Chest pain that is cardiac in etiology is termed angina pectoris. Angina is defined as a clinical syndrome “characterized by discomfort in the chest, jaw, shoulder, back, or arm” (2,3). Angina usually is provoked by physical exertion or emotional stress and is relieved with rest or nitroglycerin. Patients typically describe angina with adjectives such as “heavy,” “dull,” “pressure-like,” “suffocating,” or “squeezing,” or they use phrases such as “like a heavy weight on my chest.” Angina is classically substernal but can occur in the arm, shoulder, jaw, mandible, or upper back, with or without radiation. Pain above the mandible, below the epigastrium, localized to an area less than one fingertip in size, or that radiates into the lower extremities is rarely angina. Angina usually lasts for a few minutes and is relieved by nitroglycerin within 5 minutes or less. Continuous pain that lasts for several hours or fleeting pain that lasts for only a few seconds suggests an alternative diagnosis. Angina typically does not vary with respiration, position, or palpation.

Angina is termed stable when it occurs only with provocation, has been occurring for at least 2 months, and is symptomatically stable. According to the Canadian Cardiovascular Society Classification system (4), angina can be graded on the basis of the history (Table 1.2). Class I angina occurs only with strenuous exertion, Class II results in a slight limitation of ordinary activity and occurs only during moderate levels of exertion, Class III is associated with a marked reduction in ordinary activity and can occur with mild exertion, and Class IV angina causes limitations on activities of daily living and can occur even at rest.

Unstable angina, which is an acute coronary syndrome, can be classified as rest angina, new-onset angina, or increasing angina (5) (Table 1.3). Rest angina occurs at rest without provocation for longer than 20 minutes within 1 week of presentation. New-onset angina is angina that is at least Class
III in severity and is seen within 2 months of initial presentation. Increasing angina is stable angina that is increasing in frequency or duration, has a decreasing threshold for provocation, or has increasing intensity.

Anginal pain from myocardial infarction classically is often described as “crushing” or “as if an elephant were standing on my chest” and is usually severe and unrelenting. For many patients, it is the sentinel episode of chest pain. Others may have a history of stable angina, unstable angina, or both in the preceding 2 weeks. It is not uncommon for patients to present several days after a myocardial infarction with congestive heart failure symptoms or postinfarction angina. Some patients are completely asymptomatic or able to recall only vague “gas pains.”

Cardiac pain does not always appear as typical angina pectoris. This may be particularly the case in women, the elderly, and in those with diabetes mellitus. Patients may have pain limited to the shoulder, arm, throat, or jaw. Occasionally, patients with ACS will show predominantly sweating or shortness of breath.

Angina pectoris is most frequently caused by CAD resulting in reduced blood supply to the myocardium, but can also be due to increased demand. Conditions include hypertension, aortic valve stenosis, hypertrophic cardiomyopathy, tachycardia, etc. Chest pain may be the presenting manifestation of severe valvular heart disease or hypertrophic cardiomyopathy. When present, it manifests as typical angina caused by a supply/demand imbalance in coronary blood flow that leads to myocardial ischemia or as chest discomfort caused by pulmonary congestion resulting from left atrial hypertension or volume overload. The symptoms are usually chronic and may be associated with CHF symptoms (dyspnea, fatigue, orthopnea, edema). If either valvular heart disease or hypertrophic cardiomyopathy is suspected, a history of syncope or aborted sudden cardiac death and a family history of sudden cardiac death should be sought. A history of rheumatic fever raises the possibility of rheumatic valvular disease.

These conditions can be distinguished by the physical examination and investigations.

Chest pain is a central complaint in acute pericarditis. The pain is typically located over the precordium with radiation to the trapezius ridge and neck. The pain is often “sharp” or “knifelike,” is exacerbated by respiration and thoracic motion, is relieved by leaning forward, and is aggravated by recumbency. It is not related to exertion and can last for hours on end. Patients may complain of dyspnea, which is related to taking shallow respirations to avoid the pleuritic pain. Pericarditis is more common in men. Dyspnea on exertion and other symptoms of congestive heart failure should raise the suspicion for concomitant myocarditis.

Aortic dissection is characterized by separation of intima and media and consequent propagation as blood enters the intima/media space. The separation of the layers of the aorta with formation of a dissection flap can lead to ischemia of any of the branches of the aortic trunk, including the coronary arteries. Although much less common than acute coronary syndromes, dissection should be considered early in the evaluation of chest pain, in view of its divergent management and exceedingly high short-term mortality rate. Aortic dissection has classically been described as a severe and sudden “ripping” or “tearing” chest or back pain that radiates in a migratory fashion (6). A multicenter registry of almost 500 patients diagnosed with acute aortic dissection revealed that the pain of aortic dissection is more often sharp and typically of sudden and severe onset. The clinical manifestations of aortic dissection are quite varied, and thus the physician must have a high clinical index of suspicion to make the diagnosis.

Pulmonary embolus is a frequent cause of death. It generally results from the embolization of thrombotic material from lower extremity and deep pelvic veins. The thrombotic material can occlude any of the branches of the pulmonary artery and lead to hypoxia, pulmonary infarction, and acute right ventricular dysfunction. It is also critical to consider this diagnosis early in the evaluation of chest pain, because a recurrent pulmonary embolus may be fatal.

The chest pain of PE can be pleuritic in nature and is associated with abrupt-onset dyspnea and apprehension. Many affected patients have risk factors for PE, such as previous deep vein thrombosis, recent surgery, prolonged immobilization, malignancy, hypercoagulability syndromes, advanced age, congestive heart failure, oral contraceptive use, or pregnancy.

