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Aortic Atherosclerosis Aneurysm Dissection
TEE cannot image about 40% of the ascending aorta, including the usual site of cannulation in the ascending aorta (blind spot: interposition of trachea or right mainstem bronchus, or both, between the esophagus and the ascending aorta). Epiaortic scanning is limited by near-field drop-out (requires a standoff or “spacer” to offset the probe from the aorta). Usually a handful-sized amount of ultrasound gel placed inside the sterile sheath between the probe and aorta is sufficient.
ATHEROSCLEROSIS •
•
•
Presence of disease in the arch suggests disease in the ascending aorta and, thus, the need for epiaortic scanning before aortic cannulation. TEE identified < 30% of patients shown with epiaortic scanning to have moderate or severe atheroma in the ascending aorta or arch in one study (Ann Thorac Cardiovasc Surg 4:347–350, 1998). Multiple classification systems exist for scoring aortic atheromas. JASE classification: (from J Am Soc Echocardiogr 28:119–182, 2015) u Grade 1: normal (<2 mm thickening) u Grade 2: mild atheroma (2–3 mm or significant intimal thickening) u Grade 3: moderate atheroma (3–5 mm) u Grade 4: severe atheroma (>5 mm) u Grade 5: complex atheroma (grade 2–4 with any atheroma that is mobile or ulcerated) Embolic potential
16 Aortic Atherosclerosis Aneurysm Dissection
AORTIC ATHEROSCLEROSIS ANEURYSM DISSECTION
u Size and degree of protrusion (>5 mm
16 Aortic Atherosclerosis Aneurysm Dissection
protrusion is high-risk) (Katz et al. J Am Coll Cardiol 20:70–77, 1992) u Mobility u Complex in shape (hills and valleys) and rough in appearance (not smooth)
THORACIC AORTIC DILATATION/ANEURYSM Measure aorta in end-diastole for consistency and ensure it is perpendicular to LAX. • Ascending aorta dilatation is caused by: u hypertension u atherosclerosis u cystic medial necrosis u post-aortic valve stenosis • Aortic root dilatation u Collagen vascular and inflammatory disease u Marfan syndrome (loss of sinotubular junction); also called cystic medial necrosis – Complications of aortic root dilation – Central AR (root >5 cm) – Flail leaflets – Compression of adjacent structures – Intimal hematomas
THORACIC AORTIC DISSECTION • • •
TEE sensitivity and specificity approach 100% Fivefold increased risk in patients with bicuspid or unicuspid AV Marfan syndrome may have dissection without dilation
DIAGNOSTIC INFORMATION • •
Presence of dissection? (Presence of undulating intimal flap in 2D and/or CFD to show two channels) Location/classification (Figure 16.1)
Type A (Stanford): •
Surgical management u DeBakey type I: ascending aorta
extends into descending aorta u DeBakey type II: ascending only
DeBakey type I or Stanford A
DeBakey type II or Stanford A
DeBakey type III or Stanford B Figure 16.1 Aortic dissection classifications.
127
Type B (Stanford): • • • • • • • •
Often nonsurgical management u DeBakey type III: descending only
Location of entry tear Location of reentry tear and secondary tears Involvement of arch and major branch vessels (can be difficult to see on TEE) Involvement of coronary arteries Presence of and severity of AR Pericardial effusion and tamponade Segmental wall motion abnormalities (suggests coronary ostia involvement)
Differentiate True from False Lumen by: • • •
•
• • •
128
Size (usually true in descending aorta) u True lumen < False lumen
Pulsation u True lumen: expands in systole u False lumen: compresses in systole Flow u True lumen: systolic forward flow, which is the normal pattern u False lumen: delayed, reversed, or no flow Shape (usually true) u True lumen: round in SAX view u False lumen: crescent-shaped in SAX view Spontaneous echo contrast u True lumen: rare u False lumen: common Thrombus u True lumen: rare u False lumen: common Mimickers of dissection u Reverberation artifacts from calcification in the aortic wall or from vascular catheters; e.g., a curvilinear
echogenic line that moves with the aorta may be a reverberation artifact from a PA catheter. u Presence of innominate vein in upper esophageal aortic arch view may appear as a dissection flap.
