Causes of Chronic Chest Pain

The leading diagnostic consideration in patients with chronic chest pain is coronary artery disease. The commonest clinical presentation of coronary artery disease is recurrent angina pectoris. A helpful diagnostic feature of coronary artery disease is that the pain usually improves with specific medications. Relief of anginal pain within 3 minutes of taking sublingual nitroglycerin is strong evidence that coronary disease has caused the pain.

Decreased frequency of attacks after starting a beta blocker, calcium channel blocker, or long-acting nitrate preparation suggests that coronary artery disease is the cause.

Esophageal disease is a common cause of recurrent chest pain. Esophagitis, usually secondary to acid reflux from the stomach, frequently causes esophageal pain. The acid causes chemical damage and inflammation of the mucosa, resulting in pain that often has a burning quality. Clues to the presence of reflux esophagitis include a history of acid–peptic disease and symptoms of reflux, such as regurgitation or acid taste in the mouth. Chest pain caused by esophageal reflux tends to occur after meals and may be related to body position. Episodes of pain can be induced by bending over at the waist. They often occur at night, because the recumbent posture enhances reflux of acid into the esophagus. Relief of pain by antacids, topical lidocaine, or by specific maneuvers to reduce reflux suggests this diagnosis.

Esophageal motor disorders also commonly cause chest pain. While reflux esophagitis causes pain by irritation of the esophageal mucosa, motor disorders cause pain by contraction and spasm of the muscular wall of the esophagus. Esophageal spasm often occurs as a secondary manifestation of reflux esophagitis. As mucosal irritation and inflammation become more severe, the stimulation of local nerves leads to muscular spasm. Such patients will report a pattern of pain similar to that seen in reflux esophagitis, occurring after meals and aggravated by body position. Patients may report varying qualities of pain. With episodes of simple mucosal irritation, the pain may be reported as "heartburn," while the pain is reported as having a more severe, heavy quality during episodes of muscular spasm. Esophageal motor disorders can be independent of acid reflux disease, as in patients with achalasia or diffuse esophageal spasm. These patients show a different pattern of episodes than occurs in patients with acid reflux. The pain usually is unrelated to body position and may occur while eating instead of after meals. Dysphagia is frequently a prominent symptom in patients with primary motor disorders.

Esophageal motor disorders may be relieved by nitrates and calcium channel blockers, via relaxation of the smooth muscle wall of the esophagus. Because these agents also relieve the chest pain caused by coronary artery disease, the clinician may have difficulty using medication response as a clue to the cause of undiagnosed chest pain. The clinician must carefully interpret the results of a therapeutic trial, particularly the rapidity of response. Relief of pain within 3 minutes of a sublingual dose of nitroglycerin is more consistent with coronary artery disease than esophageal motor disorders. If relief occurs only after 10 to 15 minutes, esophageal disease is more likely. Nitrates and calcium channel blockers can relax the lower esophogeal sphincter and aggravate esophageal reflux, thereby increasing symptoms of reflux esophagitis.

Myocardial ischemia sometimes occurs in the absence of fixed obstructions of the coronary arteries, resulting in recurrent chest pain. Obstructive disease of the intramural small vessels can cause ischemia. Although such lesions occur more frequently in diabetics, small vessel disease is an infrequent cause of chest pain. It should be considered only after more likely etiologies have been excluded. Valvular aortic stenosis, hypertrophic cardiomyopathy, and thyrotoxicosis can also cause myocardial ischemia. The quality and pattern of pain in these conditions usually is similar to that of coronary artery disease. These entities nearly always are accompanied by physical examination findings typical of the underlying disease, and so their detection usually is not difficult.

Coronary vasospasm can cause myocardial ischemia in the absence of obstructive coronary disease. The pain usually has a quality similar to the pain of obstructive coronary disease, but it tends to occur in an unpredictable pattern. The pain typically is not induced by exertion and may awaken the patient from sleep. Some patients report emotional stress as a trigger. The pain frequently responds to sublingual nitroglycerin, and the frequency of episodes decreases after therapy with calcium channel blockers or long-acting nitrates. Approximately 90% of patients with coronary vasospasm have ECG changes during episodes of pain. Thus, the absence of electrocardiographic changes during pain makes coronary vasospasm unlikely.

Mitral valve prolapse (MVP) is a controversial etiology of chronic chest pain. Clinical and echocardiographic studies have demonstrated that MVP is a common finding in otherwise healthy adults. Population studies have found the incidence of chest pain to be no higher in individuals with mitral valve prolapse than in those without the disorder. Nevertheless, there have been numerous clinical reports of patients in whom mitral valve prolapse was the only identifiable etiology of recurrent chest pain. The patients in these studies have pain with various qualities and patterns, and there is no "typical" chest pain syndrome of MVP. It should be considered as a cause of recurrent chest pain only after more likely causes have been excluded, since there is no specific treatment for the disorder. The major value of diagnosing mitral valve prolapse is to identify those patients at risk of endocarditis and arrhythmias. Prospective studies have shown that patients who develop serious complications have either a late systolic murmur or abnormal electrocardiogram in conjunction with the midsystolic click. Thus, it is unnecessary to obtain echocardiography to exclude mitral valve prolapse unless a patient has findings on physical examination and/or electrocardiogram that suggest a risk of complications.

