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Acute Coronary Syndrome
Phillip A. Erwin,* Rajeev L. Narayan* and Bruce J. Darrow*
Key Pearls
• Acute coronary syndromes include unstable angina, non-ST-elevation
myocardial infarction, and ST-elevation myocardial infarction.
• Diagnosis of acute coronary syndrome is made on the basis of clinical
evaluation and targeted testing, including electrocardiogram and Troponin.
• Transition from medical stabilization to early revascularization is
indicated for ACS patients with higher clinical risk.
• Transition to outpatient recovery includes optimization of multiple
medications and additional non-medical therapies.
• Appropriate management of MI patients forms the basis of assess-
ment of hospital performance and quality of care.
Definitition and Pathophysiology
Myocardial infarction (MI) occurs when myocardial ischemia leads to
cardiac myocyte death. MI is diagnosed when biomarkers of myocyte
necrosis (primarily cardiac troponins) are detected in association with
clinical symptoms of myocardial ischemia.
1
It is important to recognize
that elevated Troponin levels alone are not sufficient for diagnosis of
MI — clinical context is required. As shown in Table 1, MI is classified
according to its presumed etiology. Type 1 MI is caused by an intracoronary event that leads to complete coronary obstruction, whereas Type 2
195
19
Chapter
*Mount Sinai School of Medicine, New York, NY, USA.
MI results when myocardial oxygen demand exceeds supply, such as in a
patient with stable obstructive coronary disease and severe anemia.
1
Acute coronary syndrome (ACS) describes a continuum of ischemia.
Myocardial ischemia without myocardial necrosis — and therefore without
biomarker elevations — is classified as unstable angina (UA). Once ischemia
progresses to cell necrosis, biomarkers become elevated and non ST-elevation
MI (NSTEMI) is diagnosed. ST-elevation MI (STEMI) is the result of complete coronary artery occlusion, with characteristic electrocardiogram (ECG)
findings and positive biomarkers.
2
Diagnosis
Evaluation of the patient with suspected ACS focuses on confirming or
excluding the diagnosis, and instituting treatment according to the
patient’s risk of an adverse outcome.
2
Diagnosis, prognosis and manage-
ment are driven by the ECG, history, exam, and cardiac biomarkers.
ECG Evaluation
The ECG should be the first parameter analyzed because characteristic
ECG findings can direct history-taking and will determine acute management (e.g. expedited revascularization of a patient with STEMI).
Comparison with old ECGs is helpful when evaluating T-wave changes
196
P. A. Erwin, R. L. Narayan and B. J. Darrow
Table 1. Types of Myocardial Infarction (MI)
1. Coronary event leading to MI.
2. Mismatch between myocardial oxygen demand and supply.
3. Sudden death with evidence of myocardial ischemia that occurs
before serum markers of myocardial necrosis can be drawn.
4a. PCI-related elevation of biomarkers.
4b. MI secondary to in-stent thrombosis.
5. MI related to CABG surgey.
Thygesen K, Alpert JS, White HD; Joint ESC/ACCF/AHA/WHF Task Force
for the Redefinition of Myocardial Infarction. (2007) Universal definition of
myocardial infarction. J Am Coll Cardiol 50: 2173–2195.
or determining whether Q-waves or left bundle-branch block (LBBB)
are new. The ECG in ACS can be dynamic, so even if the first ECG is
non-diagnostic, serial ECGs can be useful in securing a diagnosis.
2
Regardless, a lack of ECG changes — even when taken during chest
pain episodes — does not exclude myocardial infarction.
2,3
ECG
changes characteristic of UA/NSTEMI include new ST-segment
depressions ≥ 0.5 mm in multiple leads, T-wave flattening or T-wave
inversion.
2
STEMI is defined as ST elevation of ≥ 1 mm in two or more
contiguous precordial leads or adjacent limb leads, usually with reciprocal ST depressions.
