Chest Pain, Substernal

Marie K. Yamamotoya

Substernal chest pain requires a rapid and accurate assessment to identify potentially life-threatening events. Substernal chest pain of cardiac origin encompasses the entire clinical spectrum from typical angina to unstable angina and ultimately to myocardial infarction (MI) (Chapter 7.1).

Approach

In the evaluation of substernal chest pain, the initial step involves estimating the likelihood of coronary artery disease (CAD) with a thorough history, physical examination, electrocardiogram (ECG), and other potentially diagnostic tests. Serious noncardiac conditions that must be considered on initial presentation include aortic dissection, pericardial tamponade, pulmonary embolism, and tension pneumothorax.

History

A. Characteristics of pain in stable angina

 1. Quality. The pain of angina pectoris is often not described as a pain at all. Instead, it is frequently referred to as a squeezing, heaviness, or pressure sensation lasting 5 to 10 minutes. Diaphoresis, dyspnea, nausea, and vomiting often accompany the discomfort. Pain that is sharp, stabbing (especially if exacerbated by deep inspiration), pain reproducible with chest wall palpation, and pain lasting seconds or days to weeks is less likely to be from CAD.

 2. Location. Generally, angina is poorly localized in the retrosternal area, anterior chest, or epigastrium and typically radiates to the left arm, neck, or jaw.

 3. Precipitating and alleviating factors. Angina is often precipitated by conditions that increase myocardial oxygen demand, most commonly physical exertion, emotional stress, or cold weather. It is relieved promptly with rest or sublingual nitroglycerin.

 B. Characteristics of pain in unstable angina. According to the clinical practice guidelines recently developed by the Agency for Health Care Policy (1), unstable angina is defined as:

1. Angina at rest lasting greater than 20 minutes.

 2. New onset angina (< 2 months) precipitated by walking one to two blocks or by climbing one flight of stairs at a normal pace.

 3. Angina that is more frequent, longer in duration, or occurring at a lower threshold.

C. Risk factors. The Framingham Heart Study along with numerous other large epidemiologic studies has established the following risk factors for   CAD (2):

1. Sex and age: men aged 45 years or older; women aged 55 years or older; women with premature menopause without hormone replacement.

2. Family history: MI or sudden death occurring in a first-degree male relative aged 55 years or younger or in a first-degree female relative aged 65 years or younger.

3. Smoking: in men who smoke one pack per day, a three- to fivefold risk for CAD compared with nonsmokers. Those who quit smoking can reach the same risk level of nonsmokers within 2 years of stopping.

4. Hypertension: blood pressure greater or equal to 140/90 (Chapter 7.8).

5. Cholesterol: total cholesterol greater than 200; low-density lipoprotein (LDL) greater than 130; high-density lipoprotein (HDL) less than 35. An HDL level above 60 is protective.

6. Diabetes mellitus: a twofold increase in CAD, compared with nondiabetics (Chapter 14.1).

Physical examination

 A. Focused physical examination. This should include vital signs (notably blood pressure). During a symptomatic episode, the finding of a mitral regurgitation murmur, S₃ or S₄ gallop, bruits or precordial lift all suggest a high likelihood of CAD. Findings of xanthelasma, tendinous xanthomata, tobacco-stained teeth and fingernails, and decreased or asymmetrical peripheral pulses indicate the likely presence of cardiac risk factors.

Testing

 A. ECG. Despite the availability of a number of tests, the history remains very important in determining the likelihood of CAD in a patient with substernal chest pain. It is important to avoid using a normal ECG as “rule out” criteria, as many patients with unstable angina or even an acute MI may initially have a normal ECG. The diagnosis of CAD can be based on characteristic changes in the ST-T wave morphology during a symptomatic episode. Specifically, ST segment elevation greater than or equal to 1 mm in two or more consecutive leads is highly suggestive of an acute MI and is associated with the highest morbidity and mortality rate (3). ST segment depression of greater than or equal to 1 mm or T-wave inversion in two or more contiguous leads also strongly suggests ischemia or acute MI. The presence of Q waves greater than or equal to 0.04 seconds indicates previous MI. However, Q waves occurring in lead III alone may be a normal finding. As patients with initially normal ECG are still at risk for life-threatening complications and death (3% and 1%, respectively), it is important to follow serial ECGs for any evolution (3).

 B. Creatinine kinase. The most widely used laboratory test for the detection of MI is the creatinine kinase enzyme. The isoenzyme, CK-MB, is abundant in the myocardium and, therefore, is sensitive and specific for myocardial injury. With acute MI, the MB fraction typically begins to rise within 6 hours of symptom onset, peaks at 18 hours, and falls after 24 hours. Total CK and CK-MB should be measured every 6 to 8 hours for a 24-hour period.

