The History

The Big Heart Disease Lie

How I Healed my Cardiovascular Disease

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Elements of Accurate History Taking

A carefully obtained history is the cornerstone in the evaluation of a patient with known or suspected cardiac disease.1,2 A deliberate, compassionate interview forms the basis for a patient-physician relationship that may continue for days, months, or years. Unfortunately, the interview may result in adversary roles for physician and patient if the interviewer appears hurried, demands exact answers, shows impatience, insists on exploring areas that are uncomfortable to the patient, fails to establish eye contact, accepts multiple interruptions during the discussion, seems to treat dreaded diseases casually, gives nonverbal signs of personal unhappiness, or appears to be unsympathetic.2 When the medical interview is unsatisfactory due to poor communication and lack of rapport, inaccurate information often will be obtained.2 Also, important facts not revealed during a meticulous initial history usually are not detected later as workup progresses and the patient and physician become focused on high-technology studies and more aggressive therapeutic interventions.1

The patient's chief complaint, which requires further elaboration and investigation, may not identify the patient's most serious problem. Symptoms other than the patient's chief complaint must be defined.2 Rather than focusing entirely on the patient's present illness, the interviewer should note all existing symptoms and establish a present illness for each of these.2

A medical questionnaire given to the patient well in advance of the interview is useful. The patient can then record important data more accurately because of the time available for reflection and the checking of details.2 Any abnormalities indicated on the questionnaire must be defined more completely during the interview, and related areas should be discussed.2

A proper interpretation of the past history is important, and the physician should not accept a past event as a fact when the evidence is not well established. Knowledge obtained from family members about the patient's symptoms and his or her response to the illness is extremely important.2

Importantly, serious heart disease can occur in patients with mild or no symptoms. Also, knowing the sensitivity, specificity, and predictive value of an answer to a question and of the presence or absence of a physical sign provides the physician with a better perspective. The physician must determine whether or not the history obtained is sufficient to support a decision-making process about the patient.2 While many patients with severe heart disease have no symptoms, others have many symptoms associated with minor or no disease.

Some patients deny the presence of symptoms because they cannot accept the reality of the situation, whereas others may purposefully withhold information because they may lose their jobs if the truth were revealed.2 Still other patients may overstate their symptoms for personal gain. Elderly patients, sedentary patients, and patients whose physical activity is limited by another illness may have no symptoms because they do not perform adequate physical effort to produce them.2

Past and Family History

The past history may provide important clues to the presence of cardiovascular disease. A definite history of rheumatic fever may be useful in defining the cause of a heart murmur, whereas a negative history of rheumatic fever does not exclude it.2 A history of hypertension in a family member increases the likelihood that the patient has essential hypertension.2 Previous trauma may be the cause of constrictive pericarditis, a thoracic aortic aneurysm, an arteriovenous fistula, and other types of cardiac lesions. A detailed history of the use of medications, addicting drugs, and alcohol, each of which may cause heart disease, is essential. A past history of pulmonary embolism, thrombophlebitis, or systemic embolism should be ascertained.

A history of dental work, some other diagnostic or therapeutic procedure, or recent infection suggests the possibility of infective endocarditis in a patient with valvular heart disease. Patients often give a history of having had a "heart attack," which, in fact, may have been an episode of unstable angina, heart failure, or arrhythmia. The "heart attack" history often becomes "myocardial infarction" in the patient's medical record unless more information about the episode is obtained or documentation of the event is reviewed.1

Many patients are referred who have had several catheterizations, percutaneous coronary interventions, angioplasties, and one or more coronary bypass operations in addition to multiple noninvasive tests. A thorough and often time-consuming review of records from other institutions, operative notes, cineangiographic films, and noninvasive studies often will provide an accurate assessment of the patient's current status without the unnecessary repetition of expensive and potentially risky procedures.!

