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Acute coronary syndrome (ACS) is an umbrella term including unstable
angina (UA) or acute myocardial infarction (MI) which consists of ST
segment elevation MI (STEMI) and non–ST segment MI (NSTEMI).
Diagnosis is based on patient presentation, electrocardiographic
changes, and elevated cardiac biomarkers.
Treatment objectives of ACS are to alleviate ischemic symptoms,
restore blood flow to the infarct-related artery, arrest infarct expansion,
For both STEMI and NSTE-ACS, initial therapies may include oxygen,
Treatment objectives of STEMI are to restore coronary blood flow by
administering a fibrinolytic or performing percutaneous coronary
intervention (PCI). Treatment strategy depends on availability of
catheterization laboratory and skilled staff, time of initial medical
contact, and contraindication for a fibrinolytic agent.
Regardless of reperfusion strategy, patients should receive aspirin in
For patients receiving fibrinolytic therapy, unfractionated heparin (UFH),
enoxaparin, or fondaparinux should also be initiated.
For patients receiving PCI, an anticoagulant strategy consisting of either
UFH with or without a glycoprotein IIb/IIIa inhibitor or bivalirudin alone
For an invasive strategy, a P2Y12
inhibitor (clopidogrel, prasugrel, or
ticagrelor), anticoagulant (UFH, enoxaparin, bivalirudin, or fondaparinux
with UFH) along with aspirin and/or a glycoprotein IIb/IIIa inhibitor is
For an ischemia-guided strategy, an anticoagulant (enoxaparin,
fondaparinux, or UFH) along with dual antiplatelet therapy should be
Potential long-term therapies include a β-blocker; statin; aspirin;
clopidogrel, prasugrel, or ticagrelor; ACE inhibitor or ARB; aldosterone
antagonist; and sublingual NTG. Unless contraindicated, ACE inhibitors
or ARBs should be given to those with a left ventricular ejection
fraction of less than 40%, hypertension, diabetes, or chronic kidney
Lifestyle modifications include smoking cessation, weight management
through diet and exercise to reduce body weight by 10% if body mass
, diabetic treatment to achieve a near-normal
Despite advances in medical intervention and pharmacotherapy, cardiovascular
disease continues to be a leading killer in the United States. Acute coronary
syndrome (ACS) is an umbrella term that includes patients who present with either
unstable angina (UA) or acute myocardial infarction (AMI) which is further
differentiated into ST segment elevation myocardial infarction (STEMI) or non–ST
segment myocardial infarction (NSTEMI).
1–5 The terminology, non–ST segment
elevation-ACS (NSTE-ACS) includes both UA and NSTEMI.
are determined based upon the presence (NSTEMI) or absence (UA) of biomarkers
associated with necrosis. The etiology of ACS originates from the erosion or rupture
of an unstable plaque within the coronary artery leading to the formation of an
occlusive or nonocclusive thrombus. Although NSTE-ACS and STEMI lead to
hospitalization, patients presenting with STEMI are considered medical emergencies
and warrant immediate intervention.
5 Today, the management of ACS is based on
reperfusion and revascularization using both pharmacologic and nonpharmacologic
interventions such as percutaneous coronary intervention (PCI) and coronary artery
1–5 A committee composed of representatives from the
American College of Cardiology (ACC) and the American Heart Association (AHA)
periodically review the literature and publish practice guidelines to aid health care
practitioners in selecting the most effective treatments for patients with ACS.
These guidelines consist of graded recommendations based on the weight and quality
of the evidence. Although there are local variations in practice, these guidelines
serve as the foundation for care of patients with ACS.
According to AHA statistics, 652,000 hospital discharges in the United States were
attributable to ACS as the primary diagnosis in 2010. Financially, the impact of ACS
6 The cost of hospitalization for ACS is expensive and
continues to rise. In terms of direct medical expenditures, ACS costs Americans
more than $150 billion annually, with 60% to 75% of these costs related to hospital
7–9 Approximately one-third of STEMI patients die within
24 hours of onset of ischemia compared with 15% of patients with NSTE-ACS who
either die or experience reinfarction within 30 days of hospitalization.
these numbers are substantial, the risk-standardized 30-day in-hospital mortality for
Medicare beneficiaries admitted for AMI have significantly dropped during the past
In an analysis of Medicare data for all fee-for-service patients 65 years or
older with a diagnosis of ACS, Krumholz et al. estimated that the length of
hospitalization for STEMI/NSTE-ACS has decreased from 6.5 days in 1999 to 5.3
days in 2011. These trends may be reflective of application of evidence-based
guidelines as well as aggressive treatment of hypertension and
The majority of ACS results from occlusion of a coronary artery secondary to
thrombus formation overlying a lipid-rich atheromatous plaque that has undergone
fissuring or rupture (Fig. 13-1). Plaques that are susceptible to rupture have a thin
fibrous cap, large fatty core, high content of inflammatory cells such as macrophages
and lymphocytes, limited amounts of smooth muscle, and eccentric shape. Triggers
such as surges in sympathetic activity with a sudden increase in blood pressure (BP),
pulse rate, myocardial contractility, and coronary blood flow can lead to erosion,
fissuring, or rupture of the fragile fibrous cap. Once ruptured, the thrombogenic
components of the plaque consisting of collagen and tissue factor are exposed. This
promotes activation of the platelet cascade, ultimately leading to the formation of a
thrombus as well as ischemia in the corresponding myocardial area. The extent of
intracoronary thrombosis and distal embolization determines the type of ACS (Fig.
13-1). In patients with UA, the coronary artery has enough blood flow such that the
myocardial cells do not die. In patients with NSTEMI, there exists partial thrombotic
occlusion with or without distal embolization or severe stenosis and some
myocardial cells die. For STEMI, there exists total and persistent thrombotic
occlusion leading to myocardial cell death.
