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Acute Coronary Syndromes

This chapter describes the management of patients with acute, occlusive


coronary artery thrombosis
(acute coronary syndromes, or ACS). The importance of this disorder is shown
by the claim that a fatal
coronary event occurs once every minute in the United States (1). The focus of
this chapter is on the
early management of ACS, and not the diagnostic evaluation, and the
recommendations are based on
clinical practice guidelines from the American Heart Association (2,3).
I. PROTECTIVE MEASURES
The following measures are aimed at protecting the myocardium from ischemic
injury and limiting the
extent of myocardial damage.
A. Oxygen Therapy
1. INDICATIONS: Oxygen therapy is recommended for an arterial O2
saturation <90%, and for
patients with respiratory distress (2,3).
2. COMMENT: Supplemental O2 is no longer recommended as a routine
measure in ACS because O2
promotes coronary artery vasoconstriction (4), and toxic O2 metabolites have
been implicated in
reperfusion injury (5). The potential for harm from O2 therapy was confirmed in
a randomized study
of patients with acute myocardial infarction in which patients who received
supplemental O2
developed larger infarctions and more frequent arrhythmias than patients
allowed to breathe room
air (6).
B. Nitroglycerin
1. INDICATIONS: Sublingual nitroglycerin (NTG) is recommended for
immediate relief of ischemic
chest pain. NTG is also given by continuous IV infusion for recurrent chest
pain, hypertension, or
decompensated heart failure associated with ACS.
2. DOSE: The sublingual dose of NTG is 0.4 mg, which can be repeated every 5
minutes for a total of
3 doses, if needed. The IV dose is a continuous infusion, starting at a rate of 5–
10 μg/min, and
titrating upward to achieve the desired effect. Dose rates above 100 μg/min are
usually not
necessary.
3. CONTRAINDICATIONS: NTG is not recommended for right ventricular
infarction (because the
venodilator effects of NTG are counterproductive), and in patients who have
taken a
phosphodiesterase inhibitor for erectile dysfunction within the past 24 hours
(because of the risk of
hypotension) (2,3).
4. NOTE: For more information on NTG, including adverse effects and NTG
tolerance, see Chapter
45, Section V.
C. Morphine
1. INDICATIONS: Intravenous morphine is the drug of choice for ischemic
chest pain that is
refractory to nitroglycerin, and is also used for hydrostatic pulmonary edema
(because of its
venodilating and sedating effects).
2. DOSE: The effective dose of morphine can vary widely in individual patients.
The initial dose is
usually 4–8 mg as an IV bolus, followed by doses of 2–8 mg IV every 5 or 10
minutes, as needed
(2,3).
3. NOTE: For information on the adverse effects of opioids, see Chapter 43,
Section I-C.
D. Aspirin
1. INDICATIONS: Aspirin is an antiplatelet agent that is recommended for all
patients with ACS who
are not aspirin-sensitive or intolerant, and should be given as soon as possible
(decreases mortality
and re-infarction rate) (2,3).
2. DOSE: The initial dose is 162–320 mg, as a chewable tablet (enhances
absorption), and the
maintenance dose is 81 mg PO daily, using enteric-coated tablets (2,3).
3. NOTE: For patients who are aspirin-sensitive or intolerant, clopidogrel
(Plavix) is a suitable
alternative (2,3). (The dosing regimen for clopidogrel is presented later in the
chapter.)
E. β-Receptor Antagonists
1. INDICATIONS: β-receptor blockade is recommended for all patients with
ACS who do not have a
contraindication, and should be started within 24 hrs after presentation (2,3).
Oral therapy is
suitable for most cases; IV therapy is reserved for patients with persistent chest
pain or
troublesome tachycardia or hypertension.
2. CONTRAINDICATIONS: β-blockers are contraindicated in cases of high-
grade AV block,
decompensated systolic heart failure, hypotension, and reactive airway disease
(2,3), and in cases
of ACS associated with cocaine or amphetamine intoxication (risk of aggravated
coronary
vasospasm from unopposed β-receptor activity) (3).
3. DOSING REGIMENS: Metoprolol (a selective β1-antagonist) is a preferred
β-blocker for ACS.