Past and present therapeutic regimens must be reviewed carefully. Various treatment programs may have been inappropriate or suboptimal. The drugs currently used for the treatment of cardiovascular diseases have a larger number of potential side effects that can result in both cardiovascular and noncardiovascular symptoms (see Chap. 81).

Multiple risk factors for developing coronary artery disease (CAD) have been identified, including age, male sex, hypertension, hypercholesterolemia, low high-density lipoprotein (HDL) cholesterol, cigarette smoking, diabetes, and a family history of premature atherosclerosis (see Chap. 38). The presence or absence of risk factors can increase or decrease the statistical likelihood that an individual patient has CHD.

Patients should be questioned about previous health evaluations. In addition to being examined at the time of routine physicals or in association with other medical treatment, patients often have been examined for the military service, for athletics, or for insurance, and they may have been told of a heart murmur or hypertension on those occasions.2 Rejection by the military or an insurance company is often due to a cardiovascular abnormality. Many patients have not seen a physician in the recent past or ever had a careful examination of the cardiovascular system.

The increasing hemodynamic burden of pregnancy may cause an otherwise marginally compensated (2 / 16) [2003-1-4 12:15:39]

cardiac patient to become symptomatic. Specific inquiry should be made about heart failure, edema, dyspnea, or prescribed prolonged periods of bed rest during pregnancy.1 Many normal women have had a murmur detected during pregnancy (see Chap. 82). A history of illicit parenteral drug use should raise the suspicion of infective endocarditis, especially in a febrile patient (see Chap. 73). Cocaine can cause coronary artery vasospasm and also raise myocardial oxygen demand by increasing heart rate and blood pressure. Angina, myocardial infarction, and sudden cardiac death have been well documented after cocaine use (see Chap. 71).

A history of moderate to excessive alcohol consumption, an enlarged heart on prior chest roentgenogram, periods of rapid weight gain or loss, and other illnesses may provide important information, as may questions concerning prior diagnoses made by the patient or by medical personnel.1

A family history of congenital heart disease indicates a higher risk of a congenital heart lesion (see Chap. 63). The patient's mother may give a history of rubella during the first few months of pregnancy; this increases the likelihood that the patient has patent ductus arteriosus, pulmonic valve stenosis, coarctation of the pulmonary arteries, or atrial septal defect.

Although most of the common cardiovascular diseases are sporadic, there are several examples in which genetic transmission can occur (see Chap. 62). These include mitral valve prolapse and the hypertrophic or dilated cardiomyopathies. Other genetically determined disorders include some of the inborn errors of metabolism, muscular dystrophies, Ehlers-Danlos syndrome, Marfan's syndrome, and the long Q-T syndromes with or without deafness (see Chaps. 62 and 63).

Symptoms Associated with Cardiovascular Disease CHEST PAIN

Chest pain or chest discomfort is the foremost manifestation of myocardial ischemia and results from a disparity between myocardial oxygen demand and coronary blood flow in patients with CAD.3 The most common causes of myocardial ischemia are coronary atherosclerosis, coronary vasoconstriction, and coronary artery thrombosis, the latter occurring particularly in patients with acute coronary syndromes such as acute myocardial infarction and unstable angina (see Chaps. 41 and 42). An increase in myocardial oxygen demand (MV(r)O2) or demand ischemia, a decrease in or inadequate blood flow (supply ischemia), or their combination may be responsible for anginal chest pain (see Chap. 40).

The mechanism responsible for cardiac pain is not clearly understood. Nonmedullated small sympathetic nerve fibers that parallel the coronary arteries are thought to provide the afferent sensory pathway for angina; these enter the spinal cord in the C8-T4 segments.4 Impulses are transmitted to corresponding spinal ganglia and then through the spinal cord to the thalamus and cerebral cortex. Angina pectoris, like other pain of visceral origin, is often poorly localized and is commonly referred to the corresponding segmental dermatomes.

