American College of Physicians: Internal Medicine — Doctors for Adults ®


Acute coronary syndromes

From the March ACP Observer, copyright 2006 by the American College of Physicians.

Available in PDF format

Covering the spectrum from unstable angina through myocardial infarctions, acute coronary syndromes (ACS) may account for as many as 2 million hospitalizations in the U.S. every year.

What internists can do for hospitalized patients with ACS depends largely on their facility's setting and resources. If the hospital doesn't offer emergent percutaneous coronary intervention (PCI) for high-risk patients who need it, can you quickly transfer the patient to a hospital that does?

If not, then you can "administer thrombolytic therapy, which is perfectly acceptable if you don't have timely access to PCI, " said Stephan D. Fihn, FACP, director of the Northwest Health Services' research and development field program at the VA Puget Sound Health Care System in Seattle. Dr. Fihn authored the PIER module on stable chronic angina.

In the office, internists play a pivotal role in preventing a second heart attack in ACS patients—and now have a much bigger arsenal of therapeutic options, including statins, beta-blockers, ACE inhibitors, aspirin and other anti-platelet agents, to choose from. The advent of aggressive new agents may be the reason why, according to Dr. Fihn, the number of heart disease deaths has dropped over the past two decades, with cancer replacing heart disease as the No. 1 killer of Americans under age 85 in 2004.

What is also clear, however, is ACS' "changing epidemiology, especially related to diabetes," Dr. Fihn said. "We are now racing against many of the gains we've already made, and that's one of our fears. We have made great strides--which may largely be reversed through obesity and lack of physical activity."

This edition of ACP Observer Special Focus is designed to help improve your ability to diagnose, treat and manage patients with acute coronary syndromes.


An umbrella term, acute coronary syndrome (ACS) consists of three progressively damaging reactions to inadequate blood flow. They include:

  • unstable angina. Clogged with atherosclerotic plaque, a coronary artery narrows to the point that the myocardium, even at rest, doesn't receive enough oxygen.
  • a non-Q wave myocardial infarction (MI). This acute event is characterized by elevated enzyme levels and diagnostic electrocardiographic changes.
  • a Q-wave MI. The most dangerous of the three conditions, this type of MI signals a sustained occlusion that can result in extensive damage unless coronary flow is quickly restored.


A history of chest discomfort symptoms suggests an ACS diagnosis. Symptoms consistent with unstable angina include recent onset of chest discomfort, increasing discomfort with less activity or symptoms occurring at rest.

Get a detailed history, including the character, intensity, location and duration of chest discomfort, as well as exacerbating factors. Those include:

  • associated symptoms such as nausea, diaphoresis and shortness of breath.

  • atypical symptoms—including "I don't feel well"—in some coronary patients, especially women, diabetics and the elderly.

  • cardiac risk factors—such as smoking, hypertension, dyslipidemia, diabetes and obesity—or either previously documented coronary artery disease (CAD) or a family history of CAD.

Although physical findings alone do not exclude an ACS diagnosis, a thorough physical exam can help with the differential diagnosis and complications. Include the chest wall and abdomen in your exam.

Also look for abnormalities in heart rate or blood pressure; fever; tachypnea; pallor; new murmurs or gallops; and signs of congestive heart failure, including arrhythmias, shortness of breath, fatigue and leg swelling.

Many conditions can mimic acute myocardial ischemia or infarction. Of the 3 million patients admitted to the hospital annually with ACS symptoms, about 30% are diagnosed with acute MI. Your differential diagnosis should take into account cardiac, musculoskeletal, gastrointestinal, pulmonary and psychogenic etiologies of chest pain.

You can use several different tests to confirm ACS and classify it appropriately. Get an electrocardiogram (ECG) immediately for all patients with suspected ACS, then use clinical and ECG findings to estimate the likelihood that chest symptoms represent ACS.

Because an initial ECG may be nondiagnostic in 50% of all patients, serial ECGs are recommended. (For more on ECG readings and risk stratification, see "ACS: stratifying patient risk.")