The oral dosing regimen is 25–50 mg PO every 6 hrs for 48 hrs, then 100 mg
PO BID for
maintenance therapy. (Longer-acting metoprolol succinate can be used for
maintenance therapy at a
dose of 200 mg once daily.) The IV dosing regimen is 5 mg as a bolus dose
every 5 minutes, as
tolerated, to a total of 3 doses (2).
F. RAA Inhibitors
Drugs that inhibit the renin-angiotensin-aldosterone (RAA) system include
angiotensin-converting enzyme
(ACE) inhibitors and angiotensin-receptor blockers (ARBs).
1. INDICATIONS: ACE inhibitors are recommended for all cases of ACS that
do not have a
contraindication. They are especially beneficial in patients with anterior
infarction or systolic
dysfunction (ejection fraction ≤40%), and are recommended in the first 24 hrs
after presentation in
these patients (2). ARBs are reserved for patients who do not tolerate ACE
inhibitors.
2. CONTRAINDICATIONS: These agents are contraindicated in patients with
hypotension, bilateral
renal artery stenosis, renal failure, or hyperkalemia.
3. DOSING REGIMENS: ACE inhibitors are given orally (risk of hypotension
with IV ACE
inhibitors post-MI), and several drugs can be used. One of the popular ACE
inhibitors is lisinopril,
which is started at a dose of 2.5 to 5 mg once daily, and gradually increased to
10 mg daily, as
tolerated (2). For ACE inhibitor-intolerant patients the ARB valsartan has
equivalent efficacy in
acute MI (7). The initial dose is 20 mg PO BID, which is gradually increased to
160 mg PO BID,
as tolerated (2).
G. Statins
1. INDICATIONS: High-intensity statin therapy is recommended for all cases of
ACS that have been
stabilized, including those with LDL cholesterol levels <70 mg/dL (2,3). Of the
available statins,
only high-dose atorvastatin has a proven survival benefit in ACS (8).
2. DOSE: Atorvastatin, 80 mg PO daily (2,3).
3. COMMENT: The troublesome side effects of statins, such as myopathy and
hepatotoxicity, occur
with chronic therapy, and are not a concern when initiating statin therapy for
ACS. There are drug
interactions that de-serve mention; i.e., statins are metabolized by the
cytochrome P450 system
(CYP3A4), and drugs that inhibit this enzyme (e.g., amiodarone, omeprazole)
can increase the risk
of toxic reactions.
II. REPERFUSION
A. The Approach
1. The fundamental goal in ACS is to relieve the obstruction and restore flow in
the infarct-related
coronary artery. There are three methods for achieving this goal: (a)
percutaneous coronary
intervention or PCI (coronary angiography, angioplasty, and stent placement),
(b) thrombolytic
therapy, and (c) coronary artery bypass surgery.
2. The approach to reperfusion is determined by the presence or absence of ST
elevation on the ECG,
as described next.
B. ACS with ST Elevation
ACS with ST elevation ≥0.1 mv in at least 2 contiguous leads usually indicates a
transmural infarction,
from complete obstruction of the infarct-related artery. This condition, ST-
elevation myocardial
infarction or STEMI, requires emergent intervention.
FIGURE 14.1 The survival benefit of thrombolytic therapy in relation to the
time elapsed from the onset
of chest pain. STEMI = ST-elevation myocardial infarction, LBBB = left bundle
branch block. Data from
Reference 9.
1. Time-Dependence
There is convincing evidence that reperfusion with either PCI or thrombolytic
therapy can restore
flow in occluded arteries and decrease the mortality rate (2). However, the
benefit from
reperfusion therapy is time-dependent, and diminishes as the time progresses
from the onset of
chest pain. This is demonstrated in Figure 14.1 for thrombolytic therapy (9);
note that the survival
benefit is negligible after 12 hours from symptom onset.
2. Indications for Reperfusion Therapy
The major indications for reperfusion in patients with STEMI (or a new left
bundle branch block)
are as follows (2):
a. Time from onset of symptoms <12 hrs.
b. Evidence of ongoing ischemia 12–24 hours after symptom onset.
c. Acute, severe heart failure, or cardiogenic shock, regardless of the time from
symptom onset.
3. Percutaneous Coronary Intervention
Percutaneous coronary intervention (PCI) is superior to thrombolytic therapy for
restoring flow in
occluded arteries and improving outcomes (see Figure 14.2) (10-12).