The differential diagnosis of chest pain is extensive.5 In addition to angina pectoris and myocardial infarction, other cardiovascular diseases, gastrointestinal diseases, psychogenic diseases, neuromuscular diseases, and diseases of the pulmonary system must be considered (Table 10-1; see also Q+S; Table 406). An accurate interpretation of the etiology and significance of chest discomfort is critically dependent on a carefully taken history. Important clinically relevant information may be missed if the overenthusiastic use of noninvasive or invasive diagnostic methods replaces rather than augments direct physician-patient communication (see Chap. 40).

Table 10-1: Differential Diagnosis of Chest Pain

1. Angina pectoris/myocardial infarction

2. Other cardiovascular causes a. Likely ischemic in origin

(1) Aortic stenosis

(2) Hypertrophic cardiomyopathy

(3) Severe systemic hypertension

(4) Severe right ventricular hypertension

(5) Aortic regurgitation

(6) Severe anemia/hypoxia b. Nonischemic in origin

(1) Aortic dissection

(2) Pericarditis

(3) Mitral valve prolapse

3. Gastrointestinal a. Esophageal spasm b. Esophageal reflux c. Esophageal rupture d. Peptic ulcer disease

4. Psychogenic a. Anxiety b. Depression c. Cardiac psychosis d. Self-gain

5. Neuromusculoskeletal a. Thoracic outlet syndrome b. Degenerative joint disease of cervical/thoracic spine c. Costochondritis (Tietze's syndrome)

d. Herpes zoster e. Chest wall pain and tenderness

6. Pulmonary a. Pulmonary embolus with or without pulmonary infarction b. Pneumothorax c. Pneumonia with pleural involvement

7. Pleurisy

The original subjective description of angina pectoris by William Heberden6 in the late eighteenth century has not been surpassed. It is quoted in Chap. 40.

Angina pectoris is defined as chest pain or discomfort of cardiac origin that usually results from a temporary imbalance between myocardial oxygen supply and demand. It may occur only with exertion or spontaneously at rest; various subtypes are defined in Chap. 40. The quality of the chest discomfort is usually described as "tightness," "pressure," "burning," "heaviness," "aching," "strangling," or "compression." Usually the patient is able to describe a deep rather than a superficial origin of the pain. Since the qualitative description of the pain is greatly influenced by the patient's intelligence, education, and social/cultural background, a definition of other characteristics of the chest discomfort is often extremely important in evaluating the symptoms appropriately. The most important of these characteristics are the precipitating factors for the onset of pain, its mode of onset and duration, its pattern of disappearance, and its location. Classically, the discomfort is induced by exercise, emotion, eating, or cold weather.

A recognizable pattern of reproducibility of chest pain by certain activities is an important characteristic of angina. Often, patients develop pain with exertion after meals, and there is a greater tendency for arm work, which involves a greater element of isometric exercise than isotonic leg exercise, to produce distress.7-9 Occasionally, angina will dissipate despite continued exercise (the walk-through phenomenon) or will not occur when a second exercise effort is undertaken that previously produced chest discomfort (warm-up phenomenon).

Both circumstances may be attributed to the opening of functioning coronary arterial collaterals during the initial myocardial ischemia. Angina commonly occurs after the patient has eaten a heavy meal or when the patient is excited, angry, or tense. Cold showers increase blood pressure and heart rate, whereas hot showers cause an augmented cardiac output in response to vasodilation. Either may precipitate angina after exercise. The chest pain during any type of activity is often made worse by the use of tobacco. All the hemodynamic changes resulting from the use of nicotine increase the myocardial oxygen demand.

