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424
because of intense reactive medial scarring and fibrosis that occurs
in response to the spirochetal infection. Pheochromocytoma
and weight lifting (believed due to intense or repetitious Valsalva
maneuvers) also predispose to aortic dissection.
Clinical Presentation
CH
34
The most important element of any diagnostic algorithm for suspected acute aortic syndrome is a high clinical index of suspicion,
based foremost on the presenting history and physical examination (
Box 34-3). Absent an appreciation for the cardinal features
of dissection, the diagnosis can be missed in a substantial number of patients. Simple clinical prediction rules have been developed to estimate probability of acute aortic dissection.
investigators have recently confirmed the sensitivity of 12 clinical
risk markers proposed in the 2010 American College of Cardiology
Foundation/American Heart Association (ACCF/AHA) thoracic
aortic disease guidelines
2
(Table 34-1). These markers, assessed
at bedside, were divided into three distinct categories: predisposing factors, characteristics of the pain at time of presentation, and
key physical examination findings.
44
The presence of risk factor(s)
from at least one category identified 95.7% of acute aortic dissection patients in the IRAD database.
History
Diagnosis of aortic dissection may be missed on initial clinical
evaluation in about a third of cases, and an equal number are
detected only at autopsy.
the clinical presentation and occurs in over 90% of patients.
qualitatively severe and may in many cases be distinguished from
coronary ischemia by abrupt onset and maximal intensity at inception. More than 84% of aortic dissection patients described chest
pain as “worst ever” in the IRAD registry.
ized as sharp more often than tearing or ripping in nature, and may
radiate or be sensed anteriorly (suggestive of type A dissection)
or in the interscapular, lower back, or abdominal area (suggestive
of type B dissection). Visceral discomfort or limb pain may be
indicative of aortic branch vessel ischemia from malperfusion.
Syncope is a particularly ominous presenting symptom and may
reflect cardiac tamponade from intrapericardial aortic rupture,
cerebral malperfusion, and/or neurally mediated hypotension in
response to the intense pain of the dissection. In the IRAD registry,
patients with syncope were more likely to die in the hospital or
suffer a stroke. Neurological complications are noted in up to 20%
of aortic dissection patients. For example, paraplegia may develop
when critical impairment of flow to the anterior spinal artery, thoracic intercostals, or the artery of Adamkiewicz occurs. Abdominal
pain is an underrecognized symptom of acute aortic dissection;
when present, it is associated with elevated in-hospital mortality
and increased frequency of malperfusion syndromes.
Numerous other less common clinical manifestations of aortic dissection may be evident on initial evaluation and include Horner's syndrome (compression of the superior cervical ganglion), hoarseness
(pressure against the recurrent laryngeal nerve), hemoptysis (rupture into a bronchus), hematemesis (perforation into the esophagus),
ischemic enterocolitis (mesenteric artery compromise), and fever of
undetermined source (pyrogens released from the false lumen).
Box 34-3 Acute Aortic Syndromes
Aortic dissection
Intramural hematoma
Penetrating aortic ulcer
Rapid aneurysm expansion
Trauma
Adapted from Hiratzka LF, Bakris GL, Beckman JA, et al: 2010 ACCF/AHA/AATS/ACR/
ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients
with thoracic aortic disease. J Am Coll Cardiol 55:e27, 2010.
1,44
Chest pain is the dominant feature of
2,45
The pain is character-
2
43
The IRAD
2,43,44
2
It is
Percentage of Patients in the International
Registry of Acute Aortic Dissection (1996–
TABLE 34-1
2009) with Each of 12 High-Risk Clinical
Markers Observed at Time of Presentation
with Acute Aortic Dissection*
AORTIC
DISSECTION
DETECTION
RISK
CATEGORY
1 MFS
1 Family history of aortic disease 1.9
1 Known aortic valve disease 11.9
1 Recent aortic manipulation 2.8
1 Known thoracic aortic aneurysm 14.7
2 Abrupt onset of pain
2 Ripping or tearing pain 21.7
3 Pulse deficit or systolic blood
3 Focal neurological deficit
3 Murmur of aortic insufficiency (new
3 Hypotension/shock 16.0
*The aortic dissection detection (ADD) score aims to enhance early diagnosis of acute aortic
dissection. The ADD score is calculated by determining the number of categories in which any
of 12 high-risk clinical features are present in patients with symptoms suggestive of acute aortic dissection. For example, in a patient with a family history of aortic disease (category 1) and
known thoracic aneurysm (also category 1), the ADD score would be 1. Likewise, the ADD sco re is
2 in a patient with Marfan's syndrome (category 1) and a blood pressure differential (category
3). A retrospective analysis of the International Registry of Acute Aortic Dissection determined
that among 2538 patients with acute aortic dissection, 95.7% had an ADD score ≥1. The ADD
score may therefore provide the clinician with a simple and effective bedside method to inform
further diagnostic testing and/or treatment in patients with suspected aortic dissec tion. Impor tantly,
the negative predictive value for acute aortic dissection in patients with an ADD score of 0
has not yet been established.
MFS, Marfan's syndrome.
From Rogers AM, Hermann LK, Booher AM, et al: Sensitivity of the aortic dissection detection
risk score, a novel guideline-based tool for identification of acute aortic dissection on initial
presentation. Circulation 123:2213–2218, 2011.
CLINICAL CHARACTERISTICS
Severe pain intensity
pressure differential
(in conjunction with pain)
or in conjunction with pain)
44
% OF PATIENTS
N = 2538
4.3
79.3
72.7
20.3
10.8
23.6
Physical Examination
Patients with acute aortic dissection appear ill, uncomfortable,
and apprehensive. Hypertension is present in more than two thirds
of type B dissection patients and in approximately one third of
type A patients.
in approximately 40% of patients with type A dissection.
rapid equilibration of aortic and LV diastolic pressure from acute
aortic valve regurgitation, the murmur is usually of shorter duration,
lower in pitch, and of lesser intensity than the diastolic murmur
of chronic severe aortic regurgitation. Additional auscultatory
findings include a soft first heart sound and a grade 1 or 2 midsystolic murmur at the base or along the left sternal border.