Unfortunately, PCI is not
available in many hospitals. The recommendations for providing PCI to eligible
STEMI patients
(i.e., symptom onset <12 hrs, etc.) are as follows (2):
a. If the patient is at a PCI-capable hospital, the procedure should be performed
within 90
minutes of the first patient contact (in the field).
b. If the patient is at a hospital that is not capable of performing PCI, the
recommended strategy
is transfer to a PCI-capable hospital, with the goal of performing the PCI within
2 hours of the
initial patient contact.
FIGURE 14.2 Comparative effects of coronary angioplasty and thrombolytic
therapy on vascular events
(graph on the left) and clinical outcomes (graph on the right) in patients with
ST-elevation myocardial
infarction. Data from References 10-12.
4. Thrombolytic Therapy
Thrombolytic therapy is the alternative to PCI when the latter is not available, or
cannot be
performed in a timely manner. For optimal results, therapy should begin no later
than 30 minutes
after the patient arrives at the hospital (2). The major restriction to thrombolytic
therapy is a long
list of contraindications, as shown in Table 14.1.
a. LYTIC AGENTS: Fibrinolytic drugs act by converting plasminogen to
plasmin, which then
breaks fibrin strands into smaller subunits. The drugs in Table 14.2 act on
plasminogen that is
bound to fibrin (clot-specific fibrinolysis), which limits the extent of systemic
fibrinolysis and
reduces the risk of bleeding. The success rate in restoring flow is equivalent
(about 85%) for
all fibrinolytic drugs (2).
b. BLEEDING RISK: The risk of major bleeding, such as intracerebral
hemorrhage (0.5–1%),
and extracranial hemorrhage that requires blood transfusions (5–15%), is
equivalent for all the
fibrinolytic drugs (13,14).
c. Major bleeding from thrombolysis can be treated with cryoprecipitate (10 to
15 bags)
followed by fresh frozen plasma (up to 6 units) if necessary, to achieve a serum
fibrinogen
≥100 mg/mL. The use of antifibrinolytic agents such as epsilon-aminocaproic
acid (5 grams
IV over 15–30 min) is reserved for refractory cases of bleeding (because of the
risk of
thrombosis) (14).
C. ACS without ST Elevation
The absence of ST elevation on the ECG indicates less extensive myocardial
injury than a transmural MI,
or ischemia with threatened myocardial injury(troponin levels can help
distinguish between these two).
This condition, called non-ST-elevation MI, or nonSTEMI, is the result of partial
coronary occlusion, or
transient complete occlusion with spontaneous revascularization. As such, it
may not require emergent
reperfusion. The approach to reperfusion therapy in these cases is summarized
below.
1. The timing of PCI in nonSTEMI is determined by the severity of the patient’s
clinical condition (3);
a. Indications for emergent PCI include refractory or recurrent angina, severe
heart failure,
hemodynamic instability, and cardiogenic shock.
b. In clinically stable patients, clinical scoring systems are used to predict the
likelihood of a
poor outcome, and the results of these tests are used to determine the need, and
timing, of PCI
(3).
2. Thrombolytic therapy is not used in nonSTEMI cases.
III. ADJUNCTIVE ANTITHROMBOTIC THERAPY
Anticoagulation and dual antiplatelet therapy are standard practices for the early
management of ACS.
The following is a brief summary of the preferred agents and dosing regimens.
A. Anticoagulation
1. For STEMI patients who undergo PCI, unfractionated heparin (UFH) is
preferred for
anticoagulation.
a. The dosing regimen involves IV bolus doses of 70–100 Units/kg, or 50–70
Units/kg if a
glycoprotein receptor antagonist (described later) is planned, to achieve a
therapeutic
activated clotting time (250–350 sec) (2).
2. Following PCI and thrombolytic therapy, UFH is recommended for short-
term (48 hrs)
anticoagulation, using the following regimen (2).
a. 60 Units/kg IV bolus (maximum 4,000 Units) followed by an infusion at 12
Units/kg/hr
(maximum 1,000 Units/hr), and adjusted to achieve an activated PTT of 1.5 to 2
times control
(2).