Angina pectoris characteristically has a crescendo pattern at onset and "builds up." Pains, often described as "shooting" or "stabbing," that reach their maximum intensity virtually instantaneously are often not angina but are of musculoskeletal or neural origin. Angina is usually relieved within 5 to 20 min by rest, with or without the use of vasodilator drugs such as nitroglycerin, although nitroglycerin characteristically hastens relief. Failure to obtain relief with rest or nitroglycerin suggests another cause of pain or actual impending myocardial infarction. The reproducible relief of chest pain in an appropriate time frame (within 10 min) can be strong evidence favoring ischemia. A trial of nitroglycerin can be a useful diagnostic strategy. Patients with angina pectoris usually are classified functionally from class I to class IV (Table 10-2), depending on the amount of activity necessary to induce chest pain.10

Table 10-2: Canadian Cardiovascular Society Functional Classification of Angina Pectoris

I. Ordinary physical activity, such as walking and climbing stairs, does not cause angina. Angina results from strenuous or rapid or prolonged exertion at work or recreation.

II. Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, in wind, or when under emotional stress, or only during the few hours after awakening. Walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and under normal conditions.

III. Marked limitations of ordinary physical activity. Walking one to two blocks on the level and climbing more than one flight under normal conditions.

IV. Inability to carry on any physical activity without discomfort-anginal syndrome may be present at rest.

Source: Modified from Campeau L. Letter to the editor. Circulation 1976; 54:522. Reproduced with permission from the American Heart Association, Inc., and the author.

Localizing the site of chest discomfort provides additional information in determining its cause. Anginal pain is ordinarily retrosternal or felt slightly to left of the midline, beside or partly under the sternum. It is rarely isolated to the cardiac apex in the inframammary region. The chest pain of myocardial ischemia tends to radiate bilaterally across the chest into the arms (left more than right) and into the neck and lower jaw. Occasionally, radiation to the back or occiput is noted. In the arms, the pain passes down the ulnar and volar surface to the wrist and then only into the ulnar fingers, rarely into the thumb or down the outer (extensor) surface of the arm, which has a different dermatome pattern. Pain occasionally may be felt only in the arm or may start in the arm and radiate to the chest. Attention to the gestures that the patient uses in characterizing and localizing the site of pain may be useful in determining its etiology. One or two clenched fists held by the patient over the sternal area (Levine's sign) is much more indicative of ischemic pain than is a finger pointed to a small, circumscribed area in the left inframammary region. The latter more likely represents chest pain of psychogenic origin.

As indicated earlier, the duration of chest pain also may be a useful differentiating feature. Angina pectoris rarely lasts less than 1 min or more than 20 min in the absence of myocardial infarction or persistent arrhythmias. Most patients with angina report prompt relief in less than 5 min after cessation of activity or with the use of sublingual nitroglycerin. Delayed relief of chest pain by sublingual nitroglycerin may be ascribed to a placebo effect. Since nitrates are generalized smooth muscle relaxants, pain due to diffuse esophageal spasm or biliary colic also may be relieved by these same agents. Carotid sinus massage by the physician frequently will relieve anginal chest pain because of the resulting reflex bradycardia and the decrease in systolic blood pressure, thus reducing myocardial oxygen demand.!! Carotid sinus massage should be performed only in the absence of extracranial occlusive cerebrovascular disease as manifest by carotid bruits or decreased carotid arterial pulsations and with careful auscultatory monitoring of the heart rate. The Valsalva maneuver also may relieve anginal pain by decreasing myocardial wall tension as a result of the reduced venous return and left ventricular volume accompanying the increase in intrathoracic pressure. Associated symptoms-such as nausea, vomiting, faintness, fatigue, or diaphoresis-often accompany severe episodes of myocardial ischemia in both men and women.12 Severe myocardial ischemia often produces marked dyspnea due to a large increase in left ventricular (LV) diastolic filling pressure, sometimes producing an "angina equivalent" in the absence of chest discomfort.

Linked angina is a term applied to definite episodes of angina in patients with established CAD caused by gastrointestinal factors not related to an increase in cardiac work.13 Episodes typically are induced by stooping or occur after eating; they can be mimicked by esophageal acid stimulation, which can reduce coronary blood flow (CBF).13

No consideration of myocardial ischemia as a likely cause of chest discomfort is complete without carefully considering the chest pain in the context of known risk factors for CAD (see above).