An inverse correlation between the presence of pulse deficits
and mortality is observed in acute aortic dissection.
pulse deficits may obscure accurate blood pressure assessment, as
in pseudohypotension, which arises from an inability to measure
central aortic pressure when bilateral subclavian and/or femoral
artery compromise is present. Thus, invasive intraarterial monitoring may be necessary in aortic dissection patients.
Elevation of jugular venous pressure, especially with pulsus paradoxus, may indicate pericardial involvement with tamponade.
Superior vena cava syndrome can rarely occur with compression
by an expanding false aneurysm along the greater curvature of the
ascending aorta. Thoracic dullness to percussion and decreased
breath sounds suggests pleural effusion, which is more common
1,2
A murmur of aortic regurgitation can be heard
37
Due to
46
Furthermore,
in the left chest and not necessarily indicative of rupture. In fact,
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pleural effusions are quite frequent with both type A and B dissections; they are usually sympathetic in nature, reflective of the
intense inflammation associated with the acute tear.
Laboratory Testing
BIOMARKERS
Plasma smooth muscle myosin heavy chain protein, D-dimer, and
high-sensitivity C-reactive protein (CRP) have been proposed as
potentially useful biomarkers to assist with point-of-care diagnosis
of aortic dissection. In one study of 95 patients with acute aortic dissection, elevated levels of circulating smooth muscle myosin heavy
chain protein (>
ity of 98% compared with healthy controls when measured within
3 hours of presentation.
2.5 μg/L) had a sensitivity of 90% and a specific-
47
In this analysis, smooth muscle myosin
heavy chain protein levels were elevated in all patients presenting
with a proximal or type A dissection.
Soluble elastin fragment (sELAF) levels have also been proposed to be a useful biomarker for the early detection of acute aortic dissection. Despite a natural rise with age in the concentration
of sELAF levels detected in plasma, a level more than 3 standard
deviations above normal for age is associated with a 64% positivity
rate in acute aortic dissection, compared with 2% for patients with
AMI. Interestingly, patients with complete false lumen thrombosis
appear to have no detectable sELAF.
48
Suzuki et al. conducted a multicenter study of 220 patients with
suspected acute aortic dissection.49 A D-dimer level of less than
500 ng/mL when drawn within 24 hours of symptom onset was associated with a negative likelihood ratio (LR) for aortic dissection of
0.07. Consistent with these data, findings from one large meta-analysis of 734 patients demonstrated that an elevated D-dimer level had
a 97% sensitivity and 96% negative predictive value for identifying
acute aortic dissection. Conversely, an elevated D-dimer is less effective at “ruling-in” aortic dissection, with a specificity of 56% and positive predictive value of 60%.
following acute aortic dissection has been observed, with levels falling rapidly 24 hours following symptom onset.
50
An early rapid increase in CRP levels
51
Although less well
studied in aortic dissection, calponin, a counterpart protein to troponin in vascular SMCs, may provide enhanced specificity for early
detection of type A aortic dissection, but requires comprehensive
testing in advance of clinical application.
52
Other Point-of-Care Tests
The chest x-ray is abnormal in 80% to 90% of patients with aortic dissection, but is an insufficient tool to rule out this condition,
particularly when pathology is confined to the ascending aorta.
53
Findings suggestive of aortic dissection include mediastinal widening, disparity in the caliber of the ascending and descending
thoracic aortic segments, a localized bulge or angulation along
the normally smooth border of the aorta, displacement of intimal
calcium (especially in the region of the aortic knob), and a double density appearance. Associated findings may include cardiomegaly (pericardial effusion) and pleural effusion (left > right).
Effusions that occupy more than 50% of the chest cavity may be
indicative of rupture with hemothorax.
Nonspecific electrocardiographic (ECG) repolarization abnor-
malities are present in approximately 40% of dissection patients.
37
Changes indicative of active ischemia may be found in 15% of
patients, and findings suggestive of AMI (new Q waves, ST-segment
elevation) are present in a small minority (3%) of cases.
37
A thorough assessment is critical to avoid initiation of acute reperfusion
therapy in this setting.
Diagnostic Imaging
Retrograde aortography, the original diagnostic gold standard for
aortic dissection, has been almost completely replaced by transesophageal echocardiography (TEE) and computed tomographic
angiography (CTA). Magnetic resonance imaging/angiography
(MRI/MRA) is much less frequently performed in the acute
setting. Sensitivity and specificity of these three noninvasive techniques are essentially equivalent and exceed 90% in most series.
Choice of imaging technique depends chiefly on availability,
speed, safety, and local expertise in performance and interpretation. A second test is frequently needed for clarification when the
first study is abnormal but nondiagnostic. Regardless of the diagnostic sequence employed, an institutional commitment to rapid
imaging of critically ill patients is critical. Essential features to be
defined for both treatment and prognosis include presence or
absence of ascending aortic involvement, entry and reentry sites,
pericardial and aortic valve involvement, extent of the dissection,
major branch vessel compromise, and the anatomical substrate for
potential malperfusion syndrome(s).