The chest wall can cause recurrent chest pain, but the clinical diagnosis of chest wall syndromes has not been described well. The quality and location of chest wall pain vary greatly; precipitating factors are useful for diagnosis. Chest wall pain is often pleuritic and tends to be aggravated by moving the arms or torso. In most patients the pain can be reproduced by palpation or manipulation of the chest wall.

Causes of Acute Chest Pain

The clinician must make immediate management decisions for patients having new onset of chest pain or an increase in the frequency or severity of recurrent chest pain. Because some of the disorders are life threatening, it must be decided whether to admit the patient. It often is not an option to assess response to therapeutic interventions in these patients. A systematic approach to management is essential.

The leading diagnostic consideration in acute chest pain is myocardial infarction, a life-threatening condition requiring immediate medical management. The pain of myocardial infarction is similar in quality and location to angina pectoris, although usually more intense, severe, and longer-lasting. The pain often occurs at rest and is not relieved by nitroglycerin. It may be accompanied by diaphoresis, dyspnea, or nausea. The initial electrocardiogram shows new Q waves or ST segment elevations in only 70% of patients, so absence of these findings does not exclude infarction. Patients who are suspected of having a myocardial infarction usually require hospital admission.

The syndrome of unstable angina pectoris includes a diverse group of patients having chest pain due to coronary artery disease. Patients with unstable angina have a short-term risk of myocardial infarction, and therapeutic interventions have been shown to reduce this risk. The syndrome includes patients with new onset angina pectoris. These patients have exertional pain relieved by rest or sublingual nitroglycerin. The syndrome also includes patients with stable exertional pain but a changing pain pattern. Such patients report pain occurring at a lower level of exertion or at rest. Nitroglycerin may no longer provide relief.

Various pathophysiologic mechanisms may be responsible for unstable angina. The most common mechanism is progression of the severity of atherosclerotic disease. Vasospasm aggravating atherosclerotic disease can also cause unstable angina pectoris. An important cause of unstable angina in patients with prior stable angina is alteration of the patient's medication. The patient may misunderstand the physician's prescribed regimen, or the patient may not be compliant with the regimen. Nitroglycerin can become outdated and ineffective. A careful review of the patient's medications can provide clues.

It is difficult to differentiate between unstable angina and acute myocardial infarction. Hospitalization is often required to clarify the diagnosis and facilitate treatment interventions. Serial electrocardiograms and cardiac enzymes will confirm or exclude myocardial infarction. If infarction is excluded, the patient's response to medications should be carefully evaluated. If the pain episodes do not improve substantially with cardiac medications, then the patient has either refractory coronary artery disease ("preinfarction angina") or another cause of pain. Thus, further diagnostic evaluation with imaging studies or coronary arteriography may be necessary.

Dissection of the thoracic aorta is a serious and potentially catastrophic cause of acute chest pain. Because dissection requires immediate, specific treatment, the clinician must exclude this diagnosis early. The two primary types of dissection have different clinical presentations. Proximal dissections arise in the ascending aorta but sometimes extend beyond the aortic arch. Nearly all patients with proximal dissection have pain in the anterior chest, and approximately half report radiation to the posterior chest. Approximately two-thirds have evidence of previous hypertension. Most have pulse deficits, a murmur of aortic regurgitation, or neurologic deficits, and so the physical examination is important when considering this diagnosis.

Distal dissection of the thoracic aorta arises in the descending aorta below the great vessels. It occurs predominantly in men older than age 40 who have a history of hypertension, a group also at risk for acute myocardial infarction. Nearly all patients with acute myocardial infarction have anterior chest pain, but the majority of patients with distal dissection have posterior chest pain. The pain of distal dissection may be described as "tearing" or "ripping" and does not improve with nitroglycerin. Physical findings are less frequent in distal than in proximal dissection, so the diagnosis of distal dissection may be subtle and should be considered in patients who have histories of hypertension, are hypertensive at the time of pain, or have atypical pain. Radiographic studies of the aorta may be necessary to exclude the diagnosis.

Pericarditis is a moderately common disorder, and chest pain is a frequent symptom. There are many causes of pericarditis. The pain is often retrosternal and may radiate to the left arm, suggesting an ischemic etiology. The pain is usually pleuritic or affected by body position, however, aggravated by lying down and relieved by sitting up. A pericardial friction rub suggests the diagnosis, but a rub may be absent. The electrocardiogram can show ST elevations in multiple leads, a finding that may be confused with acute myocardial infarction. Not all patients with pericarditis have ECG changes, and uremic pericarditis is notable for the absence of ECG findings. Chest x-rays often show a normal cardiac silhouette. Because of its diverse presentation, pericarditis is difficult to exclude by routine clinical examination, but the diagnosis should be suspected if the patient does not have other likely causes of pain and has clinical evidence of a precipitating cause.

Pneumonia and pneumothorax also cause acute chest pain, but these disorders are usually easy to diagnose. The pain is characteristically unilaterial and pleuritic. Chest x-ray will establish the diagnosis.

A more difficult diagnostic problem is hyperventilation. Hyperventilation can cause pain that is atypical of angina pectoris. It may vary in location and may not be pleuritic. A useful clue is that the pain is often brought on by anxiety or emotions. The most useful tool for confirming hyperventilation is to demonstrate that the pain can be reproduced by rapid breathing.