Chest Pain: 10 Common Myths and Mistakes

About 6 million patients present to emergency departments (EDs) in the United States each year with acute chest pain. The decision to admit or discharge a patient with acute chest pain can have significant consequences. A practice of "admitting everyone" with such symptoms places an excessive burden on financial and acute care resources. Conversely, discharging a patient with an acute myocardial infarction (AMI) can be disastrous.

The evaluation of patients with acute chest pain has been hindered by the widespread promulgation of myths that can result in the delay of care or even harm. Our goal is to expose these misconceptions; thus, we review here the 10 most common mistakes made in the evaluation.

Failure to recognize atypical clinical presentations of acute coronary syndrome (ACS)

1. Atypical presentations in the quality, intensity, and radiation of pain are common in patients with ACS. Crushing retrosternal pain or pressure suggests a cardiac source of chest symptoms. However, only 50% of patients with AMI describe their pain in classic terms such as "crushing" or "pressure-like." Many alternative descriptors of chest pain are used, the most frequent of which include aching, cramping, and grinding (Table 1).

Moreover, women who have AMI present with atypical symptoms more frequently than do men. This may be explained in part by the fact that women are usually older and have more comorbidities (such as hypertension, diabetes, and heart failure) than men at presentation.¹ Consequently, women—as well as persons with diabetes and elderly persons—who have an AMI are more likely not to experience chest pain, or to have nonspecific complaints such as dyspnea, nausea and vomiting, unusual fatigue or weakness, palpitations, or presyncope.

The intensity of chest pain, usually assumed to be significant in AMI, may be rated from 0 to 10 on the 10-point pain scale (Table 2).² However, 33% of patients with AMI report no chest pain.³

The pattern of chest pain radiation may also be a source of confusion. Pain that radiates to the left arm and shoulder is often assumed to indicate coronary ischemia, whereas pain that radiates to the right shoulder is thought to suggest a biliary source. However, chest pain that radiates to the right shoulder is more specific for pain of cardiac origin than pain that radiates to the left shoulder.⁴ Pain that radiates to the throat, back, or epigastrium may be cardiac in origin and should not automatically be attributed to esophageal or aortic causes.

Making a disposition decision based on the patient's psychiatric history or level of anxiety

2. The appearance and mannerisms of a patient with chest pain may profoundly influence a physician's approach. A new patient with chest pain whose medication list includes numerous psychiatric drugs may be more likely to have his or her complaints dismissed as psychiatric. Birdwell and colleagues⁵ demonstrated this bias when they videotaped an actress portraying a patient who described her chest pain in a "businesslike" manner. Half of the physicians who reviewed the tape believed that the patient had a cardiac condition. However, when the actress reported the same complaint in a "histrionic" manner, only 13% believed that she had a cardiac condition.

A history of a psychiatric diagnosis or overwhelming anxiety in a patient with acute chest pain does not preclude the possibility of an acute coronary event.

Inappropriate reliance on nondiagnostic maneuvers

3. In a patient with chest pain, the clinical response to the "GI cocktail" (a mixture of liquid antacid, viscous lidocaine, and an anticholinergic), sublingual nitroglycerin, or chest wall palpation cannot reliably identify the source of pain. A decrease in chest pain after ingestion of a GI cocktail is often assumed to identify the source of pain as gastrointestinal. However, several small studies have demonstrated that patients with myocardial ischemia or ACS may report decreased chest pain when given a GI cocktail.^6,7

Many practitioners believe that decreased chest pain after a trial of sublingual nitroglycerin points to a cardiac origin. However, this marker is unreliable. In a retrospective study, an overwhelming number of patients with and without a cardiac source of chest pain experienced some pain relief with sublingual nitroglycerin.⁸ In a prospective study, 35% of patients who ultimately proved to have coronary artery disease and 41% of patients with noncardiac chest pain had more than a 50% decrease in their chest pain with nitroglycerin.⁹ This finding was confirmed in a larger, more recent study.¹⁰

Finally, reproducing a patient's chest pain with palpation is often felt to be diagnostic of a musculoskeletal cause, such as costochondritis. This is often the case, but not unfailingly so. In a prospective study, 6% of patients with atraumatic chest pain in whom costochondritis was diagnosed in the ED by a rheumatologist in fact had an AMI.¹¹

Making a disposition decision based on the ECG and one set of cardiac biomarkers

4. When obvious ST-segment elevation is present in patients with acute chest pain, the diagnosis of myocardial injury is straightforward. However, significantly more than 50% of patients with AMI have nondiagnostic ECG changes.¹² The ECG becomes even less sensitive with increasing age and in those with a previous MI.¹³ Furthermore, many ECG patterns interfere with the diagnosis of AMI. These include left bundle-branch block, Wolff-Parkinson-White syndrome, ventricular pacemaker rhythm, myopericarditis, early repolarization ST changes, T-wave abnormality associated with an intracranial bleed, left ventricular hypertrophy, and hyperkalemia.

