Acute Coronary Syndromes - Tailoring Treatment Based on Risk Stratification

Acute Coronary Syndromes - Tailoring Treatment Based on Risk Stratification

Tabas Jeffrey
US Cardiology 2006
Published: November 2005
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Approximately five million people present to the emergency department (ED) each year with chest pain, and billions of dollars are spent on assessment and treatment. Many therapies are time-dependent, so rapid identification of patients with acute coronary syndrome (ACS) -unstable angina (UA) and acute myocardial infarction (MI) - at high risk for adverse outcomes is essential. Missed or inappropriately treated ACS carries important medicolegal consequences.This raises the issue of whether doctors should treat as many people as quickly as they can.As few as 10% to 30% of patients who present with symptoms of ACS subsequently prove to have ACS.

As the proportion of patients with actual disease decreases, the benefits of the treatment decrease, while the number of adverse outcomes remains constant or potentially increases (if some patients have aortic dissection, for example). This article reviews the risk assessment and resultant management of patients with UA and non-ST-elevation MI (UA/NSTEMI). A treatment algorithm that evaluates the differences in UA/NSTEMI patients and those with STEMI will also be reviewed.

Risk Stratification
Acute MI is described as a rise and fall of serum cardiac markers, preferably troponin, and either ischemic symptoms,ischemic electrocardiogram (ECG) changes, or previous percutaneous coronary intervention (PCI).1 Angina is defined as discomfort that is induced by exercise and relieved by rest or nitroglycerine administration, and is classified according to severity, with class 3 angina occurring after walking one or two blocks or climbing one flight of steps. Unstable angina is defined as class 3 angina that is either new onset exertional angina, or increasing within the past two months, or occurring at rest for more than 20 minutes.2 As mentioned, the prevalence of actual ACS is much lower than the number of ED patients suspected of having ACS.The Multicenter Chest Pain Study showed that, between 1984 and 1986, 26% of patients admitted for possible ACS had acute MI and 28% had unstable angina.With greater recognition of missed disease by both the public and the medical community, however, these rates have declined.The same study found that, between 1990 and 1994, only 11% of these patients had acute MI and 33% had unstable angina.

The American Heart Association (AHA)/American College of Cardiology (ACC) risk stratification guidelines are shown in Tables 1 and 2. Generally, they involve a determination of:


  • whether the signs and symptoms of ACS are due to coronary artery disease (CAD); and
  • the risk of adverse events.

History, examination, ECG, and cardiac markers are used to categorize the patient with definite ACS, possible ACS, chronic stable angina, or a non-cardiac process.2 However, this approach has many limitations, including the practicality of using the suggested 28 elements to determine whether ACS symptoms are due to CAD and the 24 parameters to determine the risk of adverse events in the presence of ACS. Application of this approach can also yield perplexing results. A 35- year-old male with burning epigastric pain radiating to the chest for 25 minutes that is improved but not resolved in the ED with an antacid and with normal ECG and cardiac markers would be classified according to the guidelines as having intermediate risk of ACS due to CAD and a high risk of adverse events due to prolonged duration of chest pain at rest. In addition, most of the AHA/ACC risk stratification criteria are based on chest pain, but up to half of all acute MIs present without chest pain.

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References:
  1. Alpert J S,Thygesen K, Antman E, Bassand J P,“Myocardial infarction redefined – a consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction”, J. Am. Coll. Cardiol. (2000), 36: pp. 959–969.
  2. Braunwald E, Antman E M, Beasley J W, et al.,“ACC/AHA, 2002: Summary Article: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina)”, Circulation (2002), 106: pp. 1,893–1,900.
  3. Morrow D A, Cannon C P, Rifai N, et al., “Ability of minor elevations of troponins I and T to predict benefit from an early invasive strategy in patients with unstable angina and non-ST elevation myocardial infarction: results from a randomized trial”, JAMA (2001), 286: pp. 2,405–2,412.
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  5. Schriger D L, Herbert M E,“Platelet glycoprotein inhibitors in patients with medically managed acute coronary syndrome: does the enthusiasm exceed the science?”, Ann. Emerg. Med. (2001), 38: pp. 249–255.
  6. Boersma E, Harrington R A, Moliterno D J,White H, Simoons M L,“Platelet glycoprotein IIb/IIIa inhibitors in acute coronary syndromes”, Lancet (2002), 360: pp. 342–343.
  7. Yusuf S, Zhao F, Mehta S R, Chrolavicius S,Tognoni G, Fox K K,“Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation”, N. Engl. J. Med. (2001), 345: pp. 494–502.
  8. Brunwald E, Mark D B, Jones R H, et al., “Unstable angina: diagnosis and management”, Rockville, MD:Agency for Health Care Policy and Research and the National Heart, Lung, and Blood Institute, US Public Health Service, US Department of Health and Human Services; 1994; AHCPR Publication No. 94-0602.

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