Aortic Disease: Aneurysm, Dissection & Atheroma

RDCS Adult Echocardiography AE

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1 Introduction & Exam Overview

The RDCS AE Exam, SPI Requirement & Logistics Content Outline, Domain Weights & How to Study

2 Cardiac Anatomy

Chambers, Walls, Myocardial Layers & the 17-Segment Model Cardiac Valves & Subvalvular Apparatus Great Vessels, Pericardium, Coronary & Venous Anatomy

3 Cardiac Physiology & Hemodynamics

Cardiac Cycle, Phases & Pressure-Volume Relationships Normal Systolic & Diastolic Function Hemodynamic Principles & Response to Stress

4 Echo Modalities, Instrumentation & Contrast

2D (B-Mode) and M-Mode Imaging Spectral, Color, and Tissue Doppler Modalities Image Optimization, Artifacts, and Contrast Echocardiography

5 Standard Views, Windows & Protocol

Parasternal Long- & Short-Axis Views Apical Views Subcostal & Suprasternal-Notch Views Exam Protocol, Patient Positioning & Provocative Maneuvers

6 Quantification & Doppler Hemodynamic Calculations

Chamber Quantification: LV, LA, RA, and RV Size, Mass, and Volumes Systolic Function: Ejection Fraction Methods, Fractional Shortening & Strain Diastolic Function Grading (ASE/EACVI 2016) Core Doppler Math: Modified Bernoulli, VTI, Stroke Volume & the Continuity Equation Advanced Hemodynamics: PISA/EROA, Pressure Half-Time, dP/dt, Qp/Qs & RVSP

7 Aortic & Mitral Valve Disease

Aortic Stenosis Aortic Regurgitation Mitral Stenosis Mitral Regurgitation

8 Right-Sided, Prosthetic & Infective Valve Disease

Tricuspid & Pulmonic Valve Disease and Pulmonary Hypertension Assessment Infective Endocarditis and Vegetations Prosthetic Valves and Postoperative Evaluation

9 Ischemic Disease & Cardiomyopathies

Coronary Anatomy, Ischemic Heart Disease & Wall-Motion Abnormalities Stress Echocardiography & Myocardial Viability Mechanical Complications of Myocardial Infarction Dilated & Restrictive Cardiomyopathy Hypertrophic Cardiomyopathy, SAM & LVOT Obstruction

10 Pericardial Disease, Masses & Aorta

Pericardial Effusion & Cardiac Tamponade Constrictive Pericarditis vs. Restrictive Physiology Cardiac Masses, Tumors & Thrombi Aortic Disease: Aneurysm, Dissection & Atheroma

11 Congenital Heart Disease & Shunts

Septal Defects & Shunt Quantification Common Adult Congenital Lesions

12 Clinical Care & Safety

Patient Care, Clinical-Data Integration & Exam Protocols Bioeffects, ALARA, Infection Control & Ergonomics

Aortic Disease: Aneurysm, Dissection & Atheroma

Key Takeaways Explain This Topic AI

Ascending aortic diameter under 4.0 cm is normal; 4.0-4.4 cm is ectasia; 4.5 cm or larger meets criteria for aneurysm.

Elective surgical repair thresholds are 5.5 cm for typical ascending aortic aneurysms, 5.0 cm for bicuspid aortic valve, and 4.5-5.0 cm for Marfan or Loeys-Dietz syndrome.

Rapid aneurysm growth — ≥0.5 cm in one year or ≥0.3 cm/year over two consecutive years — is itself an indication for earlier surgical intervention.

Stanford type A aortic dissection involves the ascending aorta and is a surgical emergency; Stanford type B spares the ascending aorta and is usually managed medically.

On echo, the true lumen of a dissection is typically smaller and expands in systole, while the false lumen is larger, expands in diastole, and may show sluggish flow or thrombus.

Last updated: July 2026

Aortic Aneurysm: Definitions and Sizing Thresholds

A true aneurysm is a dilation involving all three layers of the aortic wall — intima, media, and adventitia. A pseudoaneurysm is a contained rupture: blood escapes through a defect in the wall but is contained only by adventitia, surrounding tissue, or clot, and it communicates with the true lumen through a narrow neck. Pseudoaneurysms carry a high rupture risk regardless of size and generally warrant repair once identified.

Standard measurement is performed by TTE at end-diastole, leading-edge to leading-edge, perpendicular to the long axis of the aorta, at four standardized levels: the annulus, sinuses of Valsalva, sinotubular junction, and proximal (tubular) ascending aorta.