TRANSESOPHAGEAL ECHOCARDIOGRAPHY
A surface transthoracic echocardiogram (TTE) alone is not
sufficient for diagnosis and characterization of aortic dissection
in most cases.54 However, when combined with TEE, the sensitivity
and specificity of these tests reaches 99% and 89%, respectively
(
Fig. 34-6). Transthoracic echocardiogram should not delay perfor-
mance of TEE, which can be accomplished at the bedside in the
emergency department or in the operating room within 15 to 20
minutes. Oropharyngeal anesthesia and conscious sedation are
required, with simultaneous monitoring of heart rate and rhythm,
blood pressure, and oxygen saturation. Orthogonal and longitudinal scan planes combined with M-mode, two-dimensional (2D),
and Doppler profile interrogation provide information regarding:
(1) entry and reentry sites, (2) longitudinal extent and oscillation
of the intimal flap, (3) flow velocity and direction within the true
and false lumens, (4) spontaneous contrast or thrombus within the
false lumen, (5) aortic valve competence and mechanism of regurgitation, (6) ostial coronary artery involvement, (7) pericardial effusion, and (8) global and regional LV function. In most cases, the true
lumen is differentiated from the false lumen by observing systolic
expansion and diastolic collapse, absence or minimal spontaneous
echo contrast, and/or an antegrade Doppler signal. However, vessel
diameter alone is not sufficient for making this determination. In
ambiguous cases (e.g., with a large false lumen), a pressure gradient
between true and false lumen between 10 and 25 mmHg may be
observed by continuous wave Doppler interrogation.
55,56
A series of small echo “blind spots,” however, lie in the distal portion of the ascending aorta, anterior portion of the aortic arch,
and anterior to the trachea and left mainstem bronchus. Signal
TL
FL
FIGURE 346 Proximal aortic dissection imaged by transesophageal
echocardiography (TEE). Horizontal plane TEE image of Stanford type A
aortic dissection reveals a true lumen (TL) diminished in size and false lumen
(FL) extending circumferentially. A communication through the dissection
flap that joins the TL and FL is present (arrow). (From Meredith EL, Masani ND:
Echocardiography in the emergency assessment of acute aortic syndromes. Eur J
Echo 10:i31–i39, 2009.)
425
2
CH
34
PATHOPHYSIOLOGY, CLINICAL EVALUATION, AND MEDICAL MANAGEMENT OF AORTIC DISSECTION
54
426
dropout may occur in the presence of free fluid around the
aorta or pericardium, present in some cases of traumatic aortic
penetration.
COMPUTED TOMOGRAPHIC ANGIOGRAPHY
Multislice CTA using rapid acquisition protocols and postprocess-
CH
ing of the volumetric data (multiplanar reformatting, maximum
34
intensity projection (MIP), shaded surface display, volumetric
rendering) provides highly detailed and visually familiar anatomical images (
racy of 64-slice CTA approaches 100% for aortic dissection.
intimal flap appears as a thin, low attenuation, linear or spiral
structure that separates the true and false lumens. Additional
findings include displacement of intimal calcium, delayed contrast enhancement of the false lumen, and aortic widening.
Branch vessel involvement anywhere along the course of the aorta
to the level of the iliac arteries can be precisely displayed. In addition, CTA can visualize the proximal third of the coronary arteries.
Limitations to CTA include exposure to intravenous contrast and
ionizing radiation. In addition, CTA is an anatomical study; neither aortic valve nor LV function can be rapidly assessed. Motion
artifact, mural thrombi, and image artifacts may negatively affect
study accuracy.
now widespread, and studies can be obtained, reconstructed,
and interpreted within 15 to 20 minutes. Computed tomographic
angiography has several advantages relative to MRA, including
wider availability, quicker throughput, higher spatial resolution,
absence of arterial flow-related artifacts, and the capability to
visualize calcification and metallic implants.
MAGNETIC RESONANCE IMAGING/ANGIOGRAPHY
Contemporary MRI technology affords rapid scanning with the
ability to cover a wide field of view and a comprehensive analysis
of dissection anatomy and extraaortic involvement
also see Chapter 13). Magnetic resonance imaging allows for
assessment of pericardial involvement, aortic regurgitation, proximal coronary artery involvement, and LV function. The 0.5-tesla
(T) magnet and modern gating software allow for expedited scanning across multiple levels during a single breath hold. Despite
these advances, MRI is infrequently used as the initial imaging
study in patients with suspected acute aortic syndromes. Reasons
for its limited use in the acute setting include lack of widespread
availability, difficulties with patient transport to and monitoring
within MRI scanners, and presence of implanted cardiac devices
or metallic clips. Nevertheless, MRI can provide excellent imaging
of false lumen thrombus, intramural hematoma, and penetrating
atherosclerotic ulcers.
Fig. 34-7; also see Chapter 14). The diagnostic accu-
57
Dedicated emergency department scanners are
57,58
57,58
57
The
(Fig. 34-8;
TL FL
FIGURE 348 Contrast-enhanced magnetic resonance angiography
(MRA) of aortic dissection. Maximal intensity projection (MIP) images
of a thoracoabdominal aortic dissection reveal a hyperintense true lumen
(TL) and hypointense false lumen (FL). (From Liu Q, Lu JP, Wang F, et al: Threedimensional contrast enhanced MR angiography of aortic dissection: a pictorial
essay. Radiographics 27:1311–1321, 2007.)
INVASIVE AORTOGRAPHY
The risk for catheter-related injury, length of time required to
assemble necessary personnel in an emergency situation, use of
contrast and ionizing radiation, low sensitivity (77%), and availability of highly accurate noninvasive imaging techniques have
significantly decreased use of invasive aortography as an initial
diagnostic test for acute aortic dissection.
larly limited in diagnosing noncommunicating aortic dissections,
intramural hematomas, and penetrating ulcers.
59
Aortography is particu-
2
Inadvertent injec-
tion into the false lumen or equal and rapid opacification of true
TL
FL
AB
FIGURE 347 Planar computed
tomographic angiogram (CTA)
and three-dimensional (3D)
reconstructed images of Stanford
type A aortic dissection. A,
Coronal CTA image delineates
dissection plane that separates true
lumen (TL) from false lumen (FL).
B, 3D reconstruction imaging in
same patient provides enhanced
spatial resolution after surgical repair
of aortic dissection and surrounding
anatomical structures. In this case,
aortic dissection extends from aortic
root to innominate and left subclavian
arteries, continues through aortic
arch and into descending aorta, with
termination near bifurcation of left
common iliac artery (CIA).
and false lumens without obvious aortic dilation may make cor-
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rect diagnosis of aortic dissection difficult. Invasive angiography is
a feature of any catheter-based intervention.