Both Q-wave and non-Q-wave MIs demonstrate elevated cardiac biomarkers. By serially measuring cardiac biomarkers, you can document evidence of myocardial damage that has occurred within the last 24 hours.

Establish an MI diagnosis with elevated serum levels of creatine kinase, myoglobin and cardiac troponins. Elevated troponins are the most important of the three for risk stratification—and can stay elevated for several days after a suspected MI.

If initial markers are normal, repeat measurements at six and 12 hours after the onset of symptoms. Do not, however, delay further treatment in patients with ST elevations on an ECG.

Categorize patients according to:

  • ST-elevation myocardial infarction: greater than 1 mm ST-segment elevation in two or more contiguous leads or new left bundle branch block, or evidence of true isolated acute posterior infarction; or

  • Non-ST-segment myocardial infarction elevation: no ST-segment.

Other diagnostic tests include:

  • Coronary angiography. Consider proceeding directly to diagnostic coronary angiography for the following patient subsets: those with documented ST-elevation MI or new left bundle branch block, and those with recurrent pain and persistent ST-segment depression for whom acute reperfusion with primary angioplasty is planned.

    You should also consider coronary arteriography—the gold standard for documenting the presence and severity of CAD—in hospitalized patients without ST-elevation who have acute ischemic changes and elevated cardiac biomarkers.

  • Stress testing. Use exercise stress testing in patients with low to moderate risk who are admitted with chest pain, normal or nonspecific ECG, and negative cardiac biomarkers, to assess for CAD and determine if patients need further evaluation or treatment. Consider an exercise treadmill stress test with or without radionuclide imaging or stress echocardiography (ECHO) for patients who are able to exercise. For those who cannot exercise, consider a pharmacologic stress test.

  • Echocardiography. Consider early ECHO in patients with chest pain and suspected ACS. An ECHO can detect regional wall motion abnormalities before serum marker results are known. That can be particularly helpful when you suspect non-ST-segment elevation MI or unstable angina in patients with a nondiagnostic ECG.

    Use ECHO to identify other nonischemic conditions in your differential diagnosis that can cause chest pain, such as myocarditis; valvular heart disease; aortic dissection; pulmonary embolism; and mechanical complications of acute infarction, such as mitral regurgitation, papillary muscle dysfunction or rupture, and ventriculoseptal defects.


Get a cardiology consult if the diagnosis is uncertain or if you need to optimize your diagnostic strategy and determine if invasive cardiac testing is needed. Recognize that specific tests, including exercise testing, imaging and biomarker testing, can be falsely positive or negative.

A cardiology consult is important for patients who need complex management or have high-risk features, including elevated troponin T or I; new ST-segment depression; recurrent angina/ischemia at rest or with low-level activity; heart failure; ventricular arrhythmias; and a markedly abnormal stress test.


Non-drug therapy

Consider administering oxygen routinely to all patients with uncomplicated MI during the first two to three hours after admission—and possibly for as long as six hours. This is particularly important for patients with ongoing ischemia, overt pulmonary edema or measured arterial oxygen saturation of less than 90%.

If it is available, proceed directly to primary percutaneous coronary intervention (PCI) for patients with ST-segment elevation, new left bundle branch block or true posterior acute MI. In experienced centers, PCI is the preferred approach vs. thrombolytic therapy when initial balloon angioplasty can be accomplished within 90 minutes of hospital arrival. If patients are not in such a high-volume center, consider transferring them within three hours.

Also consider stabilizing patients who have cardiogenic shock with an intra-aortic balloon pump before angiography and revascularization. You may also need to take this approach for patients with acute mitral regurgitation or ventriculoseptal defect, recurrent intractable ventricular arrhythmias with hemodynamic instability, and refractory post-MI angina.

Drug therapy

Upon admission, start patients promptly on aspirin and continue this therapy indefinitely. You can administer clopidogrel to patients who are hypersensitive or have gastrointestinal complications, but be aware of the increased risk of bleeding.

