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Tintinalli's Emergency Medicine > Section 7: Cardiovascular Disease > Chapter 49. Approach to Chest Pain >
Overview
Approximately 5 percent of all U.S. ED visits, or about 5 million visits a year, are for chest pain, but accurate diagnosis remains a challenge.1,2 This chapter covers the approach to acute chest pain, with attention to identifying patients with potentially serious disorders.
Pathophysiology of Chest Pain
Stimulation of visceral or somatic afferent pain fibers results in two distinct pain syndromes. The dermis and parietal pleura are innervated by somatic pain fibers, which enter the spinal cord at specific levels and are arranged in dermatomal patterns. Visceral pain fibers are found in internal organs, such as the heart and blood vessels, the esophagus, and the visceral pleura. These visceral pain fibers enter the spinal cord at multiple levels and map to areas on the parietal cortex corresponding to the cord levels shared with the somatic fibers. Pain from somatic fibers is usually easily described, precisely located, and experienced as a sharp sensation, whereas pain from visceral fibers is more difficult to describe and is imprecisely localized. Accordingly, those experiencing visceral pain are more likely to use terms such as discomfort, heaviness, or aching. Patients frequently misinterpret the origin of visceral pain, because it is often referred to a different area of the body corresponding to an adjacent somatic nerve. For example, diaphragmatic irritation can present as shoulder pain, and arm pain may actually represent myocardial ischemia.
Gender, age, comorbidities, medications, drugs, and alcohol may interact with psychological and cultural influences to affect the patient's perception and communication of pain.
Definitions
The phrase acute chest pain, commonly used in emergency medicine, deserves definition. The term acute means of sudden or recent onset. While there is no precise time period defined, in common practice acute means that the patient stops his or her usual activity to seek medical attention, typically within minutes to hours. Some studies of acute chest pain patients in the ED limit entry to those with chest pain of less than 24-h duration. The term chest in this context means a location described by the patient on the anterior thorax, from xiphoid to suprasternal notch and between the right and left midaxillary lines. This is because the major serious thoracic disorders typically manifest symptoms localized to the anterior thorax. While it is true that pain localized to the back, between the base of the neck and the lumbar region, is on the thorax cage, in isolation, pain localized to this region is approached differently (see Chap. 282). That said, there are occasional patients with serious and life-threatening intrathoracic disorders who will manifest a location of their most intense pain outside the boundaries noted above. In addition, some patients may have migratory pain that has moved out of the anterior chest by the time the patient reaches medical attention. Therefore, clinicians are encouraged to include within their differential diagnosis important and significant intrathoracic disorders when patients describe pain in adjacent regions; e.g., epigastric, neck and jaw, and arm. The term pain describes a noxious uncomfortable sensation. However, pain perception and description vary widely, and patients may use terms such as ache or discomfort. Alternative descriptions are common in the elderly. Similar to alternative locations, clinicians should be attuned to variation in the patient's description of the noxious sensation. In summary, acute chest pain refers to (1) recent onset, typically less than 24 h, that causes the patient to seek prompt medical attention, (2) location described on the anterior thorax, and (3) a noxious uncomfortable sensation distressing to the patient.
Initial Approach
The initial approach to acute chest pain recognizes that some causes are serious and life-threatening, and prompt medical attention may prevent death and limit morbidity. Therefore, patients should be triaged promptly. Patients with visceral-type chest pain (defined below), significantly abnormal pulse or blood pressure measurements, or with dyspnea should be placed directly into a treatment bed, a cardiac monitor initiated, an intravenous line established, oxygen administered, and an ECG ordered. Other less well-defined patients also deserve expeditious evaluation, and experienced triage officers and nurses often have a "gut" feeling about certain patients; that insight should be respected.
The initial evaluation should focus on immediate life threats: ensuring adequate airway, breathing, and circulation. The vital signs should be assessed and repeated at regular intervals as determined by the patient's condition. The initial history should focus on specific questions concerning the character of the chest pain, the presence of associated symptoms, and a history of cardiopulmonary conditions. The patient is asked to grade pain intensity in order to follow response to therapy. A 0 to 10 scale is commonly used, with 10 being the worst pain the patient can imagine and 0 being no pain at all. Focused cardiac, pulmonary, and vascular examinations should follow.
