diagnostic algorithm for acute aortic dissection imaging
TRANSCRIPT
Diagnostic algorithm for acute aortic dissection – imaging and biomarkers
Professor Toru Suzuki, MD, PhD
Chair of Cardiovascular Medicine
Department of Cardiovascular Sciences
University of Leicester
Honorary Consultant Cardiologist
Glenfield Hospital
University of Leicester Hospitals NHS Trust
Disclosure of Interest
I do not have any potential conflict of interest
AORTIC DISSECTION
PENETRATING ULCER
INTRAMURAL HEMATOMA
ulceration of an aortic atherosclerotic plaque penetrating
through the internal elastic lamina into the media. Such
lesions represent 2 – 7% of all AAS. Propagation of the
ulcerative process may either lead to IMH,
pseudoaneurysm, or even aortic rupture, or an acute AD.
intramural haematoma develops in the media of the
aortic wall in the absence of an FL and intimal tear.
Intramural haematoma is diagnosed in the presence of
a circular or crescent-shaped thickening of 0.5 mm of
the aortic wall in the absence of detectable blood flow.
disruption of the medial layer provoked by intramural
bleeding, resulting in separation of the aortic wall
layers and subsequent formation of a TL and an FL
with or without communication
D-dimer levels in acute aortic dissection
Eggebrecht et al. JACC 2004;44:804.
• Dissections show marked elevations in D-dimer compared
to control diseases in first 6 hrs after symptom onset
Time-course analysis
Diagnostic performance in early presenters
• Patients <6 hrs from onset
• 23 AD cases (19 type A, 4 type B)
31 controls (9 MI, 14 angina, 2 PE, 6 uncertain)
• NLR <0.1 against all controls in first 6 hrs after Sx onset
• PLR >10 against all controls in first 6 hrs after Sx onset
-- possible rule-in at cut-off of 1600 ng/ml
(too few number of PE cases to be definitive)
ADD clinical score and D-dimer levels
High probability on ADD score -- high D-dimer levels
Low probability on ADD score -- low D-dimer levels
Discrepancies – pitfalls or promise
• Low-probability ADD score and high D-dimer -- overlooked cases ?
• Low-probability ADD score and low D-dimer but still AAS?
AD PE
Presentation with chest pain
hsTroponin
D-dimer
PositiveNegative*#
ECG
AD or PEunlikely
AD or PElikely
Further
diagnostics
Initiation of
treatment or transfer
to a tertiary center
If suspicion
for AD or PE
remains
ST elevation (+)
CT with enhancement
STEMI
likely
ST elevation (-)
(+)(-)
Dissection Embolism
Primary step(rapid on-site)
Initial decision-making step
Repeat measurement after 3 hours
ACS
Clinical findings
Coronary Angiography
Aortic dissection biomarkers
Time after onset
Calponin (smooth muscle
troponin-like protein)
Smooth muscle
myosinCreatine kinase-BB isozyme
Cir
cula
ting levels
Refs. Myosin Suzuki T et al., Circulation 93:1244-9, 1996, Ann Intern Med 133:537-541, 2000
CK-BB Suzuki T et al., Lancet 350:784-5, 1997
Calponin Suzuki T et al., Eur. Heart J. 29:1439-45, 2008
D-dimer Suzuki T et al. Circulation 2009
TGFβ Suzuki T et al. J Am Coll Cardiol 2011
GM-CSF Son, Suzuki et al. Nature Commun 2015
TGFβ
D-dimer
GM-CSF
6.3.5 Diagnostic imaging in acute aortic dissection
The main purpose of imaging in AAD is the comprehensive
assessment of the entire aorta, including the aortic diameters,
shape and extent of a dissection membrane, the involvement
in a dissection process of the aortic valve, aortic branches, the
relationship with adjacent structures, and the presence of
mural thrombus
Computed tomography, MRI, and TOE are equally reliable
for confirming or excluding the diagnosis of AAD.
However, CT and MRI have to be considered superior to TOE
for the assessment of AAD extension and branch involvement,
as well as for the diagnosis of IMH, PAU, and traumatic aortic
lesions.
In turn, TOE using Doppler is superior for imaging flow across
tears and identifying their locations. Transoesophageal
echocardiography may be of great interest in the very unstable
patient, and can be used to monitor changes in-theatre and in
post-operative intensive care.
Imaging of aortic dissection
‘Triple-rule out’ is a relatively new term that describes an ECG-gated 64-detector
CT study to evaluate patients with acute chest pain, in the emergency
department, for three potential causes: AD, pulmonary embolism, and
coronary artery disease. The inherent advantage of CT is its rapid investigation of
life-threatening sources of acute chest pain, with a high negative predictive value.
However, it is important to recognize highly mobile linear intraluminal filling
defect, which may mimic an intimal flap on CT. The so-called ‘pulsation artefact’
is the most common cause of misdiagnosis. It is caused by pulsatile movement of
the ascending aorta
during the cardiac cycle between end-diastole and end-systole. The potential
problem of pulsation artefacts can be eliminated with ECG-gating, or else by a 180
linear interpolation reconstruction algorithm. Dense contrast enhancement in the
left brachiocephalic vein or superior vena cava, mediastinal clips, and indwelling
catheters can all produce streak artefacts in the aorta, which may potentially
simulate dissection. This difficulty can be avoided by careful attention to the volume
and injection rate of intravenous contrast material administered.
Future possibilities -- triple-rule out CT?
AD PE
Presentation with chest pain
hsTroponin
D-dimer
PositiveNegative*#
ECG
AD or PEunlikely
AD or PElikely
Further
diagnostics
Initiation of
treatment or transfer
to a tertiary center
If suspicion
for AD or PE
remains
ST elevation (+)
CT with enhancement
STEMI
likely
ST elevation (-)
(+)(-)
Dissection Embolism
Primary step(rapid on-site)
Initial decision-making step
Repeat measurement after 3 hours
ACS
Clinical findings
Coronary Angiography
Suzuki T, et al. Biomarkers of acute cardiovascular and pulmonary diseasesEur Heart J Acute Cardiovasc Care. 2016
Future possibilities – functional imaging?
Summary
• Diagnostic biomarkers for aortic disease are needed.
• Development and implementation are ongoing. Initial markers are already used clinically.
• Guidelines recognize importance of biomarker-guided diagnosis.
• Next steps -- protocol-based biomarker-guided diagnosis needs to be tested and implemented accordingly.
• Next steps – Develop acute and chronic markers. Single ‘golden standard’ important for acute diagnosis, butmultiple markers reflecting different facets of disease (e.g. pathogenesis, activity) for chronic states.