Angina pectoris should be considered a symptom and not a specific disease. Coronary arteriographic (6 / 16) [2003-1-4 12:15:39]

studies have demonstrated that more than 90 percent of patients with chest pain precipitated by exercise and relieved by rest have angiographic evidence of significant CAD. However, other diseases may be associated with classic angina pectoris (see below).

Several reports have described certain patients with typical exertional chest discomfort and arteriographically normal coronary arteries.1415 These patients are more likely to be females, have fewer coronary risk factors, have variable responses to various antianginal agents, and less commonly, have more relief of pain by sublingual nitroglycerin than patients with occlusive CAD. Although the underlying cause of this condition remains unsettled, the life expectancy of these patients appears no different from that of an age- and sex-matched population without chest discomfort (see Chap. 40).

There is some evidence that abnormal function of small coronary arteries may cause limited CBF responses to stress or pharmacologic vasodilators in a subset of patients with anginal chest pain despite angiographically normal coronary arteries (microvascular angina).16-22 In the past, investigators arguing for or against the existence of this syndrome often have used the term syndrome X to describe their patient cohort.23 Syndrome X appears to include a heterogeneous group of patients with a wide spectrum of chest pain and a variety of vascular and smooth muscle hypersensitive constrictor responses. Multiple research studies continue in an effort to explain syndrome X.24-30 It should be distinguished from the metabolic syndrome X of insulin resistance (glucose intolerance), hypertension, hyperlipidemia, and upper body obesity (see Chaps. 40 and 78).

Some patients with CAD experience angina at rest as a complication or an isolated clinical manifestation of ischemic heart disease.11 Myocardial ischemic pain at rest more likely results from an acute reduction in CBF than from an increase in MV(r)O2. Possible causative factors include isolated coronary artery spasm or embolism, coronary artery spasm superimposed on coronary atherosclerosis, and coronary thrombosis with spontaneous thrombolysis.31-34 In patients with progressive coronary atherosclerosis, however, ischemic rest pain also may result from intermittent arrhythmias that increase MV(r)O2 or decrease CBF or from labile hypertension with its increased wall stress. Chest pain at rest may occur only as nocturnal angina. In addition to the preceding mechanisms, nocturnal angina, also known as angina decubitus, may be produced by the increase in wall stress and thus MV(r)O2 secondary to redistribution of the intravascular blood volume in the recumbent position.

The relative hypercapnia and acidosis that occur during sleep also may contribute to nocturnal angina. This condition also has been accompanied by concomitant rapid eye movement sleep patterns on the electroencephalogram, which may be associated with augmented sympathetic discharge increasing MV(r)O2 or causing coronary constriction8-11 (see Chap. 40).

Despite the more malignant natural history observed in many patients with rest angina, particularly associated with ST-T-wave changes, the predictive value of the history alone is not as accurate as with exertional angina. The quality of pain is usually similar to that of exertional angina, but the discomfort may be more severe and its duration longer. In addition, angina at rest is commonly associated with nausea, vomiting, and diaphoresis. The onset of shortness of breath during or after the beginning of chest discomfort suggests that the pain is due to extensive myocardial ischemia and usually results from an acute elevation of LV filling pressure secondary to the development of a large, transiently ischemic myocardial segment. Such patients are commonly found to have multivessel occlusive CAD on arteriography.

Chest pain or discomfort resulting from myocardial infarction (MI) is qualitatively similar to angina at rest. Differentiation between the pain resulting from ischemia and that due to MI is usually impossible based on the history alone.7-9 Pain associated with transmural Q-wave MI is usually more severe and longer lasting than anginal pain and is often associated with nausea, vomiting, and diaphoresis. In addition, MI is frequently accompanied by symptoms of sustained LV dysfunction (dyspnea, orthopnea) and evidence of autonomic nervous system hyperactivity (tachycardia, diaphoresis, bradycardia).7-9 Painless or atypical presentations of MI, however, occur in up to 30 percent of patients, particularly in diabetic patients and the elderly. Thus determination of serial serum enzymes, isoenzymes, and other serum markers (e.g., troponin I), providing evidence of myocardial necrosis, and serial electrocardiograms (ECGs), indicating myocardial injury, are necessary to establish the diagnosis in most patients (see Chaps. 42 and 43).