3. Low-molecular-weight heparin (LMWH) is preferred for long-term (one
week) anticoagulation
after thrombolytic therapy. The recommended LMWH is enoxaparin, in the
following dosing
regimen (2).
a. For age <75 yrs, 30 mg IV initially, followed in 15 min by 1 mg/kg subQ
every 12 hrs
(maximum 100 mg for first 2 doses).
b. For age ≥75 yrs, the dose is 0.75 mg/kg subQ (maximum 75 mg for first 2
doses) without an IV
loading dose.
c. Regardless of age, if the creatinine clearance is <30 mL/min, the dose is 1
mg/kg subQ every
24 hrs.
4. For nonSTEMI, enoxaparin (LMWH) can be used for the duration of the
hospitalization or until PCI
is performed.
a. The recommended dose in this setting is 1 mg/kg subQ every 12 hrs, or 1
mg/kg subQ every 24
hrs if the creatinine clearance is <30 mL/min (3).
B. P2Y12 Inhibitors
1. The P2Y12 inhibitors are oral antiplatelet agents that block surface receptors
involved in ADPinduced
platelet aggregation. This mechanism of action differs from that of aspirin, so
the
antiplatelet effects of aspirin and P2Y12 inhibitors are additive.
2. Three P2Y12 inhibitors are approved for use in ACS: clopidogrel, prasugrel,
and ticagrelor.
Clopidogrel and prasugrel are prodrugs that require activation in the liver, and
their effects are
irreversible. Prasugrel has the most potent antiplatelet effects, and the highest
risk of bleeding; as a
result, prasugrel is not recommended in patients with prior stroke or TIA (2,3).
3. P2Y12 inhibitors are routinely used in combination with aspirin, and their
dosing regimens are
shown in Table 14.3. When PCI is anticipated, the loading dose of P2Y 12
inhibitors should be given
as early as possible, or at the time of the procedure.
C. Glycoprotein Receptor Antagonists
When platelets are activated, glycoprotein receptors (IIb and IIIa) on the platelet
surface begin to bind
fibrinogen, and the fibrinogen molecules form bridges between adjacent
platelets, which promotes
platelet aggregation.
1. Glycoprotein receptor antagonists (also called IIb/IIIa inhibitors) block the
binding of fibrinogen to
activated platelets, which inhibits platelet aggregation. These drugs are the most
potent antiplatelet
agents available, and are known as superaspirins.
2. The available IIb/IIIa inhibitors include abciximab (ReoPro), eptifibatide
(Integrilin), and
tirofiban (Aggra-stat). All three are given by IV infusion using the dosing
regimens in Table 14.3.
3. These drugs are used in high-risk patients who receive emergent PCI, and are
given just before or
at the start of the procedure.
4. Abciximab is the most potent, most expensive, and longest-acting IIb/IIIa
inhibitor. After
discontinuing this drug, bleeding times can take 12 hours to normalize (15).
Eptifibatide and
tirofiban are short-acting agents; after discontinuing these drugs, bleeding times
return to normal in
15 minutes for eptifibatide and 4 hours for tirofiban (15).
IV. COMPLICATIONS
The complications of ACS can be classified as electrical or mechanical. The
former are presented in
Chapters 13 and 15, and the latter are briefly described here.
A. Structural Defects
Structural defects are the result of transmural (ST-elevation) infarctions. They
can appear at any time in
the first week, but most occur in the first 24 hrs (2). Diagnosis is usually by
transthoracic ultrasound.
Temporary support with intra-aortic balloon counterpulsation is often necessary,
and emergency surgical
repair is required in most cases.
1. ACUTE MITRAL REGURGITATION is the result of papillary muscle
rupture or postinfarction LV
remodeling, and presents with the sudden onset of pulmonary edema and the
characteristic
holosystolic murmur. Diagnosis is by echocardiography, and should prompt
emergent surgical
consultation; as delays to surgery diminish the prognosis (16). Temporary
support with arterial
vasodilators (e.g., hydralazine) and the intra-aortic balloon pump can be used as
a bridge to
surgery. The mortality rate with mitral valve repair is 20% (2) vs. 70% without
surgery (17).
2. RUPTURE OF THE VENTRICULAR SEPTUM often occurs in the first 24
hrs, and is more
common following thrombolytic therapy (18). The presentation can mimic acute
mitral
regurgitation, with acute heart failure and a prominent systolic murmur.
Transthoracic ultrasound
will identify the problem. Some patients may be hemodynamically stable, but
the condition can
progress, and emergent surgical repair is required. The reported mortality rate is
20 to 80% with
surgery (the higher mortality rates are in patients with shock) (2).