Pleuritic chest pain may be a sign of pulmonary embolus, infection or inflammation of the pleura or lungs, or may result from a pneumothorax. If due to pneumonia, the pain may be accompanied by cough, sputum production, and fever.

Chest pain associated with GERD and esophagitis is often described as a “burning” sensation or simply as “heartburn” and occurs after meals or on recumbency. The pain usually starts in the epigastric region, radiates superiorly across the entire chest, and usually does not radiate into the arms. However, the pain can also be retrosternal. The patient may also complain of hoarseness, a need to clear the throat repeatedly, or a deep pressure in the throat. A history of regurgitation or water brash supports the diagnosis. The chest pain of GERD is frequently exacerbated by maneuvers that increase intraabdominal pressure, such as bending, squatting, and coughing. Many patients have risk factors for GERD, such as excessive caffeine or alcohol use, cigarette smoking, and heavy meal consumption. The pain of esophageal spasm can be very severe, may last seconds to hours, radiates to the back, and is frequently indistinguishable from angina. It is important to query the patient about associated dysphagia, weight loss, or hematemesis. Of note, the pain of esophageal spasm and esophagitis may respond to nitroglycerin.

Cholecystitis may be first seen with a pain radiating into the anterior chest. It is usually associated with nausea, vomiting, and tenderness in the right hypochondrium.

Musculoskeletal chest pain is commonly associated with a history of coughing, trauma, injury, or strenuous muscular exertion. The patient may relate a history of the pain’s varying with physical position and being exacerbated by specific thoracic or limb movements. The pain usually is of low
intensity and has a duration of several hours or days.

Chest pain can be classified as noncardiac, atypical, or typical on the basis of the presence of three features: (a) substernal location, (b) provocation with exertion or emotional stress, and (c) relief with nitroglycerin or rest. If all three features are present, the chest pain is termed typical angina; if two are present, it is termed atypical angina; and if only one is present, it is considered noncardiac chest pain.

The great majority of chest pain does not have a life-threatening cause. It is important to identify these patients early to provide effective treatment, allay patient concerns, and use health care resources appropriately.

In patients suspected of having chest pain as a result of epicardial CAD, the physician should determine whether the patient is having an acute coronary syndrome with concomitant myocardial ischemia. The ECG should be compared with a previous ECG obtained during a pain-free episode. If significant changes from the baseline ECG are present (ST-segment elevation/depression, T-wave abnormalities, Q waves, new left bundle branch block), myocardial ischemia is suggested. Unfortunately, a normal ECG or an ECG unchanged from baseline does not necessarily exclude an acute coronary syndrome.

Chest radiographs are generally not necessary diagnostic tests for myocardial ischemia. However, if the patient is complaining of dyspnea or if the pulmonary examination findings are abnormal, a radiograph should be ordered. Occasionally, the chest radiograph may reveal uncommon causes of chest pain, such as pneumothorax or chest masses.

Simple bedside maneuvers may be tried if cautiously interpreted. Anginal pain typically abates completely less than 5 minutes after nitroglycerin administration.
However, the pain of esophageal spasm and esophagitis is also relieved with nitroglycerin but may not completely resolve; a residual dull ache may be found in contrast to ischemic chest pain. A gastrointestinal (GI) “cocktail,” a mixture of antacids and viscous lidocaine, is often used as a diagnostic maneuver. Because of the variety of medications given with the “cocktail,” the possibility of spontaneous, coincidental resolution of ischemic chest pain, and the lack of good data to support this maneuver, it cannot be recommended for the routine evaluation of chest pain. However, if a patient has symptoms that are strongly suggestive of gastrointestinal origin, relief of pain with antacids or a “GI cocktail” may support the clinical diagnosis.

Biochemical cardiac markers are used to diagnose acute myocardial infarction and provide prognosis in unstable angina (11). The commonly available cardiac markers are creatine kinase (CK) and myocardial band (MB) fraction, myoglobin, and troponin I or T (TnI or TnT). Myoglobin is the enzyme most rapidly released after an acute coronary syndrome, its levels peaking within 4 to 6 hours and normalizing within 24 hours, but it is not very specific. CK-MB has traditionally been used to diagnose myocardial infarction; its levels become elevated within 12 hours of infarction, peak at 24 hours, and normalize by 72 hours. However, elevated levels of CK-MB can be found in normal individuals and in those with severe skeletal muscle injury. Troponin levels become elevated within 6 to 12 hours, peak by 48 hours, and can remain elevated for 10 to 14 days after the initial event. Because of their high cardiac specificity, troponins have become the biochemical cardiac markers of choice for diagnosing acute myocardial infarction. However, caution must be used in the interpretation of an elevated troponin level because it may represent a cardiac event that occurred in the preceding 14 days. In these cases, a myoglobin level can be checked. If it is elevated, the troponin elevation is probably a result of a recent cardiac event. However, normal troponin levels do not definitely rule out adverse cardiac outcomes in patients with chest pain. Patients with normal biochemical markers may present without injury and thus will not have biochemical evidence of myocardial necrosis. When an acute coronary syndrome is suspected, acute myocardial infarction should be ruled out by serial troponin or CK-MB measurements. The first troponin measurement should be made on initial presentation, and a second test should be repeated 8 to 12 hours after the original symptom onset. If the patient has recurrent chest pain after the initial episode, or if the first two troponin measurements are indeterminate, further measurements of cardiac enzymes should be considered.