There are two groups of cardiovascular diseases causing chest pain that is not due to coronary atherosclerosis (see Table 10-1). The first group consists of cardiac diseases causing myocardial ischemia-related angina in the absence of CAD; ischemia is due to hemodynamic changes associated with an inadequate CBF in relation to a normal or increased myocardial oxygen demand. Among these are aortic valve stenosis (see Chap. 56), hypertrophic cardiomyopathy (see Chap. 67), and systemic arterial hypertension (see Chap. 51), in which LV systolic pressure and LV wall tension are greatly increased or LV hypertrophy is present.7-9 Chest pain due to myocardial ischemia also can occur with severe aortic regurgitation (see Chap. 56). The large ventricular volume load and increased ventricular dimensions result in increased MV(r)O2, and the reduced diastolic perfusion pressure of the coronary arteries results in a relatively inadequate CBF. Occasionally, very severe anemia or hypoxia also may produce myocardial ischemia by an inadequate oxygen blood supply even in the absence of associated CAD as well as increases in angina in the presence of obstructive coronary artery disease.7-9 In addition, severe right ventricular (RV) systolic hypertension, as often occurs with pulmonic stenosis or pulmonary hypertension, may cause exertional angina, presumably on the basis of RV subendocardial ischemia.35

A second group of cardiac diseases causing chest pain that is not usually due to myocardial ischemia includes pericarditis (see Chap. 72), aortic dissection (see Chap. 88), and mitral valve prolapse (see Chap. 58). Pericarditis is a relatively common cause of chest pain.36 The chest pain of pericarditis is most often sharp and penetrating in quality, and patients often obtain relief by sitting up and bending forward (see Chap. 72). The cardinal diagnostic feature of pericardial pain is its frequent worsening by changes in body position, during deep inspiration, and occasionally, on swallowing. The chest discomfort may radiate to the shoulders, upper back, and neck because of irritation of the diaphragmatic pleura, which is innervated through the phrenic nerve by fibers originating in cervical sympathetic ganglia C3-C5. Therefore, the chest discomfort associated with pericarditis is due predominantly to parietal pleural irritation. Occasionally, the pain of acute benign, presumptive viral pericarditis may mimic that observed in acute MI. Importantly, the most common cause of pericarditis in middle-aged or older people is acute MI. The pericarditis usually occurs several days after the myocardial necrosis and must be distinguished from recurrent infarction or ischemia. Pericarditis also may be a cause of chest pain after cardiac surgery and may be a complication of aortic dissection, with leakage into the pericardium.

Aortic dissection (see Chap. 88) may be misdiagnosed on initial presentation as an acute MI; indeed, MI is a recognized complication of aortic dissection. The pain with dissection, however, is usually of sudden onset as compared with the pain of myocardial ischemia, which builds in intensity with time.37 Patients frequently characterize the pain as excruciating, the most severe discomfort that they have ever experienced, and as having a tearing quality, commonly localized to the interscapular area. The discomfort may radiate widely into the neck, back, abdomen, flanks, and legs and may migrate, depending on the location and progression of the aortic dissection and the amount of arterial luminal compression. Neurologic symptoms and signs may occur when dissection involves the cerebral arteries. With the exception of patients with Marfan's syndrome (see Chaps. 66 and 76) or idiopathic cystic medial necrosis, most patients with aortic dissection have a history of long-standing systemic arterial hypertension or evidence of it on physical examination.