Ascending Aortic Diameter Classification Typical Management
<4.0 cm Normal Routine follow-up
4.0-4.4 cm Ectasia / mild dilation Annual surveillance imaging
≥4.5 cm Aneurysm Surveillance imaging every 6 months
5.5 cm (typical patient) Surgical threshold Elective repair
5.0 cm (bicuspid aortic valve) Surgical threshold Elective repair
4.5-5.0 cm (Marfan / Loeys-Dietz syndrome) Surgical threshold Elective repair

Growth ≥0.5 cm/yr (1 yr) or ≥0.3 cm/yr (2 consecutive yrs) Rapid growth Triggers earlier intervention regardless of absolute size

Surgical thresholds are lowered for higher-risk substrates — bicuspid aortic valve, heritable connective-tissue disease — because these aortas dissect or rupture at smaller absolute diameters than degenerative aneurysms in the general population.

Aortic Dissection

Dissection begins with an intimal tear that allows pulsatile blood to enter and dissect between the layers of the aortic wall, creating a true lumen and a false lumen separated by a mobile intimal flap — an undulating, linear, hyperechoic structure crossing the aortic lumen. The true lumen is typically smaller in caliber and expands during systole; the false lumen is typically larger, expands during diastole, and more often shows sluggish flow, spontaneous echo contrast, or frank thrombus.

Classification

System Category Extent Management
Stanford Type A Involves the ascending aorta, regardless of origin site Surgical emergency
Stanford Type B Does not involve the ascending aorta Usually medical management unless complicated
DeBakey Type I Originates in and involves the ascending aorta, arch, and descending aorta Surgical emergency
DeBakey Type II Confined to the ascending aorta Surgical emergency

DeBakey Type III Originates distal to the left subclavian artery, descending aorta only Usually medical management unless complicated

TEE, ideally combined with M-mode, is highly accurate — multiplanar TEE sensitivity is approximately 97-99%, with near 100% specificity — and is the modality of choice when TTE is limited by the tracheal air interface obscuring the distal ascending aorta and proximal arch. Complications of proximal (type A) dissection include acute aortic regurgitation from flap prolapse into the LVOT or annular dilation, pericardial effusion or tamponade from rupture into the pericardial space (a leading cause of death in type A dissection), and coronary ostial involvement causing acute myocardial infarction — all findings the sonographer should actively screen for.

Aortic Atheroma

Atherosclerotic plaque within the aortic wall is graded primarily by thickness. Complex/high-risk plaque — generally defined as ≥4 mm thickness, plus any mobile component or ulceration — carries substantially increased risk of embolic stroke and is an important finding during TEE, particularly in the aortic arch and descending aorta, a recognized embolic source during cardiac surgery and aortic cannulation.

Related Acute Aortic Syndromes and Risk Factors

Aortic dissection is one of three related acute aortic syndromes . Intramural hematoma (IMH) is bleeding within the aortic media without a demonstrable intimal tear or mobile flap, appearing as crescentic or circumferential wall thickening greater than 5-7 mm without internal flow, and it is classified and managed using the same Stanford A/B framework as dissection. Penetrating atherosclerotic ulcer (PAU) is an ulcerating atherosclerotic plaque that has breached the internal elastic lamina, often in a heavily diseased descending aorta, and it can progress to IMH, pseudoaneurysm, or frank dissection. All three syndromes share the same acute presentation — severe, tearing chest or back pain — and require urgent imaging.

Major risk factors for dissection include chronic hypertension (the single most common risk factor), bicuspid aortic valve, heritable connective-tissue disease (Marfan, Loeys-Dietz, vascular Ehlers-Danlos), aortic coarctation, prior cardiac surgery or aortic instrumentation, cocaine use, and blunt chest trauma. The sizing framework above applies to the thoracic aorta; the abdominal aorta uses a separate, lower threshold, with an infrarenal diameter of 3.0 cm or greater defining an abdominal aortic aneurysm.

Marfan Syndrome and Aortic Root Dilation

Marfan syndrome, caused by an FBN1 mutation affecting connective tissue, classically produces aortic root dilation with a "tulip bulb" or pear-shaped enlargement centered at the sinuses of Valsalva. Because Marfan aortas dissect at smaller absolute diameters than the general population, surgical thresholds are lowered (4.5-5.0 cm, above), and serial imaging surveillance — tracking root diameter and, in younger patients, diameter indexed to body size as a Z-score — is essential to time elective repair before dissection occurs.