ASSESSMENT POST-DISSECTION REPAIR • • •
Residual AV incompetence Flow in coronary ostia Rule out new segmental wall motion abnormalities
129
N OTE S
130
ATHEROSCLEROSIS •
•
•
Presence of disease in the arch suggests disease in the ascending aorta and, thus, the need for epiaortic scanning before aortic cannulation. TEE identified < 30% of patients shown with epiaortic scanning to have moderate or severe atheroma in the ascending aorta or arch in one study (Ann Thorac Cardiovasc Surg 4:347–350, 1998). Multiple classification systems exist for scoring aortic atheromas. JASE classification: (from J Am Soc Echocardiogr 28:119–182, 2015) u Grade 1: normal (<2 mm thickening) u Grade 2: mild atheroma (2–3 mm or significant intimal thickening) u Grade 3: moderate atheroma (3–5 mm) u Grade 4: severe atheroma (>5 mm) u Grade 5: complex atheroma (grade 2–4 with any atheroma that is mobile or ulcerated) Embolic potential
16 Aortic Atherosclerosis Aneurysm Dissection
AORTIC ATHEROSCLEROSIS ANEURYSM DISSECTION
u Size and degree of protrusion (>5 mm
16 Aortic Atherosclerosis Aneurysm Dissection
protrusion is high-risk) (Katz et al. J Am Coll Cardiol 20:70–77, 1992) u Mobility u Complex in shape (hills and valleys) and rough in appearance (not smooth)
THORACIC AORTIC DILATATION/ANEURYSM Measure aorta in end-diastole for consistency and ensure it is perpendicular to LAX. • Ascending aorta dilatation is caused by: u hypertension u atherosclerosis u cystic medial necrosis u post-aortic valve stenosis • Aortic root dilatation u Collagen vascular and inflammatory disease u Marfan syndrome (loss of sinotubular junction); also called cystic medial necrosis – Complications of aortic root dilation – Central AR (root >5 cm) – Flail leaflets – Compression of adjacent structures – Intimal hematomas
THORACIC AORTIC DISSECTION • • •
TEE sensitivity and specificity approach 100% Fivefold increased risk in patients with bicuspid or unicuspid AV Marfan syndrome may have dissection without dilation
DIAGNOSTIC INFORMATION • •
Presence of dissection? (Presence of undulating intimal flap in 2D and/or CFD to show two channels) Location/classification (Figure 16.1)
Type A (Stanford): •
Surgical management u DeBakey type I: ascending aorta
extends into descending aorta u DeBakey type II: ascending only
DeBakey type I or Stanford A
DeBakey type II or Stanford A
DeBakey type III or Stanford B Figure 16.1 Aortic dissection classifications.
127
Type B (Stanford): • • • • • • • •
Often nonsurgical management u DeBakey type III: descending only
Location of entry tear Location of reentry tear and secondary tears Involvement of arch and major branch vessels (can be difficult to see on TEE) Involvement of coronary arteries Presence of and severity of AR Pericardial effusion and tamponade Segmental wall motion abnormalities (suggests coronary ostia involvement)
Differentiate True from False Lumen by: • • •
•
• • •
128
Size (usually true in descending aorta) u True lumen < False lumen
Pulsation u True lumen: expands in systole u False lumen: compresses in systole Flow u True lumen: systolic forward flow, which is the normal pattern u False lumen: delayed, reversed, or no flow Shape (usually true) u True lumen: round in SAX view u False lumen: crescent-shaped in SAX view Spontaneous echo contrast u True lumen: rare u False lumen: common Thrombus u True lumen: rare u False lumen: common Mimickers of dissection u Reverberation artifacts from calcification in the aortic wall or from vascular catheters; e.g., a curvilinear
echogenic line that moves with the aorta may be a reverberation artifact from a PA catheter. u Presence of innominate vein in upper esophageal aortic arch view may appear as a dissection flap.
ASSESSMENT POST-DISSECTION REPAIR • • •
Residual AV incompetence Flow in coronary ostia Rule out new segmental wall motion abnormalities
129
N OTE S
130