William Ross Brown, MD and Glenn N. Levine, MD, FACC, FAHA

1. Are most emergency room (ER) visits for chest pain caused by acute coronary syndromes (ACS)?

    No. ACS (e.g., unstable angina, myocardial infarction) account for only a small percentage of ER visits for chest pain. Depending on the study, only a small percentage of patients (1% to 11%) will be diagnosed as having chest pains caused by coronary artery disease (CAD) or ACS. ACS is the term used to describe the continuum of syndromes that include unstable angina and myocardial infarction (MI).

2. What are the other important causes of chest pains besides chronic stable angina and ACS?

    The differential diagnosis for chest pains include the following:

It is important not to assume that all chest pains are due to angina or ACS, even if someone else has made such a preliminary diagnosis. This is particularly important, as time-to-diagnosis is critical for aortic dissection, where the mortality rate increases by approximately 1% every hour from presentation to diagnosis and treatment. Additionally, the treatment of aortic dissection is dramatically different from the treatment of ACS, as anticoagulation is contraindicated with aortic dissection.

3. Does an elevated troponin level make the diagnosis ACS?

    Not necessarily. Although troponin elevations are fairly sensitive and specific for myocardial necrosis, it is well known that other conditions can also be associated with elevations in cardiac troponins. Importantly, troponin elevation can occur with pulmonary embolus and is in fact associated with a worse prognosis in cases of pulmonary embolus in which the troponin levels are elevated. Myopericarditis (inflammation of the myocardium and pericardium) may also cause elevated troponin levels. In addition, aortic dissection that involves the right coronary artery may lead to secondary MI. Further, troponins may be modestly chronically elevated in patients with severe chronic kidney disease. Troponin elevation has also been noted in patients with acute stroke. Studies to delineate the etiology of this are ongoing.

4. What is angina?

    Angina is the term used to denote the discomfort associated with myocardial ischemia or MI. Angina occurs when myocardial oxygen demand exceeds myocardial oxygen supply, usually as a result of a severely stenotic or occluded coronary artery. Patients with angina most commonly describe a chest pain, chest pressure, or chest tightness sensation. They may also use words such as heaviness, discomfort, squeezing, or suffocating. The discomfort is more commonly over a fist or larger sized wregion than just a pinpoint (though this distinction in itself is not enough to confidently distinguish anginal from nonanginal pain). The discomfort classically occurs over the left precordium but may manifest as right-sided chest discomfort, retrosternal discomfort, or discomfort in other areas of the chest. Some persons may experience the discomfort only in the upper back, in the arm or arms, or in the neck or jaw. Angina is typically further classified into stable and unstable. Stable angina refers to angina that occurs during situations of increased myocardial oxygen demand. Unstable angina can occur at any time and falls within the spectrum of ACSs.

5. What are the associated symptoms that persons with angina may experience in addition to chest discomfort?

    Patients with angina may experience one or more of the following symptoms. Some patients do not experience classic chest discomfort, but instead manifest only one or more of these associated symptoms.

6. What are the major risk factors for CAD?

Other factors that have been associated with an increased risk of CAD include inactivity (lack of regular exercise), elevated C-reactive protein, and obesity (specifically, large abdominal girth).

7. What symptoms and findings make it more (or less) likely that the patient’s chest pains are due to angina (or that the patient has ACS)?

    The answer to this question is given in Tables 15-1 and 15-2, which are taken from an excellent review article on this subject in the Journal of the American Medical Association (JAMA). The tables summarize many of the relevant questions and the value of the chest pain characteristics in distinguishing angina and ACS-MI pain from other causes. It is important to remember, no single element of chest pain history is a powerful enough predictor to use alone to rule out ACS.

8. If one is still in doubt as to the diagnosis of CAD, should a stress test be obtained?

    Yes. Stress testing for diagnostic purposes is best in patients who, after initial evaluation, have an intermediate probability of having CAD. For example, in a patient with a pretest probability of having CAD of 50%, a positive exercise stress test makes the posttest probability of CAD 85%, whereas a negative exercise stress test makes the posttest probability of CAD just 15%. Stress testing may also be used for prognostic purposes. Stress testing is discussed in greater detail in the chapters on exercise stress testing (Chapter 6), nuclear cardiology (Chapter 7), echocardiography (Chapter 5), and magnetic resonance imaging (Chapter 10). Coronary computed tomography (CT) angiography is an emerging alternate form of diagnosis and is discussed in Chapter 9.

9. Are there exceptions to the classic presentations of anginal pain?

    Yes. It is well known that women often do not present with typical anginal symptoms (e.g., substernal, exertional pain relieved by rest or NTG). In fact, women are often misdiagnosed because of a lower suspicion by doctors that they have CAD and the fact that they often experience discomfort that is not classic for angina. Older patients may have difficulty in remembering or describing their chest discomfort and so also may not describe classic anginal symptoms. Some diabetic patients appear to have an impaired sensation of chest discomfort when the heart experiences myocardial ischemia. Thus, some diabetic patients may not report chest discomfort but rather only one or more associated symptoms, such as shortness of breath or diaphoresis. Cardiac transplant patients do not experience ischemic chest pain due to denervation of the transplanted heart.

10. Who first described angina, and when?

    The association between chest pain (angina pectoris) and heart disease was first described by Heberden in 1772. He described this as a strangling sensation in the chest in his manuscript entitled, “Some Account of a Disorder of the Breast.”

11. What is Prinzmetal angina?

    Prinzmetal angina, also called variant angina, is an uncommon type of angina caused by coronary vasospasm. The coronary artery is believed to spasm, severely reducing myocardial oxygen supply to the affected myocardium. Although the spasm can occur in either a normal or a diseased coronary artery, it most commonly occurs within 1 cm of an atherosclerotic plaque. Prinzmetal angina usually does not occur with physical exertion or stress but occurs during rest, most typically between midnight and 8 am. The pain can be severe, and if an ECG is obtained during an episode, it may demonstrate ST-segment elevations. Patients with Prinzmetal angina are typically younger, often female. Treatment is based primarily on the use of calcium channel blockers, as well as nitrates.

12. What is cardiac syndrome X?

    Cardiac syndrome X is an entity in which patients describe exertional anginal symptoms, yet are found on cardiac catheterization to have nondiseased normal coronary arteries. They may also have ST-segment depressions on exercise stress testing and even perfusion defects with nuclear stress testing. Unlike Prinzmetal angina, they do not have spontaneous coronary spasm and do not have provokable coronary spasm. Although there are likely multiple causes and explanations for cardiac syndrome X, it does appear that, at least in some patients, microvascular coronary artery constriction or dysfunction plays a role. Treatment is usually individually tailored to the patient and sometimes includes cognitive behavioral therapy and imipramine, which is used in chronic pain syndromes. No one standardized recipe has been established.

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