If immediate life threats are not detected or have already been addressed, a more extensive evaluation can be preformed. This "secondary survey" consists of a history that defines symptoms more precisely. Chest pain should be assessed like other pain syndromes, with specific questions concerning quality, location, radiation or migration, severity, time and character of onset, progression, provoking factors, relieving factors, and associated symptoms. If the pain has been episodic, the frequency of pain episodes should be assessed over the past weeks to better determine progression. Risk factors for cardiopulmonary disease should be assessed. The physical examination during this phase should complete those body systems not evaluated initially as well as rechecking abnormalities noted before. Many organizations have developed structured history and physician examination forms for acute chest pain to direct the information-gathering process and organize the diagnostic approach. Such structured records are particularly helpful to less experienced physicians. Further diagnostic testing is directed by the history and physical examination.
Categorization
A useful initial approach is to classify patients into three categories: (1) chest wall pain, (2) pleuritic or respiratory chest pain, and (3) visceral chest pain. Chest wall pain is a somatic pain, usually described as sharp in quality, that can be precisely localized (often with one fingertip) and is reproducible by direct palpation and/or chest wall movement during stretching or twisting. Pleuritic chest pain is also a somatic pain, usually described as sharp in quality that is distinctly worsened by breathing or coughing. The term pleuritic is potentially confusing; more than the pleura moves during respiration, and disorders other than "pleurisy" may be worse with respiration. Visceral chest pain is poorly localized and usually described as aching or heaviness. Important causes of chest pain within each category are noted in Table 49-1.
Table 49-1 Important Causes of Acute Chest Pain
Chest Wall Pain Pleuritic Pain Visceral Pain
Costosternal syndrome Pulmonary embolism Typical exertional angina
Costochrondritis (Tietze syndrome) Pneumonia Atypical (nonexertional) angina
Precordial catch syndrome Spontaneous pneumothorax Unstable angina
Slipping rib syndrome Pericarditis Acute myocardial infarction
Xiphodynia Pleurisy Aortic dissection
Radicular syndromes Pericarditis
Intercostal nerve syndromes Esophageal reflux or spasm
Fibromyalgia Esophageal rupture
Mitral valve prolapse
A very useful principle in the clinical assessment of acute chest pain is that, with rare exception, chest pain diagnosis is a composite picture, no one fact or observation make the diagnosis. The challenge to the clinician is to take the often-confusing history and nondiagnostic physician examination and select the useful features that guide further assessment, management, and disposition.
Assessment of risk factors for cardiovascular disease can play a role in patient assessment. Specifically, the presence of risk factors for coronary artery disease (cigarette smoking, diabetes, hypertension, hypercholesterolemia, family history), aortic dissection (middle aged, male gender, hypertension, Marfan syndrome), and pulmonary embolism (hypercoagulable diathesis, malignancy, recent immobilization or surgery) are useful in judging the probability of these diagnoses. Likewise, age can be used to assess the probability of atherosclerotic disease; clinically significant coronary artery disease is rare in patients under the age of 30. Acute cocaine use has been associated with acute myocardial infarction, and chronic cocaine use is associated with accelerated atherosclerosis and severe coronary artery disease (see Chap. 168). However, youth or absence of risk factors does not completely eliminate any potentially serious cause of acute chest pain.
The patient's medical record should be reviewed. The current ECG should be compared with previous tracings. Results of prior cardiac studies (echocardiograms, stress testing, or catheterizations), esophageal studies (endoscopy, oral contrast swallowing studies), gastrointestinal studies (ultrasound, computed tomography), or pulmonary studies (spirometry) should be reviewed and present symptoms interpreted in comparison with these results. In general, cardiac stress studies within the previous 6 months and coronary angiography within the prior 2 years are considered to likely reflect the current state of the coronary circulation.