4
New or presumed new LBBB should be man-
aged in the same way as STEMI.
4
History
Symptoms typical of ACS include retrosternal chest pain or pressure that
may radiate to the arms (usually left) or jaw. Chest pain or pressure may
be associated with dyspnea, diaphoresis, nausea, epigastric discomfort,
or fatigue — although any of these symptoms may occur in isolation
without chest pain.
2,5,6
The symptoms typically worsen with exertion and
improve with rest or nitrates.
7
Less consistent with ACS is pain that is
positional, pleuritic, described as sharp or stabbing, or is reproducible
with palpation.
7
Nonetheless, these symptoms are not absolute and their
presence or absence is not diagnostic in isolation. In particular, women
and diabetics may present with atypical symptoms.
2
The history should
elicit the duration of the symptoms, risk factors for coronary artery
disease, and contraindications to treatments such as thrombolysis or
nitrates.
2
Physical Exam
At the time of presentation, findings consistent with ACS or a poor prognosis can guide management (e.g. S3, hypotension, pulmonary edema).
8
The exam may also reveal a non-coronary cause of symptoms such as
uncontrolled hypertension, arrhythmia, pericarditis, or aortic dissection.
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Acute Coronary Syndrome
It is important to document not only abnormalities, but also the absence
of signs of complications of MI that may appear later in the patient’s
hospital course (e.g. murmur of ventricular septal defect).
Cardiac Biomarkers
Evaluation of ACS symptoms should include serum Troponin measurement.
Detection of Troponin has both diagnostic and prognostic value. Troponin
may not be detectable for several hours from the start of MI, so it is not until
three negative sets of Troponin levels have been drawn 6–8 hours apart that
MI can be excluded.
2,7
Nonetheless, it is important to recall that troponin
levels can be elevated from a non-ACS cause, such as myocarditis.
1
Initial Treatment and Stabilization
Initial treatment should begin when the diagnosis of ACS is suspected and
should be guided by the patient’s risk of mortality from a cardiac event.
2,8
The TIMI Risk Score is a validated predictor of outcome in UA/NSTEMI
(see Table 2). Aspirin (162–325 mg) should be given promptly to every
patient undergoing evaluation for ACS unless there is a contraindication;
clopidogrel may be substituted in case of aspirin allergy.
2
Control of pain
with nitrates or opiates is standard treatment, but is not clearly associated
with improved outcome.
2
UA/NSTEMI
All patients with a high risk of UA/NSTEMI and without contraindications
should be given clopidogrel 300–600 mg, unfractionated or low-molecular
weight heparin, and a high-dose statin.
2,9
Beta-blockers may be given if not
contraindicated by bradycardia or heart failure.
2
It is reasonable to consult
a cardiologist before biomarker result if the patient is hemodynamically
unstable or has refractory pain, or once ACS is diagnosed. Determination
of whether the patient will undergo conservative versus early invasive
management (cardiac catheterization with possible revascularization
within 48 hours of presentation) should be guided by risk factors and
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P. A. Erwin, R. L. Narayan and B. J. Darrow
clinical circumstances. Patients with TIMI risk scores ≥ 3 (Table 2), hemodynamic instability, PCI within six months, prior coronary bypass surgery,
ejection fraction < 40%, sustained ventricular tachycardia, or recurrent
angina should be considered for an early invasive strategy.
2,4,10
Patients
managed conservatively can be medically optimized before further risk
stratification and a follow-up appointment with a cardiologist.
Stress testing with adjunct imaging may be utilized safely in low
TIMI risk patients (specifically those with negative serum biomarkers and
without dynamic ST-T deviations) to help stratify patients and determine
suitability for percutaneous intervention.
2
In patients with low clinical
suspicion of disease, this can be performed on an inpatient or outpatient
basis. In those patients suspected of having obstructive coronary disease,
stress testing may be safely performed after the acute event has resolved
and should be performed as an inpatient procedure to allow for rapid risk
assessment and treatment planning. Use of stress testing in this sense
should be thought of as assisting with risk stratification and allowing
clinicians to decide if invasive therapy is warranted.