INTRAVASCULAR ULTRASOUND
Low-frequency (<
20 MHz) intravascular ultrasound (IVUS) affords
maximal signal penetration of the aortic wall and nearly 100% diagnostic accuracy for aortic dissection in a procedure that can be
completed in less than 10 minutes.
58,60
This method provides clear
delineation of several key findings, including entry points, longitudinal and circumferential extent, luminal dimensions and contour,
and thrombus if present. Intravascular ultrasound is infrequently
used as a second imaging technique for diagnosis in patients for
whom false-negative results on invasive aortography are suspected,
and femoral access has been obtained. Intravascular ultrasound may
also have a role during performance of endovascular procedures.
427
CH
34
PATHOPHYSIOLOGY, CLINICAL EVALUATION, AND MEDICAL MANAGEMENT OF AORTIC DISSECTION
CORONARY ANGIOGRAPHY
Selective coronary angiography is neither indicated nor advisable in anticipation of emergency surgery for type A dissection.
61
Operative mortality is generally not related to myocardial ischemia
but rather to aortic rupture, so performance of angiography consumes valuable time before life-saving surgery. Systematic preoperative coronary angiography for hemodynamically stable chronic
type A dissection patients is a subject of debate.
54,62
Preoperative
coronary angiography is reasonable in type A dissection patients
who have a history of previous coronary artery bypass graft surgery,
or in type B patients with unstable angina prior to planned aortic
and/or coronary intervention. Identification of high-grade atherosclerotic disease of native coronary arteries and/or coronary artery
bypass graft(s) affords determination of the optimal operation
for patients requiring ascending aortic surgery. However, in these
instances, the potential for incorporating additional surgical procedures beyond repairing the dissection should be evaluated on a
case-by-case basis.
Differential Diagnosis
Other Acute Aortic Syndromes
Aortic transection from deceleration injury and traumatic aortic valve disruption with acute severe aortic regurgitation occur
in the setting of high-speed vehicular accidents or vertical falls.
The nontraumatic acute aortic syndromes, however, are often not
distinguishable from classic dissection on clinical grounds alone,
but rather are delineated with cross-sectional imaging.
FIGURE 349 Aortic intramural hematoma (IMH). Axial multidetector
computed tomographic angiographic (CTA) image acquired at level of aortic
arch reveals circumferential rind (arrows) that does not enhance with contrast.
(From Takahashi K, Stanford W: Multidetector CT of the thoracic aorta. Int J
Cardiovasc Imaging 21:141–153, 2005.)
IMH from aortic aneurysm with mural thrombus, severe atherosclerosis, or aortitis with medial inflammation and edema.
PENETRATING ATHEROSCLEROTIC AORTIC ULCER
An inflamed atherosclerotic plaque that disrupts normal aortic wall architecture may result in erosion of the internal elastic
membrane, allowing luminal blood to burrow into the media of
the aorta and beyond. Penetrating atherosclerotic aortic ulcers
(PAUs) are most commonly seen in the mid- to distal descending thoracic aorta in older persons with a heavy burden of atherosclerotic disease. They appear as irregular craters or outpouchings
of contrast (Fig. 34-10) and may result in IMH formation or frank
dissection. Ganaha et al. observed in a retrospective analysis of 65
symptomatic IMH patients with PAU that ulcer depth (>1.0 cm) and
diameter (>2.0 cm) positively correlated with disease progression
(i.e., IMH expansion, aortic rupture, propagation of dissection).66
Others suggest that PAU location in the proximal segment of the
descending thoracic aorta, and refractory symptoms rather than
presence of an ulcer per se is most worrisome.
67
Medical management with vigilant clinical and radiological follow-up is advised for
the initially uncomplicated descending thoracic PAU. Surgery or
endovascular stent grafting when feasible can be undertaken for
failed medical therapy, pseudoaneurysm, or rupture.
AORTIC INTRAMURAL HEMATOMA
Intramural hematoma (IMH) is defined as a contained collection of
blood within the wall of the aorta, without evidence of an intimal
flap, entry tear, or double lumen (
for IMH include primary rupture of the nutrient vasa vasorum or
a limited intimal tear that cannot be detected with imaging.
Fig. 34-9). Mechanisms to account
62–64
Intramural hematoma is observed clinically in about 20% of cases
of suspected acute aortic dissection and is discovered at autopsy
in 5% to 13% of acute aortic syndrome cases.
2,64
Approximately 10%
*
of aortic IMHs undergo spontaneous resorption. Predicting evolution to dissection, rupture, aneurysm formation, or false aneurysm
development is difficult. Type A IMH thickness greater than 11 mm
is an independent risk factor for death, surgery, or progression to
dissection.
4.8 cm is a high-risk feature.
64,65
Likewise, an ascending aortic diameter greater than
2,62–65
Aortic IMH is managed according
to the same principles that pertain to aortic dissection, including
surgery for type A disease, surveillance imaging, and intervention
for downstream complications.
Diagnosis of IMH by TEE requires visualization of crescentic or circumferential wall thickening of more than 0.7 cm or identification of
fresh thrombus within the aortic wall. Computed tomographic angiography and MRA are more accurate than TEE for distinguishing
FIGURE 3410 Penetrating atherosclerotic ulcer (PAU). Transesophageal
echocardio graphic (TEE) image of anterior aortic arch wall demonstrates
outpouching from ulcer-like crater. (From Firschke C, Orban M, Andrássy P, et al:
Images in cardiovascular medicine. Penetrating atherosclerotic ulcer of the aortic
arch. Circulation 108:e14–e15, 2003.)
