Pocket Medicine




•  True aneurysm (dilation of all 3 layers of aorta) vs. false (rupture contained by adventitia)

•  Location: root (annuloaortic ectasia), thoracic aortic aneurysm (TAA), thoracoabdominal aortic aneurysm (TAAA), abdominal aortic aneurysm (AAA)

•  Type: fusiform (circumferential dilation) vs. saccular (localized dilation of aortic wall)

Epidemiology (Circ 2010;121:e266; Nat Rev Cardiol 2011;8:92)

•  In U.S., ~15,000 deaths/y from aortic ruptures; overall ~50,000 deaths/y from Ao disease

•  TAA: ~1.7:1; ~60% root/ascending Ao; 40% descending Ao; arch & TAAA rarer

Risk factors: HTNatherosclerosis; congenital (bicuspid AoV, Turner’s); connective tissue diseases (Marfan, Ehlers-Danlos type IV, Loeys-Dietz); aortitis (Takayasu’s, GCA, spondyloarthritis, IgG4, syphilis); familial syndromes; chronic AoD; trauma

•  AAA: ~4–8% prev. in those >65 y; 5–10× more common in  vs. ; mostly infrarenal

Risk factors = similar to atherosclerosissmoking, HTN, hyperlipidemia, age, FHx

Pathophysiology (NEJM 2009;361:1114; Nat Med 2009;15:649)

•  LaPlace’s law: tension across a cylinder ∝ [(ΔP × r) / (wall thickness)]

•  TAA: medial degeneration = muscle apoptosis, elastin fiber weakening, mucoid infiltration

•  AAA: atherosclerosis & inflammation → matrix degeneration → medial weakening

•  Inflammatory and infectious (“mycotic”) aneurysms relatively rare

Screening (Annals 2005;142:203; JAMA 2009;302:2015; Circ 2010;121:e266)

•  TAA: no consensus guidelines; ? screen if bicuspid AoV or first-degree relative

•  AAA: ✓ for pulsatile abd mass; U/S  >60 y w/ FHx of AAA &  65–75 y w/ prior tobacco

Diagnostic studies (Circ 2005;111:816 & 2010;121:e266)

•  Contrast CT: quick, noninvasive, high Se & Sp for all aortic aneurysms

•  TTE/TEE: TTE most useful for root and proximal Ao; TEE can visualize other sites of TAA

•  MRI: preferred over CT for aortic root imaging for TAA; also useful in AAA but time-consuming; noncontrast “black blood” MR to assess aortic wall

•  Abdominal U/S: screening and surveillance test of choice for infrarenal AAA

Treatment (Circ 2006;113:e463; 2008;177:1883; 2010;121:1544 & e266)

•  Risk factor modification: smoking cessation, statin to achieve LDL-C <70 mg/dL

•  BP control: bB (↓ dP/dt) ↓ aneurysm growth (NEJM 1994;330:1335); ACEI a/w ↓ risk of rupture (Lancet 2006;368:659), ARB may ↓ rate of aortic root growth in Marfan (NEJM 2008;358:2787); no burst activity/exercise requiring Valsalva maneuvers (eg, heavy lifting)

•  Indications for surgery: individualize based on FHx, body size, gender

TAA: sx; asc Ao ≥5.5 cm (? 5.0 cm Marfan, bicuspid AoV; 4.2–4.4 cm Loeys-Dietz); descending >6 cm; ↑ >0.5 cm/y; aneurysm ≥4.5 cm and planned AoV surgery

AAA: infrarenal ≥5.5 cm (NEJM 2002;346:1437) but consider ≥5.0 cm in ; sx; ↑ >0.5 cm/y; inflam/infxn

•  Endovascular aneurysm repair (EVAR) (NEJM 2008;358:494; Circ 2011;124:2020)

↓ short-term mort., bleeding, LOS; but long-term graft complic. (3–4%/y; endoleak, need for reintervention, rupture) necessitate periodic surveillance, with no proven Δ in overall mortality, except ? in those <70 y (NEJM 2010;362:1863, 1881 & 2012;367:1988)

Guidelines support open repair or EVAR for infrarenal AAA in good surg candidates

In Pts unfit for surgery or high peri-op risks: ↓ aneurysm-related mortality but no Δ in overall mortality over medical Rx (NEJM 2010;362:1872). EVAR noninferior (? superior) to open repair in ruptured AAA w/ favorable anatomy (Ann Surg 2009;250:818).

TEVAR (thoracic EVAR) for descending TAA ≥5.5 cm may ↓ peri-op morbidity, no proven mortality benefit (Circ 2010;121:2780; JACC 2010;55:986;  J Thorac CV Surg 2010;140:1001)

Complications (Circ 2010;121:e266; Nat Rev Cardiol 2011;8:92)

•  Pain: gnawing chest, back or abdominal pain; new or worse pain may signal rupture

•  Rupture: risk ↑ w/ diameter, , current smoking, HTN

TAA: ~2.5%/y if <6 cm vs. 7%/y if >6 cm; AAA: ~1%/y if <5 cm vs. 6.5%/y if 5–5.9 cm

rupture p/w severe constant pain and hemorrhagic shock; ~80% mortality at 24 h

•  Acute aortic syndromes (qv)

•  Thromboembolic ischemic events (eg, to CNS, viscera, extremities)

•  Compression of adjacent structures (eg, SVC, trachea, esophagus, laryngeal nerve)

Follow-up (Circ 2010;121:e266; Nat Rev Cardiol 2011;8:92; JAMA 2013;309:806)

•  Expansion rate ~0.1 cm/y for TAA, ~0.3–0.4 cm/y for AAA

•  AAA: q3y if 3–3.9 cm; q6–12 mo if 4.0–5.4 cm (? q2y if 4–4.4)

•  TAA: 6 mo after dx to ensure stable, then annually.

•  Screen for CAD, PAD and aneurysms elsewhere, esp. popliteal. About 25% of Pts w/

TAA will also have AAA, and 25% of AAA Pts will have a TAA: consider pan-Ao imaging.