A practice to be decried is the use of therapeutic trials in acute chest pain; usually in the form of (1) a "gastrointestinal (GI) cocktail" containing an antacid, antispasmodic, and local anesthetic for gastroesophageal reflux, (2) nitroglycerin for myocardial ischemia, and (3) nonsteroidal anti-inflammatories for chest wall pain. The placebo effect makes it difficult to interpret a positive response; patients with definite myocardial ischemia have been reported as experiencing complete pain relief with a GI cocktail. In addition, nitroglycerin is a smooth muscle dilator and may produce relief in esophageal spasm and biliary colic as well as myocardial ischemia. The analgesic properties of nonsteroidal anti-inflammatories are not specific for any location.
Ischemic Equivalents
A confounding observation is that many patients with acute coronary syndrome (ACS, defined below), perhaps as high as 40 percent, do not describe chest pain as their predominant symptom.3 The absence of chest pain leads to delayed or inadequate anti-ischemic therapy and increased inhospital mortality.4
Truly silent myocardial ischemia does occur, but these patients are not likely to come to the ED. For those that do, ischemic equivalents or atypical presentations are important to note: dyspnea at rest or with less exertion compared to the patient's previous baseline; shoulder, arm, or jaw discomfort; nausea; lightheadedness; generalized weakness; acute change in mental status; or diaphoresis. Epigastric or upper abdominal discomfort can be the presenting symptom of myocardial ischemia. Patients with sensory impairment due to diabetes, advanced age, psychiatric disease, or altered mental status are more likely to present with atypical symptoms with ACS. Atypical presentations of ACS also occur more frequently in women and non-white populations compared to white males.5
Differential Diagnosis
When patients present with acute chest pain due to myocardial ischemia, the term acute coronary syndrome, or ACS, is used because, on initial assessment, it is not possible to determine if the patient has an acute myocardial infarction (AMI) or unstable angina (UA). ACS is a common cause of acute chest pain; in a typical ED population of adults over the age of 30 presenting with visceral-type chest pain, about 15 percent will have AMI and 25 to 30 percent will have UA.1
The pain of myocardial ischemia is almost always retrosternal and diffuse, usually described as a heaviness or pressure, and commonly radiates, usually to the neck or left arm (see Chap. 50). In exertional angina, the pain is episodic, lasting minutes (usually 20 min). UA is a potentially serious condition and patients are at high risk for early AMI or death. In AMI, the pain is usually persistent (>20 min), severe, and associated with symptoms of dyspnea, diaphoresis, or nausea.
In ACS, the most useful test is an ECG for both detecting myocardial ischemia and risk stratification. Using the initial ECG, the incidence of AMI is approximately 80 percent for patients with new ST-segment elevation greater than 1 mm in two contiguous leads, about 20 percent in patients with new ST-segment depression or T-wave inversion, but less than 4 percent in patients without either of these two patterns.
Pulmonary embolism is common and life-threatening and is a diagnosis that can be missed in the ED due to the frequently atypical nature of its presentation. Pulmonary embolism can manifest with any combination of chest pain, dyspnea, syncope, shock, and/or hypoxia (see Chap. 56). The pain associated with a PE occurs when inflammation of the parietal pleura overlying the infarction causes chest pain that is generally sharp and related to respiration. Dyspnea, fever, cough, and/or hemoptysis also may be present, and the chest wall may be tender to palpation. Patients with massive PEs often present with unstable vital signs and the classic presentation of sharp, pleuritic chest pain and dyspnea associated with tachypnea, tachycardia, and hypoxemia. A clinical scoring system may be useful in categorizing patients into low (about 10 percent), intermediate (about 40 percent), and high (about 80 percent) prevalence for PE.6
Risk factors for aortic dissection include atherosclerosis, uncontrolled hypertension, coarctation of the aorta, bicuspid aortic valves, aortic stenosis, Marfan syndrome, Ehlers-Danlos syndrome, and pregnancy (see Chap. 58). The pain of aortic dissection, i.e., midline substernal chest pain, is classically described as tearing, ripping, or searing and radiating to the interscapular area of the back. Typically, the pain is at its worst at symptom onset and is often felt above and below the diaphragm. Symptoms of "secondary" pathologies resulting from arterial branch occlusions, such as stroke, AMI, or limb ischemia, may overshadow the clinical presentation of the dissection and make an accurate diagnosis difficult. No combination of clinical factors or chest radiography findings are adequate to exclude the diagnosis of aortic dissection, and specific imaging studies are usually required.7
Spontaneous pneumothorax may occur due to sudden changes in barometric pressure, in smokers or patients with chronic obstructive pulmonary disease or idiopathic pleural bleb disease, or in those with another pulmonary pathology (see Chap. 66). Patients usually complain of a sudden, sharp, lancinating, pleuritic chest pain and dyspnea. Auscultation of the lungs may reveal absence of breath sounds on the ipsilateral side and hyperresonance to percussion, but clinical impression alone is unreliable. Diagnosis of a simple pneumothorax is made by chest radiography.