428
ACUTE ANEURYSM EXPANSION
Acute painful expansion of a previously established aortic aneurysm may herald impending rupture. Aortic aneurysm due to atherosclerosis (especially abdominal or descending thoracic in
location) is particularly susceptible to sudden expansion, although
CH
this phenomenon occurs with aortitis and other diseases such as
34
MFS. Imaging studies in the former disease states may reveal wall
thickening and periaortic stranding or hematoma, as well as a
measurable increase in aortic dimensions when compared with
available past studies. Rapid expansion of the Marfan aorta occurs
for reasons not related to inflammation, but when present may be
even more worrisome. Urgent surgical referral is indicated.
Nonaortic Diseases
Chest or back pain may be the presenting symptom of a variety
of conditions including AMI, unstable angina, pericarditis, musculoskeletal pain, pulmonary embolism (PE), pneumonia, pleuritis, and cholecystitis. Attention to the patient's description of the
nature and quality of the pain, presence of predisposing factors,
physical examination, and initial laboratory studies should allow
early differentiation.
Initial Medical Treatment
Patients with acute aortic syndromes should be treated with
intravenous medications to lower the arterial blood pressure
as expeditiously as possible (
is a function of LV contraction velocity (expressed mathematically as change in pressure divided by change in time [dP/dT]),
β-adrenergic receptor antagonists, given to attenuate LV systolic
Fig. 34-11). Since aortic wall strain
Intravenous b-Adrenergic Receptor
TABLE 34-2
Antagonists for Management of Acute Aortic
Dissection
THERAPY
Metoprolol
Labetalol 10-20 mg bolus, repeat 20-40 mg
Esmolol 0.5 mg/kg bolus, then 50 μg/kg/
Propranolol 0.05-0.15 mg/kg every 4-6 h as
5 mg bolus every 5 min for 3 doses;
additional doses of 5-10 mg every
4-6 h as needed
bolus every 10-15 min as needed
Maintenance infusion 1-2 mg/min;
maximum total dose of 300 mg
min infusion
needed
DOSE
RECEPTOR
SELECTIVITY
HALFLIFE
β1 > β2 (3-6 h)
α1-, β1-, and β2
(≈ 5.5 h)
β1 (9 min)
β1 ≈ β2 (5-7 h)
contractile force and decrease heart rate, are first-line therapeutic agents (
Table 34-2). In patients with a contraindication or
intolerance to β-adrenergic receptor antagonists, a heart rate–
slowing nondihydropyridine calcium channel blocker, such as
diltiazem or verapamil, may be an effective substitute.
Target systolic blood pressure and heart rate are 110 mmHg and
60 beats/min or less, respectively, but medications may require
titration according to clinical evidence of impaired end-organ
perfusion. β-Adrenergic receptor antagonists alone are often insufficient for achieving blood pressure control, so administration of
a direct vasodilator may be necessary. Sodium nitroprusside is
Suspected dissectionStep 1
Directed history and exam
ECG, biomarker testing
Diagnostic Imaging (CTA TEE)
Initiate IVs medical treament
Step 2
YES (Type A) NO (Type B)
Emergency surgical consultation
Step 3
Operative management
Cannulation, perfusion
Aortic valve considerations
Management of arch complications
Step 4
FIGURE 3411 One proposed management pathway for acute aortic dissection. In Step 1, a low index of clinical suspicion for acute aortic dissection should
prompt early diagnostic testing while medical therapy is initiated. Step 2 involves determination of ascending aortic involvement, which significantly influences
importance of emergent surgical consultation. In Step 3, patients with type A aortic dissection are referred for surgery, and patients with complicated type B aortic
dissection are referred for endovascular therapy or surgery. Patients with uncomplicated type B aortic dissection are continued on medical therapy and monitored
for changes in clinical status. In Step 4, a care plan is established that emphasizes importance of long-term medical therapy, radiological surveillance, and lifestyle
modifications to decrease risk of postdissection complications. Long-term medical therapy should include β-receptor antagonists and angiotensin receptor blockers
(ARBs) or angiotensin-converting enzyme inhibitors (ACEIs) to achieve resting heart rate of 60 beats/min or less and BP of 120/80 mmHg or less, respectively. BP, blood
pressure; CTA, computed tomographic angiography; ECG, electrocardiogram; HR, heart rate; IV, intravenous; TEE, transesophageal echocardiography. (Adapted from
Hiratzka LF, Bakris GL, Beckman JA, et al: 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic
disease. J Am Coll Cardiol 55:e27–e129, 2010.)
OR
Intra-op TEE
2
Ascending aortic involvement?
Complicated? Uncomplicated?
Malperfusion syndrome
Rupture
Rapid expansion
Refractory pain
Endovascular (TEVAR) open repair
Long-term medical treatment
Radiologic surveillance
Pain, HR, BP controlled
Continued medical
treatment
the agent of first choice in aortic dissection patients with hyper-
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tension refractory to initial β-blocker therapy, but should not be
initiated without adequate heart rate control because reflex tachycardia unfavorably influences the dP/dT profile. The starting dose
is 25 μg/min by continuous infusion, and adjustments are usually
made in increments of 10 to 25 μg. At infusion rates above 2 μg/
kg/min, the circulating concentration of the metabolite cyanide
−
(CN
) exceeds the rate of excretion by the kidneys. After a total
nitroprusside load of 500 μg/kg, endogenous molecular CN− buffers are depleted, increasing the probability of complications from
drug toxicity, including death. In clinical practice, measuring levels of thiocyanate, a byproduct of CN
−
metabolism, is critical to
prevent drug-induced CN− toxicity, particularly in patients with
renal insufficiency. Alternative intravenous vasodilators available
for use in the acute setting include enalaprilat, hydralazine, and
nicardipine.
68
Concomitant analgesia for pain control is essential
and may favorably influence blood pressure and heart rate.
For acute aortic dissection patients with hypotension, cardio-
genic shock from hemopericardium should be considered.
Volume resuscitation or pressor therapy may be necessary to
maintain vital organ perfusion, but these are merely temporizing
measures. Pericardiocentesis for relief of tamponade is not recommended, and surgery should be performed emergently.