When the cause of chest pain remains unclear in a clinically stable patient with a nondiagnostic ECG, assays of cardiac biomarkers (myoglobin, creatine phosphokinase-MB [CPK-MB], and troponin I and T) are the next step used to identify an AMI. However, because the initial sensitivity of these markers is low, a decision to discharge a patient with chest pain should not be based on just one set of laboratory values. A meta-analysis revealed that the likelihood that levels of any of these common biomarkers will be elevated on initial evaluation in patients with AMI is less than 50% (Table 3).¹⁴

Even when the ECG and biomarkers are considered in combination, as in the Erlanger protocol,¹⁵ they will still miss about 40% of acute myocardial infarctions, although the sensitivity is improved.

About 1% to 2% of patients with AMI are inappropriately discharged from the ED, which means that 98% to 99% of MIs are properly identified. This high rate of detection is the result of a careful, focused history taking and physical examination that suggest a cardiac source of pain. The history and physical examination must drive the decision to admit the patient, aided by information gleaned from the ECG and biomarkers.

Overreliance on serum troponin values

5. Because of the high sensitivity and specificity of troponin I and T levels, these proteinshave become the cardiac biomarkers of choice for the American College of Cardiology, the American Heart Association, and the European Society of Cardiology.¹⁶ Troponin levels, like those of the traditional marker CPK-MB, begin to rise within 6 to 8 hours after the onset of myocardial damage. However, a discharge decision based on a negative troponin value in a patient with 6 hours or more of chest pain may be risky because the onset of chest pain (myocardial ischemia) does not always coincide with the onset of myocardial damage. Therefore, serial troponin levels taken at 3- to 6-hour intervals are recommended.

Although troponin has greaters pecificity than myoglobin and CPK-MB for myocardial damage, elevated levels may be present in patients with nonischemic heart disease or noncardiac disease. Cardiac causes such as heart failure, cardiac amyloidosis, myocarditis, and the use of cardiotoxic drugs such as doxorubicin, 5-fluorouracil, and trastuzumab can produce nonischemic troponin elevations. Noncardiac causes such as pulmonary embolism, sepsis, high-dose chemotherapy, stroke, subarachnoid hemorrhage, preeclampsia, positive heterophil antibody, and renal failure can also produce such elevations. Therefore, elevated troponin levels do not invariably signify myocardial damage.

Patients with renal failure and elevated troponin levels require special attention. In one study, 17% of 52 asymptomatic patients receiving hemodialysis had elevated troponin T values.¹⁷ These were assumed to be false-positive results. However, recent evidence suggests that elevated troponin levels in patients receiving hemodialysis portend higher mortality rates.^18-21

An exclusive focus on ruling out MI

6. Clinicians often become too focused on the diagnosis of MI and are relieved if it is excluded. However, if a patient's pain is classified as noncardiac once an MI is ruled out, the possibility of unstable angina may be ignored. Of patients with untreated unstable angina, 10% will have an MI or die within 28 days and 20% within 1 year.²²

Sending a patient to the ED to rule out an AMI

7. Results of the history taking, physical examination, serial 12-lead ECGs, and 3 sets of biomarkers (usually at 6-hour intervals) must all be negative in order for an AMI to be ruled out. The amount of time required for this evaluation precludes the possibility of its being undertaken in the ED unless there is a special subunit dedicated to this process.

A more appropriate request from the office-based physician is to ask the ED physicians to risk-stratify a patient with suspicious chest pain. If the patient appears to be at high risk for ACS (for example, if he has coronary artery disease; a suggestive history; or abnormal physical examination, ECG, or biomarker results), he should be admitted for evaluation to a coronary unit or ICU with the possibility of early invasive therapy. However, if the patient appears to be at lower risk, he may be admitted to a telemetry unit for possible early noninvasive evaluation with stress testing.

Overreliance on the absence of traditional coronary risk factors or overlooking uncommon risk factors in the decision to admit or discharge a patient with chest pain

8. Although cardiac risk factors are common in patients with ACS, they are not a prerequisite. In a study of more than 120,000 men with acute coronary disease, 81% had at least 1 traditional cardiac risk factor.²³ This means that nearly 1 in 5 had no traditional risk factors. In addition, patients who present with ACS are often unaware that they have an underlying risk factor, such as hypertension or hyperlipidemia.