Esophageal rupture (Boerhaave syndrome) is a rare but potentially life-threatening cause of chest pain. Patients classically present with a history of substernal, sharp chest pain of sudden onset that occurs immediately after an episode of forceful vomiting (see Chap. 75). The patient is usually ill-appearing, dyspneic, and diaphoretic. The physical examination is often normal but may reveal evidence of pneumothorax or subcutaneous air. Chest radiography may be normal or may demonstrate pleural effusion (left more common than right), pneumothorax, pneumomediastinum, pneumoperitoneum, and/or subcutaneous air. The diagnosis can be confirmed by a study with water-soluble contrast.
The pain of acute pericarditis is typically acute, sharp, severe, and constant (see Chap. 55). It is usually described as substernal, with radiation to the back, neck, or shoulders, and is exacerbated by lying down and by inspiration. It is classically described as being relieved by leaning forward. A pericardial friction rub is the most important diagnostic finding. The ECG may show diffuse ST-segment elevation and T-wave inversion. In addition, depression of the PR segment is a highly specific ECG finding for pericarditis.
Pneumonia can produce chest pain or discomfort that is usually sharp and pleuritic (see Chap. 63). It is usually associated with fever, cough, and possibly hypoxia. Physical examination may reveal rales over the affected lobes, decreased breath sounds, and signs of consolidation (i.e., bronchial breath sounds). A chest radiograph confirms the diagnosis.
Mitral valve prolapse (MVP) is the most frequently diagnosed cardiac valvular abnormality and is more commonly diagnosed in women than in men. The discomfort of MVP often occurs at rest, is atypical for myocardial ischemia, and can be associated with dizziness, hyperventilation, anxiety, depression, palpitations, and fatigue (see Chap. 54). The discomfort may be related to papillary muscle tension, and many patients benefit from the administration of -adrenergic blocking agents. Two-dimensional echocardiography is the diagnostic tool of choice and, with physical examination findings, helps to stratify patients into high- and low-risk categories for developing serious complications. Palpitations and every type of supraventricular or ventricular dysrhythmia have been associated with MVP.
Musculoskeletal or chest wall pain syndromes are characterized by highly localized, sharp, positional chest pain. Pain that is completely reproducible by light to moderate palpation of a discrete area of the chest wall often represents pain of musculoskeletal origin, although chest wall tenderness occurs in some patients with PE and myocardial ischemia. Costochondritis is an inflammation of the costal cartilages and/or their sternal articulations and causes chest pain that is variably sharp, dull, and/or increased with respirations. Tietze syndrome is a particular cause of costochondral pain related to fusiform swelling in one or more upper costal cartilages and has a pain pattern similar to that of other costochondral syndromes. Xiphodynia is another inflammatory process that causes sharp, pleuritic chest pain reproduced by light palpation over the xiphoid process. Texidor twinge or precordial catch syndrome is described as a short, lancinating chest discomfort that occurs in episodic bunches lasting 1 to 2 min near the cardiac apex associated with inspiration and poor posture and inactivity.
Gastrointestinal disorders cannot be reliably discriminated from myocardial ischemia by history and examination alone. Dyspepsia syndromes, including gastroesophageal reflux, often produce pain described as burning or gnawing, usually in the lower half of the chest, and often accompanied by a brackish or acidic taste in the back of the mouth (see Chap. 75). The recumbent position usually exacerbates the symptoms, and although the pain is typically relieved with antacids, this therapeutic response also can be observed in myocardial ischemia. Esophageal spasm is often associated with reflux disease and is characterized by a sudden onset of dull, tight, or gripping substernal chest pain, frequently precipitated by the consumption of hot or cold liquids or a large food bolus and often lasting for hours (see Chap. 75). The pain also responds to sublingual nitroglycerin (although supposedly with a slight delay).