C. Troponin I and T. Both troponin I and T proteins are located on the contractile apparatus of the myocardium. These proteins are highly sensitive for myocardial injury. The prospective study conducted by Hamm et al. showed that in the 47 patients diagnosed with acute MI, 94% were positive for troponin T and 100% for troponin I (4). In addition, the negative predictive value of troponin T was 98.9% and that of troponin I was 99.7% (4).

 D. Noninvasive and invasive testing. Both exercise and pharmacologic stress tests are used to assess for CAD in patients with stable angina. Unstable angina, uncontrolled hypertension, severe aortic stenosis, unstable arrythmias, and recent MI (4–6 weeks) are contraindications to stress testing.

 1. Exercise ECG is a relatively inexpensive test with an overall sensitivity and specificity of 50% to 70%. It is most useful for those patients with a moderate pretest probability. Protocols are used to incrementally increase treadmill speed and elevation until the maximal heart rate for age is achieved. The ECG is monitored for ST depression and any ventricular arrythmias. The patient is also monitored for any fall in blood pressure or complaints of chest discomfort or dyspnea.

 2. Exercise ECG with thallium or technetium sestamibi. The use of these radioisotopes improves the sensitivity and specificity of exercise ECG to approximately 90%. Thallium is distributed in proportion to blood flow. Areas of decreased uptake during exercise followed by normal uptake at rest suggest ischemia, whereas areas of persistent defect indicate infarction. Technetium is a newer agent with the advantage of a slow washout and added contrast, which results in fewer false-positive findings than thallium.

3. Exercise echocardiogram. This method detects wall motion abnormalities during exercise and has comparable sensitivity and specificity to exercise ECG. It is preferred in patients with abnormal resting ECGs and in patients with a low pretest probability. The disadvantages include difficulty imaging obese patients and the need to image as close to peak exercise as possible.

 4. Dipyridamole or adenosine stress testing. The use of intravenous coronary vasodilators (dipyridamole or adenosine) in combination with a radioisotope (thallium or technetium sestamibi) is useful in patients who are unable to exercise. Areas of redistribution suggest ischemia, whereas areas of persistent defects indicate infarction. The use of phosphodiesterase inhibitors and the presence of reactive airway disease are contraindications.

5. Dobutamine echocardiogram. This method is also used for those who are unable to exercise. Dobutamine increases myocardial oxygen demand by increasing contractility and essentially “exercises” the heart. The echo monitors for any wall motion abnormalities.

 6. Coronary angiography. Considered the “gold standard” test, this procedure provides the most detailed structural information of all the tests discussed. It is indicated in those patients who are at high risk for CAD by noninvasive tests and for those with persistent symptoms despite medical therapy. As diagnosis is closely tied to therapy, only those patients who are candidates for invasive procedures (e.g., percutaneous transluminal coronary angioplasty or coronary artery bypass graft) should be considered.

Diagnostic assessment

 In patients presenting with substernal chest pain, the key to diagnosis involves quickly and accurately assessing for the likelihood of myocardial ischemia or infarction. An initial history, physical examination, and ECG will help in the risk assessment of the patient for significant CAD. Those who are at high to intermediate risk need to then be evaluated for presence of unstable angina. Once established, further steps involve the simultaneous evaluation with serial ECGs and enzymes along with therapy to reduce ischemia. Cardiac angiography is the final step in evaluation and treatment. For those at low risk for CAD and not meeting criteria for unstable angina, further evaluation involves noninvasive diagnostic testing with the possibility for cardiac angiography and revascularization.

References

1. Braunwald E, Mark DB, Jones RH. Unstable angina: diagnosis and management. Clinical Practice Guideline Number 10. AHCPR Publication No. 94-0602. Rockville, MD: Agency for Health Care Policy and Research and the National Heart, Lung, and Blood Institute, Public Health Service, US Department of Health and Human Services, March 1994.

2. Anderson KM, Wilson PWF, Odell PM. An updated coronary risk profile. A statement for health professionals. Circulation 1991;83:356–362.

3. Karlson BW, Hallgren HP, Liliequist JA. Emergency room prediction of mortality and severe complication in patients with suspected acute myocardial infarction. Eur Heart J 1994;15:1558–1565.

4. Hamm CW, Goldmann BU, Heeschen C. Emergency room triage of patients with acute chest pain by means of rapid testing for cardiac troponin T or troponin I.
N Engl J Med 1997;337:1648–1653.>

Book Source Details

• Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
• Author(s): Robert B. Taylor (editor)
• Year of Publication: 2000
• Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.

Other Book Chapters Related to Angina

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Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2008 Williams & Wilkins.

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• Back to symptom: Angina: Introduction (review 38 causes)
• Next Book Extract About Angina: Acute Nonpleuritic Chest Pain (Field Guide to Bedside Diagnosis)
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More About This Book: Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter Authors: Robert B. Taylor (editor) Publisher: Lippincott Williams & Wilkins Copyright: 2000 ISBN: 0-78172-094-X

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