A number of nontraditional cardiac risk factors have been described. Systemic lupus erythematosus confers a 9-fold increase in cardiac risk on young patients and a 50-fold increase in risk on women aged 35 to 44 years. This increased risk seems unrelated to corticosteroid use or the presence of other risk factors.²⁴

Cocaine use is a risk factor for AMI. Acute use of cocaine can produce vasospasm and vasoconstriction, platelet aggregation, dysrhythmias, and ischemia from adrenergic stimulation. Chronic use is associated with myocyte toxicity and accelerated atherosclerosis, which results in a 6-fold increase in the risk of MI.

Recent evidence shows an increased risk of AMI in the 3 days following the onset of an upper respiratory tract infection.²⁵ Although the reason for this association is not clear, a systemic inflammatory response may be responsible.

Discharging from the ED with a diagnosis of "noncardiac chest pain" a patient who had normal results on a recent stress test or cardiac catheterization

9. Many clinicians have faced the dilemma of a patient who presents with symptoms consistent with ACS but had "normal" results on a recent stress test or cardiac catheterization. Could this patient still be having a significant coronary event?

Current evidence suggests that stress tests are 68% to 90% sensitive for coronary artery disease, depending on the type of study performed.²⁶ The sensitivity of the test depends on the pretest probability of disease, the coronary artery involved (left anterior descending more than left circumflex artery), and the degree of obstruction (more than 75%). Coronary angiography, once the gold standard of diagnosis, is not 100% sensitive for exclusion of coronary artery disease. Coronary angiography detects the later stage of atherosclerosis (negative remodeling stage), when larger plaques significantly impinge on the coronary lumen. Angiography may fail to detect the early stage of atherosclerosis (positive remodeling stage), when smaller plaques cause minimal or no luminal impingement. This stage is detectable only by intravascular coronary ultrasonography.

ACS is caused by rupture of a soft, cholesterol-rich nonobstructive plaque. These smaller plaques represent early-stage lesions or smaller late-stage lesions. Such plaques may defy detection by stress testing and coronary angiography. Larger plaques, which are more readily detected by these modalities, impede coronary flow and cause chest pain but are less likely to rupture and cause ACS.

If you suspect ACS, do not make a disposition decision based on previous investigations.

Assuming that patients who present to the ED with chest pain are similar to patients who present to the office with chest pain

10. An approach to the patient who presents to the office with acute chest pain may be quite different from that used with a patient who arrives in the ED with the same complaint. Patients who present to the office tend to be younger and infrequently have a cardiac source of pain. Patients who arrive in the ED with acute chest pain are generally older and more often have acute coronary disease.²⁷ Consequently, the evaluation and management of these types of patients may differ significantly.

CLINICAL HIGHLIGHTS

• Proton pump inhibitors (PPIs) can mask a Helicobacter pylori infection because they are associated with a marked reduction in the bacterial load. Because the results of serological tests are not affected by drugs that reduce the bacterial load, testing for H pylori antibodies is recommended when the diagnosis is in doubt. Consider switching the patient from a PPI to an H₂-receptor antagonist several weeks before either noninvasive testing (stool antigen or urea breath tests) or endoscopy for histology and possibly culture; H₂ blockers do not affect H pylori status.

• NSAID use—one of the major causes of refractory ulcer—can be inadvertent. Because many over-the-counter medications (eg, cough-cold remedies) contain NSAIDs, inquire about the use of these and other products from health food or vitamin stores during the history taking.

• Zollinger-Ellison syndrome may be a hidden cause of refractory peptic ulcers. It is characterized by peptic ulcers of the upper GI tract that are difficult to manage and which rapidly recur when antisecretory drug therapy is withdrawn. H pylori infections are typically absent. A fasting plasma gastrin level higher than 1000 pg/mL or a basal acid output of more than 15 mEq/h suggests the diagnosis.

• The location of the ulcer provides clues to its possible etiology. For esophageal ulceration, consider a pill-induced ulcer and acid hypersecretory states. For gastric ulcers, consider cancer, primary lymphoma, and use of NSAIDs or other ulcerogenic drugs. For duodenal ulcers, consider use of NSAIDs or other ulcerogenic drugs, acid hypersecretory states, other infectious processes, and Crohn disease.

• Histological features that suggest NSAID use include focal erosion of the luminal epithelium, macroerosion, and the presence of prominent capillaries in suberosive areas of the lamina propria. Ultrastructural damage is characterized by a proliferative phenomenon of “desquamation” of contiguous epithelial cells. The findings may include chemical gastritis.