Peptic ulcer disease is classically characterized as a postprandial, dull, boring pain in the midepigastric region (see Chap. 77). Patients often describe being awakened from sleep by discomfort. Duodenal ulcer pain is usually relieved after eating food, in contrast to gastric ulcer symptoms, which are often exacerbated by eating. Symptomatic relief is usually achieved by antacid medications. Acute pancreatitis and biliary tract disease present with right upper quadrant or epigastric pain and tenderness but also can present with chest pain.
Panic disorder (PD) is defined as a syndrome characterized by recurrent unexpected panic attacks (discrete periods of intense fear or discomfort) with at least four of the following symptoms: palpitations, diaphoresis, tremor, dyspnea, choking, chest pain or discomfort, nausea, dizziness, derealization or depersonalization, fear of losing control or dying, paresthesias, chills or hot flushes (see Chap. 292). The diagnosis can be made only in the absence of direct physiologic effects of a substance disorder, a general medical condition, or symptoms better accounted for by another mental disorder. Several studies have used standardized screening tools to evaluate ED chest pain patients for PD and have reported an incidence of 17 to 32 percent. In a small trial, investigators found that ED physicians can successfully diagnose PD by using a brief screening procedure, and they suggested that PD patients could benefit from the initiation of specific pharmacologic therapy (serotonin reuptake inhibitors) in the ED.8 Many patients with PD and other anxiety disorders have elevated baseline sympathetic tone, that may be an independent risk factor for coronary artery disease (CAD). In fact, when all ED chest pain patients were screened for PD, 25 percent of those screening positive had a discharge diagnosis of ACS (9.3 percent) or stable angina pectoris (15.7 percent).9 Thus, PD always must be considered a diagnosis of exclusion.
Ancillary Testing
Ancillary testing in acute chest pain generally utilizes electrocardiography, measurement of serum markers of myocardial injury, and/or imaging studies to detect intrathoracic pathology. The specific studies are chosen according to the clinical circumstances. That said, because ACS is the most common potentially serious cause of acute chest pain, clinical studies and common practice focus on the use of the ECG and serum marker measurement to detect or exclude acute myocardial injury. The remainder of this chapter will focus on this topic. The use of ancillary tests in other conditions are discussed in their respective chapters.
Electrocardiography
Due to the importance of early diagnosis of AMI (and, hence, reduced delay of thrombolytic treatment), the American College of Cardiology/American Heart Association (ACC/AHA) guidelines for management of patients with AMI recommend standing orders that all patients with "ischemic-type pain" have a 12-lead ECG performed within 10 min of arrival and that the ECG be handed directly to the treating physician for immediate interpretation.10 Considering the difficulty of defining "ischemic-type" pain and the frequency of atypical presentations, it may be prudent to extend this protocol to all adult patients with chest pain or other symptoms of possible ischemia.
The normal myocardium depolarizes from endocardium to epicardium and repolarizes in the opposite direction. Ischemic myocardium remains electrically less positive than nonischemic myocardium at the end of depolarization. This creates an electrical potential between normal and ischemic myocardium during depolarization and results in ST-segment elevation in an overlying electrode. Conversely, if the electrode is located over normal myocardium opposite an ischemic region, ST-segment depression will be seen. If ischemia is limited to the subendocardial area, an overlying electrode will be separated from the ischemic tissue by a layer of normal myocardium, resulting in an electrical potential pointed inward from the normal to ischemic tissue, resulting in ST-segment depression.
Myocardial ischemia can also delay the repolarization process. In extensive or transmural ischemia, the direction of repolarization is reversed so that recovery occurs from endocardium to epicardium, resulting in T-wave inversions in an overlying electrode. In subendocardial ischemia, the delay does not alter the normal recovery process (epicardium to endocardium), so T waves are not inverted. However, because normal epicardium repolarization is unopposed due to delayed subendocardial repolarization, the T wave in an overlying electrode may be larger than normal (called hyperacute T waves)
After infarction, the area of necrosis is electrically silent, not able to depolarize. During ventricular depolarization, initial electrical activity will be generated in normal myocardium, away from the infarcted area. This results in an electrical potential directed from the infarcted area toward normal myocardium, causing an abnormal initial negative deflection (pathologic Q waves) in the QRS complex of overlying electrodes. Occasionally, small Q waves (called septal Q waves) are seen in the limb or lateral precordial ECG leads. Pathologic Q-waves are distinguished by their duration (greater than 40 ms) and depth (greater than 25 percent of the corresponding R wave).