Psychogenic chest discomfort is a common type of recurrent chest pain that may be difficult to separate from angina pectoris, particularly when it occurs in patients with multiple risk factors for CAD or in otherwise asymptomatic patients with well-documented CAD. The most common psychogenic cause of chest discomfort is anxiety38 (see Chap. 80). Psychogenic chest pain is often described as sharp or stabbing, is commonly localized to the left inframammary area, and is usually sharply circumscribed. Descriptors such as "stabbing" or "lightning-like" may be used to describe extremely short (<1 min) episodes of pain. At times, the pain may persist for many hours or several days. Patients often note psychogenic pain at rest. Also, nonvocal communication, such as a flat or worried facial expression, retarded motor activity, and hand wringing, may indicate underlying depression. Observation of the patient during pain that occurs spontaneously or during exercise testing often provides insight into a potential psychogenic etiology. Patients with anxiety often have multiple complaints such as breathlessness, giddiness, and palpitations. Associated symptoms, such as air hunger, circumoral paresthesias, globus hystericus, and multiple somatic complaints, may suggest a neurasthenic personality or hyperventilation syndrome.

Pain originating in the gastrointestinal tract, particularly that of esophageal origin, is commonly confused with ischemic chest pain.39 Diffuse esophageal spasm, a neuromuscular motor disorder of the esophagus characterized by chest pain, is the extracardiac condition most frequently confused with angina pectoris. Esophageal spasm may occur at any age but is more common in individuals in the fifth decade. The pain is usually retrosternal; may be burning, squeezing, or aching in quality; and often radiates to the back, arms, and jaw. It usually begins during or after a meal and can last minutes or hours. In some patients, the pain may be precipitated or exacerbated by exercise, and relief may be obtained with nitroglycerin, which also relaxes esophageal smooth muscle. A useful feature in the differentiation of diffuse esophageal spasm from ischemic chest discomfort is its frequent association with pain as a result of swallowing, dysphagia, and the regurgitation of gastric contents. Episodes of pain frequently are precipitated either by extremely hot or cold drinks or by an emotional upset. The diagnosis of diffuse esophageal spasm is based on the history, the exclusion of cardiac and musculoskeletal causes of chest pain, and the demonstration of abnormal esophageal motility on cineesophagograms or by esophageal manometry.

Reflux esophagitis results from mucosal irritation produced by failure of the lower esophageal sphincter to prevent regurgitation of highly acidic gastric contents into the distal esophagus.40-42 The pain is usually epigastric or retrosternal, burning in quality, and frequently precipitated by the recumbent position or by bending over. "Heartburn" and regurgitation often occur after meals or ingestion of coffee or after postural changes. Patients are often awakened by chest discomfort due to acid reflux occurring in the recumbent position. Many of these patients are obese and report relief of discomfort from food, antacids, or elevation of the head of the bed. Dysphagia may result from stricture formation secondary to long-standing esophageal reflux. An upper gastrointestinal series may demonstrate hiatal hernia, but this does not establish the diagnosis of esophagitis or esophageal reflux. Esophagoscopy and esophageal biopsy may demonstrate mucosal lesions and are useful for assessing the severity of inflammation and for excluding malignancy. Sphincter incompetence may be documented by the use of esophageal manometry. Esophageal acid perfusion testing (Bernstein test) often will provoke the patient's characteristic symptoms, and distal esophageal pH monitoring will detect gastroesophageal reflux.41

Acute esophageal rupture, a serious and often rapidly lethal event, causes severe retrosternal pain secondary to the chemical mediastinitis produced by acidic gastric contents.7-9 Spontaneous rupture usually results from a prolonged bout of vomiting or retching after a heavy meal. Rupture is a recognized iatrogenic complication of esophageal instrumentation. The pain varies in location depending on the rupture's site and position. The diagnosis is based on symptoms and signs of mediastinal air following vomiting or esophageal instrumentation.