12 Eighty percent of patients presenting
with ACS have two or more active plaques.
Most infarctions are located in a specific region of the heart and are described as
such (e.g., anterior, lateral, inferior). Some patients exhibit permanent
electrocardiographic (ECG) abnormalities (Q waves) after an AMI. In the past,
patients with Q-wave infarctions were generally believed to have more extensive
necrosis and a higher in-hospital mortality rate. Patients with a non–Q-wave infarct
were believed to have a greater likelihood of experiencing postinfarction angina and
early reinfarction. More recently these distinctions have come into question. Some
cardiologists believe there is no difference in prognosis. The terminology has
changed because most patients who have STEMI are treated emergently, preventing
the development of Q waves. An anterior wall infarction carries a worse prognosis
than an inferior or lateral wall infarction because it is more commonly associated
with development of left ventricular (LV) failure and cardiogenic shock.
An important part in establishing the diagnosis of ACS is obtaining the patient’s
“story,” which can elicit crucial hallmark symptoms such as increasing the frequency
of exertional angina or chest pain at rest, new-onset severe chest discomfort, or
increasing angina with a duration exceeding 20 minutes. The pain is typically midline
anterior chest discomfort that can radiate to the left arm, back, shoulder, or jaw, and
may be associated with diaphoresis, dyspnea, nausea, and vomiting as well as
unexplained syncope. Patients with STEMI will usually complain of unrelenting chest
duration, or intensity. Presentation may differ by sex, age, and presence of various
comorbidities. Men commonly complain of chest pain, whereas women often present
with nausea and diaphoresis. Elderly patients may present with hypotension or
cerebrovascular symptoms rather than chest pain. Additionally, onset of ACS does
not occur at random, and many episodes appear to be triggered by external factors or
conditions. MI occurs with increased frequency in the morning, particularly within
the first hour after awakening; on Mondays; during winter months or colder days; and
during emotional stress and vigorous exercise.
The physical examination is important in guiding initial therapy. Signs of severe
LV or right ventricular dysfunction may be present (see Chapter 14, Heart Failure).
The patient may have severe hypertension as a result of pain or, conversely, may be
hypotensive. Significant tachycardia (heart rate > 120 beats/minute) suggests a large
area of damage. On cardiac auscultation, presence of a fourth heart sound (S4
denotes an ischemia-induced decrease in LV compliance. New cardiac murmurs may
be heard, resulting from papillary muscle dysfunction. The cerebral and peripheral
vasculature should be assessed. Patients with a history of cerebrovascular disease
may not be eligible for fibrinolytic therapy. Peripheral pulses should be examined to
assess perfusion and to obtain a baseline before invasive procedures are instituted.
In addition to the patient’s history and presentation, the diagnosis of ACS is based on
the electrocardiogram (ECG) and laboratory results from a cardiac injury profile. A
12-lead ECG should be obtained within 10 minutes of presenting to the emergency
department (ED). The ECG is an indispensable tool in the diagnosis of ACS and has
become the key point in the decision pathway (Fig. 13-2). Key findings on ECG
consist of ST segment elevation, ST segment depression, or T-wave inversion.
definition, STEMI consists of ST segment elevation in two or more contiguous leads
and either exceeding 0.2 mV (2 mm) in leads V1
greater in other leads (Fig. 13-3). NSTE-ACS consists of ST segment depression
exceeding 0.1 mV (1 mm) in two or more contiguous leads or T-wave inversions
exceeding 0.1 mV (1 mm). Additionally, the 12-lead ECG is helpful in determining
the location of an infarct. Q waves may be found in lead V6
leads II, III, AVF for an inferior infarct; in lead I, AVLfor a lateral infarct; and in the
When a cardiac cell is injured, proteins are released into the circulation. The
measurement of these sensitive and specific proteins (troponins T or I and creatine
kinase [CK]) is routine in establishing the diagnosis of AMI (Fig. 13-4). There are
three isoenzymes of CK, of which the MB band is the most specific for the
myocardium. Troponin is the preferred biomarker for assessment of myocardial
damage owing to its high cardiac specificity and sensitivity (90.7% and 90.2%,
respectively) as well as the development of newer sensitive troponin assays.
Troponins T and I are detectable in blood within 4 to 12 hours after the onset of MI,
and peak values are observed at 12 to 48 hours. Troponin levels may also stay
elevated for 7 to 10 days after myocardial necrosis. As seen in Figure 13-4, the
horizontal line depicts the upper reference limit (URL) for the cardiac biomarker in
the clinical chemistry laboratory.
1,2,5 The URL represents the 99th percentile of a
reference control group without MI. Because cardiac troponin T and I are not
normally detected in the blood of healthy people, the definition of an abnormally
increased level is a value that exceeds that of 99% of a reference control group. For
the diagnosis of NSTEMI or STEMI, the patient should have one troponin value or
two CK-MB values greater than the URL. Cardiac biomarkers are not typically
elevated in patients with UA. Presently, no current marker is detectable immediately
upon onset of MI, and therefore repeated measurements of cardiac enzymes after
admission are warranted. A cardiac injury profile will be measured at presentation
and every 3 to 6 hours for the first 12 to 24 hours and periodically thereafter.
Unfortunately, several conditions other than AMI, such as tachyarrhythmias, heart
failure (HF), myocarditis and pericarditis, hypotension or hypertension, acute
pulmonary embolism, end-stage renal disease and cardiac trauma are associated with
elevated troponin. As a result, it is important to assess other diagnostic criteria such
as ECG changes, chest pain, presence of atherosclerotic risk factors, and
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