The ECG is an important tool in the detection of acute infarction and conduction blocks.11 Also, the ECG can help identify the infarct-related artery and help predict reperfusion. The sensitivity of the initial ECG for the diagnosis of AMI has been extensively studied. Approximately half of patients with AMI have diagnostic changes on their initial ECG with new ST-segment elevation greater than 1 mm in two contiguous leads. Another 20 to 30 percent will have new ST-segment or T-wave inversion suggestive of myocardial ischemia. About 10 to 20 percent will have ST-segment depressions and T-wave inversions similar to that seen on previous tracings. About 10 percent have nonspecific ST-segment and T-wave abnormalities. Only about 1 to 5 percent of AMI patients will have a truly normal initial ECG.
The sensitivity of the initial ECG in unstable angina is less well defined, probably because the diagnosis is clinical as there is no "gold standard" against which to evaluate a diagnostic test. In addition, the initial ECG would not be expected to be abnormal if a patient with UA presents during a pain-free period.
The positive predictive value of the different ECG patterns has also been studied. For new ST-segment elevation, the positive predictive value for AMI is about 80 percent. For new ST-segment depression and T-wave inversions, the positive predictive value is about 20 percent for AMI and between 14 and 43 percent for UA. With acute chest pain and an initial ECG showing preexisting ST-segment depressions and T-wave inversions, the positive predictive value is about 4 percent for AMI and 21 to 48 percent for UA. Thus, the standard 12-lead ECG is useful in conjunction with the clinical history for detection of ACS.
Variations on the standard 12-lead ECG have been proposed. One approach uses a continuous 12-lead ECG monitor that records (but does not print) a new 12-lead ECG every 20 s. When the ST-segment baseline is altered from the previous tracing, an alarm is raised and a copy of the new ECG is shared or printed. This technology is potentially useful for monitoring patients with ongoing pain and a nondiagnostic initial ECG.12 Because of the costs, concerns regarding labile ST-segment and T-wave changes from patient movement and respiration, and a lack of ED-based prospective studies, continuous 12-lead ECG monitoring cannot be recommended for routine use.
Electrocardiograms with added leads—for a total of 15, 18, and 22 leads—have been studied. In general, adding more leads increases the sensitivity for AMI detection, but reduces specificity. The only generally agreed upon extension to the standard 12-lead ECG is the use of right-sided precordial leads in the setting of acute inferior myocardial infarction in order to detect right ventricular involvement.13
Risk stratification based on the initial ED ECG also has been suggested as a way of improving ED decision making. Although the initial ECG cannot exclude AMI, stable ED patients whose initial ECG is without ischemic changes are at low risk of subsequent life-threatening complications and usually can be managed in a non-intensive-care setting. Conversely, patients whose initial ECG demonstrates ischemic changes (ST-segment depression or T-wave inversion), even in the absence of confirmed AMI, are at significantly greater risk of short- and long-term morbidity and mortality and should be managed accordingly.
Serum Markers of Myocardial Injury
Creatine Kinase, Creatine Kinase Isoenzymes, and Isoforms
Creatine kinase (CK; adenosine triphosphate creatine N-phosphotransferase) is an intracellular enzyme involved in the transfer of high-energy phosphate groups from ATP to creatine. Although found in small quantities in many tissues, CK is present in large concentrations in cardiac and skeletal muscle and the brain. The enzyme is a dimer composed of two subunits, each of which may be the M (muscle) type or the B (brain) type, thus creating three distinct dimers, or isoenzymes: CK-BB, CK-MM, and CK-MB. Type CK-BB predominates in brain tissue, whereas skeletal muscle consists mostly of CK-MM, in addition to CK-MB in small amounts. The "cardiac isoenzyme," CK-MB, accounts for 14 to 42 percent of total cardiac muscle enzyme activity, thus the predominant enzyme in the heart is actually CK-MM.