Indications for Surgery
Anatomical location of disease, patient comorbidities, initial complications from the dissection, and acuity of presentation (i.e.,
acute vs. chronic) are key factors that influence surgical indications for treatment of aortic dissection (
evidence to support a relationship between clinical outcome and
operator experience in repair of aortic disease. Increasing hospital
volume for open abdominal aortic aneurysm repair is associated
with improved survival, particularly at centers that perform over 50
abdominal aortic aneurysm repairs annually.
lished are clinically useful parameters for evidence-based referral
of patients with thoracic aortic disease. Ongoing public health initiatives have proposed examining the following variables to define
centers of excellence for surgical repair of thoracic aortic disease:
procedural volumes (operator and facility), outcome, time to
Box 34-4 Indications for Surgery
Acute Dissection
Type A
All patients
Type B
With complications:
Rupture
Extension
Rapid aneurysm expansion
Malperfusion syndrome
Marfan's syndrome (MFS)
Chronic Dissection
Type A
Maximal dimension ≥5.5 cm
MFS with maximum dimension ≥4.5-5 cm
Increase in dimension ≥1 cm/yr
Severe aortic regurgitation
Symptoms suggestive of expansion or compression
Type B
Maximal dimension ≥5.5-6 cm
Increase in dimension ≥1 cm/yr
Symptoms suggestive of expansion or compression
Adapted from Hiratzka LF, Bakris GL, Beckman JA, et al: 2010 ACCF/AHA/AATS/ACR/
ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients
with thoracic aortic disease. J Am Coll Cardiol 55:e27, 2010.
Box 34-4). There is evolving
69,70
Less well estab-
2
diagnosis and intervention, and logistical measures including distance to nearest referral center and services available.
2,71
Type A Aortic Dissection
Recommendations pertaining to patient selection for surgical,
endovascular, or medical treatment of acute aortic dissection are
derived from consensus expert opinion because randomized trials are lacking.
dissections, regardless of the site of entry.
2
Emergency surgery is indicated for all acute type A
2,72
Surgery is performed to
prevent rupture with exsanguination or tamponade and to relieve
aortic regurgitation when present. The extent and complexity of surgery (resection/grafting of the ascending aorta, valve resuspension
or replacement, coronary artery reimplantation) is determined on
a case-by-case basis. Incorporation of the aortic arch in the primary
repair is indicated when the tear traverses this segment of the aorta
or when it has become acutely aneurysmal.
73
Indications for and
timing of surgical repair for the unusual case of chronic stable type
A aortic dissection are unresolved. In this situation, surgeon preference and patient comorbidities weigh heavily in decision making,
as does any information related to aortic enlargement over time.
Outcomes with conservative management may not be inferior to
surgical repair in the chronic phase, as suggested by limited single
center experiences and retrospective data.
12,75
Endovascular stent
grafts are not approved by the U.S. Food and Drug Administration
(FDA) for use in the ascending aorta or arch.
Type B Aortic Dissection
Uncomplicated type B dissection is treated medically, with emphasis on tight heart rate and blood pressure control. Serial imaging
is performed to monitor disease evolution. Lifestyle modifications,
including the possibility of career change, may be necessary to
avoid strenuous lifting, pushing, or straining that requires intense or
repetitive Valsalva maneuvers.
Surgery for acute type B dissection is generally reserved for
those patients who have failed initial conservative therapy and
have a complicated course, as indicated by refractory or recurrent
pain, continued extension, early aneurysmal expansion, rupture,
malperfusion syndrome, dissection location within a previously
known aneurysmal aortic segment, and for patients with MFS. The
importance of refractory pain in otherwise uncomplicated type B
dissection is increasingly appreciated. In one recently published
prospective analysis of 365 type B dissection patients without
conventional high-risk features, the presence of pain or persistent hypertension despite medical therapy was associated with a
35-fold increase in mortality, compared with the absence of these
clinical features.
74
Presently there are insufficient data to provide comprehensive guidelines for appropriateness of endovascular stent grafting,
percutaneous fenestration, and branch vessel stenting as alternatives to surgery for type B aortic dissection (
Chapter 36). Several nonrandomized small prospective trials and
registries have shown that endovascular stent grafting for acute,
subacute, or chronic type B dissection can be an effective lowerrisk alternative to surgery.
adoption of endovascular stent graft treatment for complicated
type B dissection, although randomized trial data are lacking. Most
high-volume centers have moved in this direction, and it is unlikely
that a pivotal trial versus surgery will be conducted in patients with
traditional indications for surgery in type B dissection.
The Investigation of Stent Grafts in Aortic Dissection (INSTEAD)
trial randomized 140 stable
section to optimal medical therapy or optimal medical therapy
plus endovascular stent grafting.
powered for the primary endpoint of aorta-related death at
2 years following randomization, a substantially greater number of
patients who underwent stent grafting demonstrated recovery of
true lumen size and contour and false lumen thrombosis (91%)
compared with those who received optimal medical therapy
2
Table 34-3; also see
75–77
Recent years have seen increasing
type B patients 2 weeks following dis-
78
Although this trial was under-
429
CH
34
PATHOPHYSIOLOGY, CLINICAL EVALUATION, AND MEDICAL MANAGEMENT OF AORTIC DISSECTION
430
Probability of Death (%)
Society of Thoracic Surgeons Class I and II
TABLE 34-3
PATIENT SUBGROUP
CH
Acute traumatic dissection I C
34
Acute type B dissection with
ischemia
Symptomatic PUA/AIH IIa C
Chronic dissection from
trauma
Acute type B dissection
without ischemia
Subacute dissection IIb B
Chronic dissection IIb B
Degenerative descending
aortic dissection >5.5 cm
Aortic arch dissection with
morbidity prohibitive for
surgery
AIH, aortic intramural hematoma; PUA, penetrating atherosclerotic aortic ulcer.