Although peptic ulcer disease and biliary colic are less commonly confused with chest pain of cardiac origin, myocardial ischemic pain occasionally may be described as burning in character and located near the epigastrium.

Diseases involving the neuromuscular-skeletal systems may cause pain affecting dermatome patterns similar to those occurring with angina pectoris.7-9 The thoracic outlet syndromes, in which various neural and vascular structures are compressed, may produce symptoms that are sometimes confused with cardiac chest pain. Although compression of the neurovascular bundle by a cervical rib or the scalenus anterior muscle may cause discomfort radiating to the head and neck, the shoulder region, or the axilla, most patients experience pain in the upper extremity resulting from somatic nerve compression, usually in the distribution of the ulnar nerve.8-44 The presence of associated paresthesias, the presence of pain unrelated to physical exercise, the worsening of discomfort, and its aggravation by certain body positions are useful differentiating characteristics. The diagnosis of thoracic outlet syndrome can be confirmed in many patients by careful physical and neurologic examination.

Tietze's syndrome, or idiopathic costochondritis, is an occasional cause of anterior chest wall pain that is aggravated by movement and deep breathing. The reproduction of the chest pain syndrome by direct pressure over the involved costochondral junction or the relief of pain after local infiltration with lidocaine is a helpful diagnostic maneuver.43 Degenerative arthritis of the cervical and thoracic vertebrae may cause bandlike pain confined to the chest, neck, or back that often radiates to the arms.7-9 Radiologic evidence of degenerative changes involving the cervical and thoracic vertebrae is often found in asymptomatic elderly patients. The production or exacerbation of pain by various postures, movement, sneezing, or coughing is more useful in the diagnosis of chest discomfort due to vertebral disease.7-9

The preeruptive stage of herpes zoster may be characterized by bandlike chest pain over one or more dermatomes. The advanced age of the patient, additional symptoms of malaise, headache and fever, the presence of hyperesthesia of the involved area on physical examination, and the eventual eruption of typical lesions 4 or 5 days after the onset of symptoms will result in the correct diagnosis. Chest wall pain and tenderness may occur for unknown reasons.44 The discomfort may be reproduced by pressure over the painful area and by movements of the thorax such as bending, twisting, or turning. The variable duration of the pain and the absence of relief by nitroglycerin distinguish it from angina.

The syndrome of acute massive pulmonary embolism with its associated acute pulmonary hypertension and low cardiac output occasionally may simulate acute MI, since myocardial ischemia may be present in both conditions. The quality of chest pain may be identical to that observed in patients with nonradiating ischemic chest pain or may be pleuritic, as described below. The associated signs of severe dyspnea, tachypnea, and intense cyanosis, accompanied by profound anxiety and agitation, however, favor the diagnosis of pulmonary embolism8-11 (see Chap. 54). The clinical setting may suggest the diagnosis because of the known increased likelihood of pulmonary embolism in the postpartum or postoperative state, during long trips, in patients with congestive heart failure and peripheral edema, and in those with deep-vein thrombophlebitis. Measurements of arterial blood gases, abnormal pulmonary perfusion-ventilation scans, and if needed, pulmonary arteriography will establish the correct diagnosis.7-9

Other pulmonary conditions associated with chest discomfort, such as pneumothorax, are rarely confused with ischemic chest pain because of additional characteristic clinical features. Spontaneous pneumothorax usually occurs in otherwise healthy males in the third and fourth decades. The clinical presentation is usually characterized by the abrupt onset of agonizing unilateral pleuritic chest pain associated with severe shortness of breath. The plain or expiratory chest film provides the definitive diagnosis. Chest pain associated with pneumonias of various etiologies, as well as pulmonary infarctions as a consequence of pulmonary embolus, may result from pleural irritation. The discomfort is sharp, varies acutely with breathing, and frequently is accompanied by a reduced inspiratory effort. Associated signs of pulmonary parenchymal infection or infarction usually indicate the underlying diagnosis.

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