurement of free testosterone levels in their evaluation.

Luteinizing hormone and follicle-stimulating hormone levels should be measured in patients found to be testosterone deficient in order to distinguish primary from secondary testicular failure. Those men found to have secondary androgen deficiency should be evaluated further to assess for systemic disease (for example, hyperprolactinemia or hemochromatosis) and/or pituitary tumor.

Testosterone replacement is recommended to maintain secondary sex characteristics, improve sexual function and sense of well being, and improve bone density in patients who have androgen deficiency and who do not have identified contraindications. The choice of replacement medication and delivery system will depend on individual patient factors and preference.

Testosterone treatment is not recommended in men with breast or prostate cancer, elevated PSA, and/or unevaluated prostate abnormality, those at high risk for prostate cancer, those with severe lower urinary tract symptoms, or in men with hematocrit greater than 50 %, untreated sleep apnea or poorly controlled heart failure.

Men treated with testosterone replacement should be evaluated 3-6 months after it is initiated, and then annually thereafter. This follow-up should include measurement of testosterone, hematocrit and PSA levels, and a prostate exam. Bone density should be measured 1-2 years after initiation of testosterone replacement in patients with low bone density or fragility fracture; the subsequent interval of remeasurement of bone density remains controversial.

Urologic consultation is recommended when prostate abnormalities or rising PSA is detected while a man is taking testosterone.

Dr. Golden is professor of medicine and public health and Dr. Hopkins is program director for the internal medicine/pediatrics combined residency program at the University of Arkansas, Little Rock.

Reference

Testosterone Therapy in Men With Androgen Deficiency Syndromes: An Endocrine Society Clinical Practice Guideline (J. Clin. Endo. Metab. 2010;95:2536-59).

Background

Testosterone deficiency is a poorly understood entity among many physicians and patients. In order to provide an evidence-based foundation for diagnosis and management, the Endocrine Society published an updated guideline on this condition early this year.

Conclusions

The symptoms of androgen deficiency in men vary with the age of onset and degree of testosterone deficiency.

The signs and symptoms most consistent with testosterone deficiency include decreased libido, erectile dysfunction, gynecomastia, loss of body hair, hot flushes/sweats, bone loss and/or low-impact fractures, azoospermia/infertility, and incomplete sexual development. A variety of less-specific symptoms also may be attributable to testosterone deficiency: decreased energy or mood, sleep disturbance, poor concentration, modest anemia, and increased body fat with decreased muscle bulk/mass.

Testosterone deficiency can result from defects in testicular production of androgens (primary testicular failure), at the hypothalamic-pituitary level (secondary failure), or from combined mechanisms. The distinction is important because combined and secondary defects might be caused by specific diseases that may require treatment; and the potential to restore fertility in some patients with secondary testicular failure with correct hormone stimulation. Testosterone levels decline by 1%-2% per year in older men, and the circadian variability of levels present in younger men is also commonly lost with aging.

Randomized trials of testosterone replacement in men with testosterone deficiency have shown consistent improvement in bone density, lean body mass with concomitant reduction in fat mass, and sense of physical well-being; the trials were less consistent in effects on muscle strength, libido, erectile function, quality of life, depression, cognition, and muscle strength. Testosterone replacement has not been demonstrated to reduce fractures. Many of the trials are limited by small sample size and short follow-up.

Implementation

Androgen deficiency should not be diagnosed without the presence of both symptoms and low testosterone levels.

Screening is not indicated in the general population or in men who are being evaluated for unrelated health issues. There is not a consensus case definition for androgen deficiency; there are few data on the performance of screening criteria; and the long-term implications of replacement is unclear in the most commonly affected populations: older men and men with chronic illness.

Patients should not be evaluated for androgen deficiency during an acute illness because illness can suppress testosterone levels.

High-dose glucocorticoids, opiates (particularly methadone and long-acting opiates), eating disorders, and excessive exercise can affect testosterone levels and should be asked about in the evaluation of a patient who is potentially androgen deficient.

A morning total testosterone level is the recommended initial test for androgen deficiency; this should be repeated to confirm deficiency.

Patients who have total testosterone levels near the lower limit of normal and in whom protein binding may be abnormal, such as those who have concomitant obesity, diabetes, chronic illness, or thyroid disease, might require measurement of free testosterone levels in their evaluation.

Luteinizing hormone and follicle-stimulating hormone levels should be measured in patients found to be testosterone deficient in order to distinguish primary from secondary testicular failure. Those men found to have secondary androgen deficiency should be evaluated further to assess for systemic disease (for example, hyperprolactinemia or hemochromatosis) and/or pituitary tumor.

Testosterone replacement is recommended to maintain secondary sex characteristics, improve sexual function and sense of well being, and improve bone density in patients who have androgen deficiency and who do not have identified contraindications. The choice of replacement medication and delivery system will depend on individual patient factors and preference.

Testosterone treatment is not recommended in men with breast or prostate cancer, elevated PSA, and/or unevaluated prostate abnormality, those at high risk for prostate cancer, those with severe lower urinary tract symptoms, or in men with hematocrit greater than 50 %, untreated sleep apnea or poorly controlled heart failure.

Men treated with testosterone replacement should be evaluated 3-6 months after it is initiated, and then annually thereafter. This follow-up should include measurement of testosterone, hematocrit and PSA levels, and a prostate exam. Bone density should be measured 1-2 years after initiation of testosterone replacement in patients with low bone density or fragility fracture; the subsequent interval of remeasurement of bone density remains controversial.

Urologic consultation is recommended when prostate abnormalities or rising PSA is detected while a man is taking testosterone.

Dr. Golden is professor of medicine and public health and Dr. Hopkins is program director for the internal medicine/pediatrics combined residency program at the University of Arkansas, Little Rock.

Reference

Testosterone Therapy in Men With Androgen Deficiency Syndromes: An Endocrine Society Clinical Practice Guideline (J. Clin. Endo. Metab. 2010;95:2536-59).