3. LEFT VENTRICULAR FREE-WALL RUPTURE presents with the return of
chest pains and new
ST-segment abnormalities on the ECG. Accumulation of blood in the
pericardium often leads to
rapid deterioration from pericardial tamponade. Diagnosis is by cardiac
ultrasound, and
pericardiocentesis can be life-saving. Immediate surgery is the only course of
action, and mortality
rates as low as 12% have been reported with a new “patch and glue” surgical
technique (19).
B. Cardiac Pump Failure
1. About 10% of cases of ST-elevation MI (STEMI) are associated with cardiac
pump failure and
cardiogenic shock (20). About 15% of cases occur at presentation, and the
remainder develop
during the hospitalization (2).
2. Management involves emergent PCI (or thrombolysis if PCI is not available)
and coronary bypass
surgery, if necessary. In one multicenter study, revascularization with PCI or
bypass surgery within
6 hours was associated with a 13% absolute decrease in mortality when
compared with medical
management and delayed surgery (21).
3. The hemodynamic management of cardiogenic shock is described in Chapter
8 (see Sections III-C
and IV). An important consideration in postinfarction cardiogenic shock is
providing hemodynamic
support without producing undesirable increases in myocardial O 2 consumption.
Table 14.4 shows
the superiority of the intra-aortic balloon pump over pharmacologic support in
that regard.
V. ACUTE AORTIC DISSECTION
Aortic dissection involving the ascending aorta can be mistaken as ACS, and
can also be a cause of ACS.
However unlike ACS, aortic dissection is a surgical emergency that is often fatal
if not managed
appropriately.
A. Pathophysiology
Aortic dissection occurs when a tear in the aortic intima allows blood to dissect
between the intimal and
medial layers of the aorta, creating a false lumen. When the dissection involves
the ascending aorta,
retrograde propagation can result in coronary insufficiency, aortic insufficiency,
and pericardial
tamponade (22).
B. Clinical Manifestations
1. The most common complaint is the abrupt onset of chest pain, which is often
sharp, and can be
substernal (ascending aortic dissection) or in the back (descending aortic
dissection). Most
importantly, the chest pain can subside spontaneously for hours to days (23,24),
and this can be a
source of missed diagnoses. About 5% of patients have no pain (22).
2. The most common clinical findings are hypertension (50% of patients) and
aortic insufficiency
(50% of patients) (23,24). Unequal pulses in the upper extremities (from
obstruction of the left
subclavian artery in the aortic arch) are found in only 15% of patients (24).
3. The chest x-ray can show mediastinal widening (60% of cases) (24), or can
be normal (20% of
cases) (22). The ECG can show ischemic changes (15% of cases) or evidence of
MI (5% of cases),
but the ECG is normal in 30% of cases (22).
C. Imaging Studies
1. The diagnosis of aortic dissection requires one of four imaging modalities:
magnetic resonance
imaging (MRI) (sensitivity and specificity 98%), transesophageal
echocardiography (sensitivity
98%, specificity 77%), contrast-enhanced computed tomography (sensitivity
94%, specificity
87%), and aortography (sensitivity 88%, specificity 94%) (25). As indicated
MRI is the most
sensitive and specific imaging modality for the diagnosis aortic dissection.
D. Management
The goals of management in aortic dissection are control of hypertension and
surgical intervention.
1. Antihypertensive Therapy
Antihypertensive therapy should NOT increase cardiac stroke output because
increased flow in the
aorta will augment the shear forces that promote further dissection. For this
reason, β-receptor
antagonists are preferred because they decrease the force of ventricular
contraction (negative
inotropic effect). The drug regimens that are used for blood pressure control in
aortic dissection are
presented in Table 14.5.
a. The β-blocker that is most favored is esmolol (Brevibloc), which has a short
duration of
action (9 minutes) and can be rapidly titrated to achieve the desired end-point.
b. An alternative drug is labetalol, a combined α−β− blocker that can be given in
IV bolus doses
or by continuous infusion.
2. Outcomes
With medical management alone, the mortality in acute aortic dissection
increases 1–2% per hour
after the onset of symptoms (22). Surgical repair reduces the mortality rate to
10% at 24 hours and
12% at 48 hours (22).