2
STEMI
Patients with STEMI should have their management discussed immediately
with a cardiologist to determine whether they are candidates for percutaneous
intervention (PCI), thrombolysis, or conservative management. If PCI is
available, or the patient can be rapidly transferred to a hospital performing
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Acute Coronary Syndrome
Table 2. TIMI Risk Score for UA/NSTEMI (1 Point Each)
Age ≥65
≥ 3 risk factors for CAD (HTN, HL, DM, smoking, family history)
Documented coronary stenoses ≥ 50%
Aspirin use in past 7 days
≥ 2 anginal episodes in past 24 hr
ST deviation greater than 0.5 mm
Elevated cardiac biomarkers
Antman EM, et al. (2000) The TIMI Risk Score for Unstable Angina/
Non-ST Elevation MI. JAMA 284: 835–842.
PCI, patient outcomes are better than with thrombolysis. Concurrent medical
therapy is otherwise similar to treatment of NSTEMI.
4
Addition of a glycoprotein IIb/IIIa antagonist may be made at the discretion of the consulting
cardiologist.
11
Transition to Maintenance Therapy
Hospital discharge marks the transition from treatment for ACS to outpatient management of stable chronic ischemic coronary disease. In addition
to medical therapy, lifestyle modifications, smoking cessation, and participation in cardiac rehabilitation are recommended.
2,12
Medications for secondary coronary prevention include antiplatelet
agents; aspirin (75–325 mg daily) forms the foundation.
2,12
In addition to
aspirin, clopidogrel (75 mg daily) for up to one year after an acute coronary
syndrome has been shown to be beneficial in secondary prevention.
2,4,12
Indefinite use of beta-blockers has been shown to reduce cardiac events and
should be prescribed before discharge.
2,4
High-dose statin therapy with
target low-density lipoprotein-cholesterol (LDL-C) below 70–100 mg/dl
should also be instituted prior to discharge if not contraindicated.
2,9,12
An echocardiogram is usually the test of choice to determine cardiac
function and guide transitional therapy. For patients with left ventricular
ejection fraction less than 40%, ACE-Inhibitors (ACE-I), have a mortality
benefit
4
and are indicated. In those patients who are intolerant of ACE-I’s,
angiotensin receptor blockers (ARBs) may be substituted.
4
Finally, in
STEMI patients with left ventricular dysfunction, eplerenone, an aldosterone antagonist, has been shown to reduce mortality.
2,12,13
The use of these
medications should be offset by clinical parameters that may limit their use,
including hypotension, bradycardia, or hyperkalemia. Additionally, these
medications may require outpatient titration to achieve maximum benefit.
Quality Measures in Acute Coronary Syndromes
As the above treatments are recognized as standard of care for patients
with ACS, regulatory groups have established core measures for hospital
200
P. A. Erwin, R. L. Narayan and B. J. Darrow
performance in the care of patients with acute MI.13Table 3 summarizes
the core measures established by the Center for Medicare and Medicaid
Services and The Joint Commission. These guidelines are subject to
regular review; Table 3 lists requirements as of January 2012.
References
1. Thygesen K, Alpert JS, White HD. (2007) Joint ESC/ACCF/
AHA/WHF Task force for the redefinition of myocardial infarction.
Universal definition of myocardial infarction. J Am Coll Cardiol 50:
2173–2195.