Patients with suspected acute MI or unstable angina should receive intravenous beta-blockers unless they have significant bradycardia, hypotension, severe asthma or active bronchospasm, high-degree heart block, or moderate to severe congestive heart failure.

Prescribe intravenous nitroglycerin for the first 24 to 48 hours to most patients with unstable angina, acute uncomplicated MI with ongoing chest discomfort, and MI complicated by congestive heart failure, large anterior infarction, persistent ischemia or hypertension.

For pain, administer intravenous morphine sulfate to patients whose symptoms persist after three sublingual nitroglycerin doses or who have recurrent symptoms.

Add anticoagulation with subcutaneous low-molecular weight heparin or intravenous unfractionated heparin to antiplatelet therapy for patients with likely or definite ACS.

In patients with ST-elevation MI, administer clopidogrel with aspirin to those who are not at high risk for bleeding if PCI is planned; continue clopidogrel therapy for at least one month and as long as 12 months. If you instead plan to use a noninterventional approach, immediately administer clopidogrel along with aspirin and continue clopidogrel, again for at least one month.

Patients not undergoing immediate intervention should receive intravenous thrombolytic therapy if they have ST-elevation or new left bundle branch block MI and chest pain for less than 12 hours, or if they present more than 12 hours after the onset of persistent chest pain.

Administer glycoprotein IIb/IIIa antagonists along with aspirin and heparin in patients with non-ST-elevation MI, and as adjunctive therapy in patients with ST-elevation MI undergoing PCI.

Most patients also need an angiotensin-converting enzyme (ACE) inhibitor within the first 24 hours post-MI. These patients include those with ST-segment elevation in two or more anterior precordial leads; or clinical heart failure in the absence of hypotension (systolic blood pressure of less than 100 mm Hg) or of known ACE-inhibitor contraindications.

Other candidates for ACE inhibitors include those with acute MI, with or without a reduced left ventricular ejection fraction, especially diabetics. You can also use angiotensin receptor blockers post-MI if there are contraindications to ACE inhibitors, especially in patients with left ventricular dysfunction.

Consider initiating the beta-blocker carvedilol or metoprolol three to 21 days post-MI in stable patients with left ventricular ejection fraction of less than or equal to 40% and no significant contraindications. Also consider eplerenone, a selective aldosterone blocker, beginning three to 14 days post-MI in patients with left ventricular ejection fraction of less than or equal to 40% and clinical heart failure or diabetes.


In patients not undergoing immediate coronary angioplasty and reperfusion, consider cardiac catheterization of patients who develop or continue to have:

  • unstable angina or non-ST-segment elevation MI and recurrent ischemic symptoms
  • heart failure
  • left ventricular dysfunction
  • dysrhythmias
  • persistent elevated cardiac protein levels
  • persistent ischemic ECG abnormalities

Also consider exercise stress testing for lower-risk, stable patients who don't have such complications (or a pharmacologic stress test for those who can't exercise). Get a submaximal stress test four to seven days post-MI or a symptom-limited exercise test at 14 to 21 days post-MI.

Consider adding imaging—such as myocardial perfusion or ECHO--to improve the sensitivity and specificity of these tests. Imaging can be especially helpful in patients with left bundle branch block, marked baseline ST-T wave abnormalities, pacemaker dependency, left ventricular hypertrophy, use of digitalis or type 1 antiarrhythmics, and Wolff-Parkinson-White syndrome.

Emphasize secondary prevention measures as part of outpatient management and patient education. For all post-MI patients, address and manage hypertension, diabetes, lipids, smoking cessation and exercise as important components of cardiac rehabilitation and comprehensive follow-up.

And consider screening for depression. Ask patients about their energy level, eating and sleeping habits, mood swings, loss of interest in usual activities, and crying spells.

The PIER module for acute coronary syndromes is online.


The information included herein should never be used as a substitute for clinical judgment and does not represent an official position of ACP.


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