Adapted from Svensson LG, et al: Expert consensus document on the treatment of descending
thoracic aortic disease using endovascular stent-grafts. Ann Thorac Surg 82:S1, 2008.
alone (19%; P
gesting positive aortic remodeling in type B dissection patients following endovascular stent graft placement. It is unclear whether
positive aortic remodeling will impact clinical outcomes longer
term. Endoleak, stroke, and other device complications including
migration and thrombosis have been reported.
Indications for percutaneous balloon fenestration include false
lumen compression of the true lumen with end-organ hypoperfusion.
In this procedure, a balloon catheter is used to create a transverse
tear across the dissection flap to attenuate compressive forces on the
true lumen and improve flow to compromised organs. Placement of
a bare metal stent (BMS) into side branch vessels to restore blood
flow may be performed to enhance regional perfusion.
Surgery for chronic type A aortic dissection is indicated for treatment of symptomatic aortic regurgitation with LV dysfunction or
for management of aneurysmal disease according to conventional
size criteria (≥
for descending thoracic aneurysm, ≥5.5 cm for thoracoabdominal
aortic aneurysm, or ≥1.0 cm/yr increase in maximal dimension).2
Of note, in high-risk patients, such as those with MFS, elective aneurysm repair may be recommended at smaller aortic diameters.
Recommendations for Thoracic Stent Graft
Insertion
CLASSIFICATION
I A
IIa B
IIb C
IIa with comorbidities
IIb without comorbidities
IIb C
<0.001). These data are concordant with others sug-
76
5.5 cm for ascending aortic aneurysm, ≥5.5-6.0 cm
LEVEL OF
EVIDENCE
B/C
7
Aneurysmal enlargement and recurrent dissection are more likely
with long-term patency or partial thrombosis of the false lumen.2
It has been proposed that partial thrombosis of the false lumen
confers a worse outcome on patients with type B aortic dissection due to associated increases in pressure within the false lumen
that may compromise true lumen-mediated blood flow to critical
15–17
organs.
Prognosis
The European Cooperative study group reported 1- and 2-year
mortality rates for patients with type A dissection of 60% and 50%,
respectively.
vors will experience rupture, extension, or require surgery for aneurysm formation within 5 years of recovery from the initial event.7
Outcome in acute type A dissection is heavily influenced by treatment strategy; in-hospital mortality rates following presentation are
65% and 6% with medical therapy and surgical repair, respectively.
Nevertheless, surgical outcomes are poor in patients demonstrating signs of ischemia in renal, mesenteric, or peripheral arterial circulatory beds prior to dissection repair.
tool for in-hospital mortality incorporating these variables offers
clinicians, patients, and families a useful method by which to
understand the complexities and hazards of the acute dissection
process
For type B dissection, overall in-hospital mortality rates approach
15%.
medically, 1-month survival is 90%, whereas for patients who require
surgical intervention for the indications listed previously, 1-month
survival is only 75%. Independent predictors of early mortality
include advanced age, rupture, and malperfusion syndromes. The
excess mortality risk imposed by early complications necessitating
surgical treatment, and thus operation on acutely sicker patients, has
prompted investigation of endovascular stent grafting for selected
patients. Nearly 2 decades of experience with thoracic endovascular aortic repair have yielded encouraging results regarding
short- and long-term efficacy rates for this treatment strategy. One
retrospective analysis of 87 patients undergoing endovascular stent
placement to treat acute type B dissection demonstrated a 30-day
survival rate of 81%, despite the presence of hemodynamic instability or shock in 62% of the study population.
patient cohort for whom the prevalence of hemodynamic collapse
was only 16%, endovascular graft placement was associated with
short- and long-term survival rates of 90% and 87%, respectively.
The most feared complications of type B aortic dissection are
rupture, redissection, or development of malperfusion syndromes.
Complete or partial false lumen patency or maximal descending thoracic aortic diameter of 4.0 cm or greater are risk factors
for development of subsequent descending thoracic aortic
aneurysms.
54
Approximately one third of aortic dissection survi-
7
A bedside risk prediction
72
(Fig. 34-12).
37
For patients with uncomplicated type B dissection managed
80
In a type B dissection
78
79
81
90
80
70
60
50
40
30
20
10
0
0 0.5 1.0 1.5
Observed
Model
2.0 2.5
Model Score
3.0 3.5 4.0 4.5 5.0
FIGURE 3412 Observed versus
predicted mortality rate for patients
with acute type A dissection in the
International Registry of Aortic Dissection.
Variables used in the risk model include age,
female gender, abrupt onset of pain, abnormal
electrocardiogram (ECG), pulse deficit, renal
failure, and hypotension/shock/tamponade.
(From Mehta RH, Suzuki T, Hagan PG, et al:
Predicting death in patients with acute type A
aortic dissection. Circulation 105:200–206, 2002.)
Long-Term Surveillance
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Because of the lifelong risk of subsequent aortic and cardiovascular complications, vigilant clinical and radiographic followup is mandatory for all hospital survivors. Medical management
remains targeted to strict blood pressure (≤
heart rate (≤60 beats/min) goals.2 Statin therapy is indicated for
treatment of atherosclerosis. Strenuous exercise is discouraged,
and patients need be educated regarding the chronic nature of this
disease, self-awareness of dissection-associated symptoms, and the
importance of medication adherence. Imaging of the entire aorta
is recommended pre-discharge and at 1, 3, 6, and 12 months, then
annually thereafter.
82
The continued high rates of death and disability from acute
aortic dissection reinforce the urgent need for improvements in
aggressive treatment of identifiable risk factors (notably hypertension), genetic and biomarker screening, clinical awareness, regional referral networks, consistent care protocols both
during and after hospitalization, and possibly, surgical centers of
excellence in aortic repair.