REFERENCES
1. Roger V, Go AS, Lloyd-Jones D, et al. Heart disease and stroke statistics—
2012 update: a report
from the American Heart Association. Circulation 2012; 125:e2–e220.
2. Ogara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for
the management of STelevation
myocardial infarction. J Am Coll Cardiol 2013; 61:e78–e140..
3. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline
for the management of
patients with non-ST-elevation myocardial acute coronary syndromes.
Circulation 2014; 130:e344–
e426.
4. McNulty PH, King N, Scott S, et al. Effects of supplemental oxygen
administration on coronary
blood flow in patients undergoing cardiac catheterization. Am J Physiol Heart
Circ Physiol. 2005;
288:H1057–1062.
5. Bulkley GB. Reactive oxygen metabolites and reperfusion injury: aberrant
triggering of
reticuloendothelial function. Lancet 1994; 344:934–936.
6. Stub D, Smith K, Bernard S, et al; AVOID Investigators. Air versus oxygen in
ST-segment elevation
myocardial infarction. Circulation 2015; 131:2143–2150.
7. Pfeffer MA, McMurray JJV, Velazquez EJ, et al. Valsartan, captopril, or both
in myocardial
infarction complicated by heart failure, left ventricular dysfunction, or both. N
Engl J Med. 2003;
349:1893–96.
8. Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid
lowering with statins
after acute coronary syndromes. N Engl J Med. 2004; 350:1495–504.
9. Fibrinolytic Therapy Trialists Collaborative Group. Indications for
fibrinolytic therapy in suspected
acute myocardial infarction: collaborative overview of early mortality and major
morbidity results
from all randomized trials of more than 1000 patients. Lancet 1994; 343:311–
322.
10. The GUSTO IIb Angioplasty Substudy Investigators. A clinical trial
comparing primary coronary
angioplasty with tissue plasminogen activator for acute myocardial infarction.
New Engl J Med
1997; 336:1621–1628.
11. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous
thrombolytic therapy for
acute myocardial infarction: a quantitative review of 23 randomized trials.
Lancet 2003; 361:13–20.
12. Stone GW, Cox D, Garcia E, et al. Normal flow (TIMI-3) before mechanical
reperfusion therapy is
an independent determinant of survival in acute myocardial infarction.
Circulation 2001; 104:636–
641.
13. Llevadot J, Giugliano RP, Antman EM. Bolus fibrinolytic therapy in acute
myocardial infarction.
JAMA 2001; 286:442–449.
14. Young GP, Hoffman JR. Thrombolytic therapy. Emerg Med Clin 1995;
13:735–759.
15. Patrono C, Coller B, Fitzgerald G, et al. Platelet-active drugs: the
relationship among dose,
effectiveness, and side effects. Chest 2004; 126:234S–264S.
16. Tepe NA, Edmunds LH Jr. Operation for acute postinfarction mitral
insufficiency and cardiogenic
shock. J Thorac Cardiovasc Surg. 1985; 89:525–30.
17. Thompson CR, Buller CE, Sleeper LA, et al. Cardiogenic shock due to acute
severe mitral
regurgitation complicating acute myocardial infarction: a report from the
SHOCK trial registry. J Am
Coll Cardiol 2000; 36:1104–1109.
18. Prêtre R, Ye Q, Grünenfelder J, et al. Operative results of “repair” of
ventricular septal rupture after
acute myocardial infraction. Am J Cardiol. 1999; 84:785–8.
19. Haddadin S, Milano AD, Faggian G, et al. Surgical treatment of
postinfarction left ventricular free
wall rupture. J Card Surg 2009; 24:624–631.
20. Samuels LF, Darze ES. Management of acute cardiogenic shock. Cardiol
Clin 2003; 21:43–49.
21. Hochman JS, Sleeper LA, While HD, et al. One-year survival following
early revascularization for
cardiogenic shock. JAMA 2001; 285:190–192.
22. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syndromes. Circulation 2005;
112:3802–3813.
23. Khan IA, Nair CK. Clinical, diagnostic, and management perspectives of
aortic dissection. Chest
2002; 122:311–328.
24. Knaut AL, Cleveland JC. Aortic emergencies. Emerg Med Clin N Am 2003;
21:817–845.
25. Zegel HG, Chmielewski S, Freiman DB. The imaging evaluation of thoracic
aortic dissection. Appl
Radiol 1995; (June):15–25.