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.