The quantitative and temporal patterns of appearance and disappearance of CK and its isoenzymes in the blood occur in a reproducible manner but can vary considerably depending on the amount of CK released from cells, the amount of perfusion of damaged tissues, and the rate of clearance by the reticuloendothelial system. The CK levels usually become abnormally high within 4 to 8 h after coronary artery occlusion (onset of symptoms), peak between 12 and 24 h, and return to normal between 3 and 4 days (Figure 49-1). Reports of the sensitivity of total CK vary from 93 to 100 percent, whereas the specificity is lower (57 to 86 percent), owing to the presence of CK in other tissues. Thus, this marker's usefulness is limited. The CK-MB isoenzyme curve parallels the total CK curve, with levels detectable 4 to 8 h after onset of symptoms (see Figure 49-1). Type CK-MB may peak slightly earlier than total CK, and it is cleared more rapidly, usually within 48 h (vs. 72 to 96 h). Using CK-MB and the ratio of CK-MB to total CK, most studies have reported sensitivity and specificity to be greater than 95 percent. Cutoff values vary between techniques, laboratories, and populations, but CK-MB values in healthy controls may be up to 5 g/L and up to 5 percent of total CK. Historically, CK-MB had been universally adopted as the gold standard for diagnosis of AMI. Although specificity is generally improved over total CK, 37 conditions other than AMI have been associated with elevated CK-MB levels (Table 49-2). Fortunately, most of these conditions can be easily differentiated from AMI on clinical grounds. The relatively rapid return of elevated CK-MB levels to normal is another potential disadvantage, because of the possibility of missing the diagnosis in patients presenting later in the course of AMI. However, this rapid clearance may be used to a different advantage, because it enables the identification of infarct extension and reinfarction.
Fig. 49-1.
Typical pattern of serum marker elevation after AMI. Abbreviations: CK-MB =creatine kinase-MB isoenzyme; cTnI = cardiac troponin I; cTnT = cardiac troponin T; LD1 = lactate dehydrogenase isoenzyme 1; MLC = myosin light chain.
Table 49-2 Conditions Associated with Elevated CK-MB Levels
Common Uncommon Rare Unclear
Unstable angina, acute coronary ischemia Congestive heart failure Isolated case in normal person Acromegaly
Inflammatory heart diseases Coronary artery disease after stress test Hypothermia
Cardiomyopathies Angina pectoris Rocky Mountain spotted fever
Circulatory failure and shock Valvular defects Typhoid fever
Cardiac surgery Tachycardia Chronic bronchitis
Cardiac trauma Cardiac catheterization Lumbago
Skeletal muscle trauma (severe) Electrical countershock Febrile disorder
Dermatomyositis, polymyositis Noncardiac surgery
Myopathic disorders Brain and head trauma
Muscular dystrophy, especially Duchenne Peripartum period
Extreme exercise Miscellaneous drug overdoses
Malignant hyperthermia CO poisoning
Reye syndrome Prostatic cancer
Rhabdomyolysis of any cause
Delirium tremens
Ethanol poisoning (chronic)
Abbreviation: CK-MB =creatine kinase, subunits muscle and brain.
The 4- to 8-h delay in CK-MB detection after onset of symptoms has been overcome in part with the development of rapid assays for CK-MB isoforms (subforms). The isoenzymes CK-MM, CK-MB, and CK-BB are dimeric molecules consisting of three different combinations of two monomers, M and B. On its release from damaged cells, the M monomer found in tissue CK (Mt) is acted on by an enzyme present in serum, carboxypeptidase N, which cleaves off the C-terminal lysine. This action results in its conversion into the M monomer found in serum CK (Ms). Newly released unmodified CK-MtB (or CK-MB2) is enzymatically changed into CK-MsB (or CK-MB1). Because the rate of this conversion is limited, CK-MB2 activity reflects new recent release into the serum. By measuring MB2 activity (>1 U/L) and the MB2:MB1 ratio (>1.5), infarction can be detected before the total level of CK-MB exceeds the normal range. Although this method has reported early ( ................
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