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CH
34
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CHAPTER
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35 Surgical Therapy for Aortic
Dissection
Joseph Huh, Joseph S. Coselli, Scott A. LeMaire
The treatment of aortic dissections remains technically challenging
to surgeons. Patients can present with a wide range of anatomical
and physiological derangements. Surgical decisions are made on
the basis of three primary considerations: anatomical location
of the dissection, time since the onset of dissection, and resulting
complications of dissection. The DeBakey and Stanford classifications define dissections according to their anatomical location;
both systems place great importance on the involvement of the
ascending aorta
the ascending aorta and extends varying distances into the thoracoabdominal aorta, often reaching the aortic bifurcation. Type II
dissection is confined to the ascending aorta. Type III dissection initiates in the descending thoracic aorta and extends variable distances
into the thoracoabdominal aorta. Timing of the operation is important
because surgical repair becomes safer as the dissection becomes
older and the aorta less fragile. Risks posed by tissue fragility must be
weighed against the competing risk of acute complications, which
include rupture, heart failure, and malperfusion. Although arbitrary, dissection is considered acute
in the aortic wall. After 14 days, the dissection is described as chronic.
Additionally, aortic dissections can produce a wide variety of lifethreatening complications that may mandate emergent surgical
repair or correction. Aortic rupture can occur anywhere along the
dissected aorta. Lethal proximal aortic complications include pericardial tamponade, acute aortic valve regurgitation, and myocardial
infarction (MI) from coronary artery malperfusion. In subsequent
aortic segments, malperfusion of branch vessels can cause stroke,
paraplegia, mesenteric ischemia, renal failure, and limb-threatening
ischemia (
combined with severe physiological derangement and extreme
tissue fragility, make aortic dissection one of the most challenging
conditions faced by cardiovascular surgeons. These considerations
are the foundations of operative indications and strategies for aortic
dissection. Surgical strategies for treating proximal aortic dissections
involving the ascending aorta and transverse aortic arch differ distinctly from strategies for treating distal aortic dissections involving
the descending thoracic and thoracoabdominal aorta; therefore, the
proximal and distal aortic segments will be discussed independently.
1
(Fig. 35-1). DeBakey type I dissection initiates in
within the first 14 days after the initial tear
Fig. 35-2). The potential for these acute complications,
Acute Proximal Dissection
Without treatment, nearly half of patients with acute proximal aortic dissection die within 48 hours.
aggressive pharmacological treatment is initiated immediately, and
the focus can then shift to confirming the diagnosis and assessing
treatment options (see Chapter 34).
Indications for Operation
Proximal aortic repairs performed in the chronic phase uniformly
have better outcomes than those performed in the acute phase.
Unfortunately, the high risk associated with early operation is outweighed by the even higher risk of a fatal complication (e.g., aortic
rupture) during medical management. Therefore, the presence of an
acute proximal aortic dissection has traditionally been considered
an absolute indication for emergency surgical repair. Many authors
continue to advocate this approach.
operative management of acute proximal aortic dissection has been
proposed in specific clinical scenarios: in elderly patients; in patients
with severe malperfusion; when dissection occurs after previous
cardiac operation; and to enable transport to a specialized center.
2
Once the diagnosis is suspected,
3,4
Although controversial, delayed
ELDERLY PATIENTS
Emergent repair of proximal aortic dissection in patients with
advanced age remains controversial. In recent literature, operative mortalities of nearly 50% have been reported for octogenarian
patients.
ranted in the elderly because “it does not reverse the unfavorable
prognosis of the disease.”
national registry identified a significant trend toward nonoperative
management of acute aortic dissections (AAD) with increasing age.
However, elderly patients who survived operative treatment had better long-term survival than patients who were treated medically.
risk situation. Surgical results of institutions and communities have
to be considered to optimize best outcomes.
erative strategies, such as total arch replacement and root replacement, should be weighed against the mortality risk associated with
prolonged operations. In patients whose limited physiological
reserve makes them poor candidates for emergency aortic repair,
delayed management with initial medical optimization followed
by elective surgery may be a reasonable alternative.
SEVERE MALPERFUSION
Branch-vessel obstruction due to dissection creates a spectrum of
malperfusion that ranges from mild (e.g., diminished pulse in an
extremity) to severe (e.g., bowel infarction). In most cases of mild
to moderate malperfusion, surgical repair of the proximal aorta
redirects flow into the true lumen and restores adequate peripheral
blood flow; however, patients in whom ischemia has caused severe
end-organ dysfunction are unlikely to benefit from immediate
ascending aortic repair.11 Stroke with resulting coma and bowel
infarction with peritonitis remain ominous conditions after type
I aortic dissection. Deeb et al. reported that eight of nine patients
who underwent early proximal aortic repair in the setting of severe
malperfusion (as defined in
the hospital. All deaths were attributed to irreversible ischemic
organ damage and severe reperfusion injury after cardiopulmonary bypass (CPB). On the basis of these results, these surgeons
initiated a policy of delayed surgical treatment in patients with
severe malperfusion. This strategy consisted of aggressive pharmacological treatment to reduce dP/dt (rate of rise of left ventricular
[LV] pressure), confirmatory arteriography, percutaneous fenestration or stenting (if needed) to restore flow to compromised
branch vessels, and elective operation after complete recovery
from malperfusion. Of the 20 patients treated with this strategy, 17
underwent delayed operation an average of 20 days after presentation.
the three patients who died without operation (one from rupture,
two from reperfusion injury) and the two patients who died after
delayed surgery. The overall survival for these patients treated without immediate operation (15/20, 75%) was significantly better than
the dismal survival obtained with a strategy of immediate surgery.
Fabre et al. have also advocated percutaneous intervention before
operation in patients with severe ischemic sequelae.
DISSECTION AFTER PRIOR CARDIAC OPERATIONS
Delayed management with elective operation has been proposed
for patients who have had cardiac surgery in the remote past.
Presence of prosthetic aortic valves, aortic suture lines, coronary
5,6
Neri et al. concluded that surgical treatment is not war-
7
A demographic study that used a Taiwanese
Clearly, acute proximal aortic dissection in the elderly is a high-
9,10
Aggressive intraop-
Box 35-1) died before discharge from
12
To reduce selection bias, the authors’ analysis also included
13
8
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