Coronary artery disease (CAD) is pervasive, complex, and kills more Americans each year than any other disease process.1 Many patients with symptomatic CAD use the ED as their initial point of entry into the medical system. Early recognition, risk stratification, and timely intervention are critical to securing a favorable outcome. Emergency physicians must therefore be expert both in the diagnosis of symptomatic CAD as well as the implementation of the complex, stepwise management protocols currently being recommended. This review highlights the advances in our understanding of ACS: its pathophysiology, clinical diagnosis, risk stratification, and therapeutics. There is a particular focus on the subgroup of unstable angina (UA) and non-STsegment elevation myocardial infarction (NSTEMI).
ACS is a term referring to patients with clinical evidence of acute myocardial ischemia: UA, NSTEMI, and ST-segment elevation myocardial infarction (STEMI).2 ACS represents a continuum of diseases with variations in pathophysiology, presentation, prognosis, and response to therapeutic intervention. The subgroup of UA/NSTEMI defines the phase of symptomatic CAD that occurs after stable angina. Angina is considered unstable when one of three situations exists: it is occurring for the first time, it occurs at rest, or it is accelerating in terms of frequency or severity. The presentation of NSTEMI is similar to that of UA, with the addition of an elevation in biochemical markers for myocardial infarction (MI).2 The presentation of STEMI is similar to that of NSTEMI, with the addition of diagnostic ST elevation on ECG testing. ACS is an area of abundant clinical research, with new studies, practice protocols, and therapeutics being introduced on almost a monthly basis. Sorting out what is bona fide and practical represents an ongoing challenge for the practicing emergency physician.
The spectrum of ACS has produced intense scientific interest, leading to an enormous amount of high-quality literature. Even so, it is important to remember that pharmaceutical industry sponsorship of trials is frequent.
Much of the data referenced in this review are from large randomized, controlled clinical trials. A number of large meta-analyses are also cited.
In 2002, the American College of Cardiology (ACC) and the American Heart Association (AHA) issued practice guidelines on the diagnosis and management of UA and NSTEMI using a strict evidence-based approach.2 These guidelines are evaluated in this issue of Emergency Medicine Practice as they apply to patients in the ED. (The June 2003 issue of Emergency Medicine Practice presents an evidencebased discussion of the management of patients with STEMI who are suitable for reperfusion by percutaneous coronary intervention or thrombolytics.) The Cochrane Library contains several pertinent reviews that are also discussed; the most applicable relate to the use of glycoprotein (GP) inhibitors and low-molecular weight heparin (LMWH).3,4
The American College of Emergency Physicians (ACEP) issued an updated clinical policy titled "Critical Issues in the Evaluation and Management of Adult Patients Presenting with Suspected Acute Myocardial Infarction or Unstable Angina," which is discussed in this text.5
Of the 6 million ED visits for chest pain each year, approximately 800,000 patients are diagnosed with MI and an additional 1.5 million with UA or NSTEMI. Approximately 60% of those hospitalized are over 65, and half are women.6
ACS occurs when myocardial perfusion proves inadequate to meet demand. The result is angina—a characteristic sensation of pain or pressure within the chest that may radiate to the jaw or upper extremities, associated with diaphoresis, nausea, and dyspnea. In addition, angina may present without pain, manifesting only as shortness of breath, syncope, or nausea. A patient with exertional angina may experience these symptoms due to insufficient coronary flow through a fixed stenosis. A patient with rapidly accelerating angina, rest angina, or acute MI will experience symptoms when there is a sudden interruption in the blood supply to the myocardium. A common mechanism is when a previously stable atherosclerotic plaque ruptures, leading to platelet aggregation, thrombus formation, and myocardial ischemia.7 The severity and duration of the ischemia, the likelihood of MI, and the eventual prognosis are determined by what happens next to this thrombus. In many cases, the thrombus quickly erodes, washes downstream, and symptoms abate. Alternatively, the thrombus may wax and wane but never fully occlude, causing a stuttering form of ischemia. Finally, the thrombus may consolidate and fully occlude, resulting in an MI. (See Figure 1)
Less common causes of ACS include spasm of epicardial or intramural coronary arteries, progressive atherosclerotic narrowing in the absence of thrombus, and, rarely, inflammatory processes leading to coronary artery occlusion.7
From a prognostic standpoint, UA/NSTEMI represents a continuum from low risk to high risk, depending on many thrombus-related elements as discussed above, the location of the occlusion, the presence of collaterals, and comorbid disease. It is interesting to note that in some cases UA/ NSTEMI may carry a worse prognosis than STEMI, since the thrombus in UA is nonocclusive and the downstream vascular territory is exposed to ongoing risk, which predisposes the patient to renewed ischemia, STEMI, and the risk of lethal arrhythmia.
1. "But the ECG was normal."
The ECG should be interpreted and acted on early. However, it lacks sufficient sensitivity to exclude a cardiac etiology on its own, especially if other risk factors are present. Up to 8% of those who present with NSTEMI will have a normal (or nondiagnostic) ECG.30
2. "I know the troponin was elevated, but the patient has renal failure."
Recent data show that the troponin T level retains its prognostic value in all degrees of renal dysfunction.
3. "Thrombolytics work well in STEMI, so why can't I use them for UA?"
The pathophysiology is similar, but complete coronary occlusion is usually not present in UA/NSTEMI. Giving these people thrombolytics can worsen their outcomes.
4. "Aspirin is too inexpensive to be effective."
While it is true that aspirin is one of the least expensive interventions, it has a proven benefit that is equal to or greater than any other pharmacologic intervention. Give aspirin early and give it to everyone who does not have a contraindication (in which case use clopidogrel or ticlopidine).
5. "The admitting physician insisted that the patient did not have ‘cardiac chest pain."
Be an expert. If you know the data about atypical presentations, the timing of the rise in cardiac biomarkers, and ECG test performance characteristics, you can educate consultants about the likelihood of a cardiac cause for a given patient.
6. "I know that he had persistent tearing back pain, but the chest x-ray was negative."
Giving a patient with an aortic dissection aspirin, LMWH, clopidogrel, and a GP IIb/IIIa inhibitor will not improve his or her outcome! Be aware that this is a difficult diagnosis to make and may be fatal when treated inappropriately.
7. "The heart rate was only 82 bpm, so I didn't think that she could tolerate beta-blockade."
Beta-blockers are very beneficial in patients with myocardial ischemia. The goal heart rate should be between 50 and 60 bpm. These are inexpensive and effective agents; always use them when indicated.
8. "Everyone with possible ACS should be treated with GP IIb/ IIIa inhibitors."
The patients who will benefit most from this expensive intervention are those who are likely to undergo PCI. Patients at higher risk based on cardiac biomarkers and ECG changes may benefit as well.
9. "Only those patients with ST elevation will benefit from PCI."
Increasing data are being reported to support the expanded role of PCI in the acute treatment of UA/NSTEMI. High-risk patients should be considered for this potentially beneficial intervention.
10."All patients with cocaine-associated chest pain need to be admitted to the hospital."
Recent data support discharging a certain subgroup of patients with cocaine-associated chest pain after a period of observation with serial ECGs and biomarkers.132 This period of observation was 9-12 hours. Those patients without ischemic ECG changes or positive cardiac biomarkers were safely discharged home.
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.
To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the reference, where available. In addition, the most informative references cited in the paper, as determined by the authors, will be noted by an asterisk (*) next to the number of the reference.
Thomas Macfarlane; Eric R. Snoey
April 1, 2004