2. Anderson JL, et al. (2007) ACC/AHA 2007 guidelines for the management of patients with unstable angina/non–ST-elevation myocardial
infarction — executive summary: A report of the American College of
Cardiology/American Heart Association Task Force on Practice
Guidelines (Writing Committee to Revise the 2002 Guidelines for the
Management of Patients With Unstable Angina/Non–ST-Elevation
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Acute Coronary Syndrome
Table 3. National Hospital Inpatient Quality Measures for Myocardial
Infarction
1. Administration of aspirin at arrival and at discharge.
2. ACE-I or ARB prescribed at discharge for LVEF <40%.
3. Smoking cessation counseling.
4. Beta-blocker prescribed at discharge to patients without contraindications.
5. Fibrinolysis administered within 30 min of hospital arrival for STEMI
patients at institutions where PCI is unavailable and in whom delays in
transfer are expected.
6. Primary PCI for patients presenting with STEMI to institutions capable
of performing such procedures within 90 min of arrival.
7. LDL-Cholesterol assessment on admission.
8. Lipid-lowering therapy (e.g. statins) prescribed at discharge
Krumholz HM et al. (2008) ACC/AHA 2008 performance measures for adults with STelevation and non-ST-elevation myocardial infarction: A report of the American College
of Cardiology/American Heart Association Task Force on Performance Measures
(Writing Committee to Develop Performance Measures for ST-Elevation and NonST-Elevation Myocardial Infarction). J Am Coll Cardiol 52: 2046–99.
Myocardial Infarction) developed in collaboration with the American
College of Emergency Physicians, American College of Physicians,
Society for Academic Emergency Medicine, Society for Cardiovascular
Angiography and Interventions and Society of Thoracic Surgeons. J Am
Coll Cardiol 50: 652–726.
3. Turnipseed SD, et al. (2009) Frequency of Acute Coronary Syndrome
in patients with normal electrocardiogram performed during presence
or absence of chest pain. Acad Emerg Med 16: 495–499.
4. Antman EM, et al. (2004) ACC/AHA Guidelines for the management
of patients with ST-elevation myocardial infarction — Executive
Summary. Circulation 110: 588–636.
5. Panju AA, et al. (1998) Is this patient having a myocardial infarction?
JAMA 280: 1256–1263.
6. Swap, CJ, Nagurney, JT. (2005) Value and limitation of chest pain
history in the evaluation of patients with suspected acute coronary
syndromes. JAMA 294: 2623–2629.
7. Cannon CP, and Lee TH. (2008) Approach to the patient with chest
pain. In: Libby P, et al. (eds), Braunwald’s Heart Disease, 8th ed.
Saunders Elsevier, Philadelphia: pp. 1195–1206.
8. Antman EM, et al. (2000) The TIMI risk score for unstable
angina/non-ST elevation MI. JAMA 284: 835–842.
9. Cannon CP, et al. (2004) Intensive versus moderate lipid lowering
with statins after acute coronary syndromes. N Engl J Med 350:
1495–1504.
10. Cannon CP, et al. (2001) Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated
with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med 344:
1879–1887.
11. Keeley EC, Boura JA, Grines CL. (2003) Primary angioplasty versus
intravenous thrombolytic therapy for acute myocardial infarction: A
quantitative review of 23 randomised trials. Lancet 361: 13–20.
12. Kushner FG, et al. (2009) Focused Updates: ACC/AHA guidelines for
the management of patients with ST-elevation myocardial infarction
(updating the 2004 guideline and 2007 focused update) and
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P. A. Erwin, R. L. Narayan and B. J. Darrow
ACC/AHA/SCAI guidelines on percutaneous coronary intervention
(updating the 2005 guideline and 2007 focused update): A report of
the American College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines. J Am Coll Cardiol 54:
2205–2241.
13. Krumholz HM, et al. (2008) ACC/AHA 2008 performance measures
for adults with ST-elevation and non–ST-elevation myocardial infarction: A report of the American College of Cardiology/American Heart
Association Task Force on Performance Measures (Writing
Committee to Develop Performance Measures for ST-Elevation and
Non–ST-Elevation Myocardial Infarction). J Am Coll Cardiol 52:
2046–99.
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Acute Coronary Syndrome