Cardiac outpouchings

Cardiac outpouchings are focal protrusions of a cardiac chamber wall that range from incidental normal variants to life-threatening pathology requiring urgent surgery. A structured approach — considering location, neck width, wall motion, wall thickness, and presence of fibrosis (LGE on CMR) — is essential for accurate classification and appropriate management.

The framework applies across modalities: CT excels at morphology, neck geometry, and pericardial relationships; CMR adds wall motion characterization, myocardial signal, and late gadolinium enhancement (LGE) for fibrosis detection.

Key reference: Hassani C, Walker CM, Urdaneta F, et al. Cardiac Outpouchings: Practical Approach to Normal Variants and Pathologic Conditions at CT and MRI. RadioGraphics. 2023;43(5):e220063. DOI: 10.1148/rg.220063

1 Right atrium

RA Aneurysm

A focal dilation that can arise from any location including the right atrial appendage (RAA). Key features:

• Wall motion: variably normal, akinetic, or dyskinetic
• Prevalence: ~50% are asymptomatic; the remainder present with arrhythmia (AF/flutter), chest pain, dyspnea, or fatigue
• Complications: thrombosis (→ pulmonary embolism or paradoxical embolism via PFO), mass effect on adjacent structures, rupture
• Management: no established universal strategy; surgical excision is preferred when there is thrombus, arrhythmia refractory to medical therapy, major dilation, or cardiac compression. Serial imaging surveillance for asymptomatic cases

RA Pseudoaneurysm

Defined by a wall defect or tear through which blood communicates with contained pericardium or hematoma. Etiologies:

• Post-traumatic
• Post-iatrogenic (catheterization, surgery)
• Malignancy (high suspicion when found incidentally without trauma history)

Complications: thrombosis and embolism. Surgical repair is generally indicated.

Subthebesian Pouch

Synonyms: subthebesian recess, sinus of Keith, subeustachian sinus

A normal variant arising from the inferior RA wall between the IVC junction and tricuspid valve:

• Prevalence: 20–47% at CT (threshold >5 mm)
• Clinical significance: generally low; large pouches may create a re-entrant circuit associated with supraventricular tachycardia and can pose technical challenges during AF ablation
• Frequently associated with a prominent thebesian valve

2 Left atrium

LA Diverticulum

A congenital outpouching (arising from the common pulmonary vein during embryologic development) or, less commonly, acquired:

AF ablation relevance: LA diverticula lie along the planned ablation line. Must be reported in AF ablation candidates — risk of catheter entrapment or perforation.

LA Accessory Appendage

Morphologically resembles a small LA appendage: lobulated walls, narrow neck, smaller than 1 cm:

• Prevalence: 6.5–28% of CT studies
• Location: anterior and left lateral LA walls
• Distinction from diverticulum: more lobulated walls, narrower neck, characteristic location
• Must be reported in AF ablation candidates for the same reasons as LA diverticulum

LA Aneurysm

Usually congenital, larger (>1 cm), and clinically significant:

• Complications: AF/tachyarrhythmia, thrombosis, systemic embolism
• Management: surgical resection is usually recommended even in asymptomatic patients (~150 reported cases in the literature)

3 Interatrial septum

Atrial Septal Aneurysm (ASA)

A developmental bulging at the fossa ovalis due to redundant septal tissue:

• Diagnostic criteria (echocardiography/CMR): base ≥15 mm AND protrusion ≥10–15 mm into either atrium, OR total excursion ≥10–15 mm
• Prevalence: ~2–3% of the general population; female predominance
• Associated with PFO in 50–70% of stroke patients — the combination of ASA + PFO is a high-risk combination for cryptogenic stroke and is a candidate for percutaneous or surgical PFO closure
• Also associated with: supraventricular arrhythmias, mitral/tricuspid valve prolapse
• Larger and more mobile ASAs carry higher stroke risk

Atrial Septal Pouch (ASP)

A distinct entity from PFO — incomplete fusion of septum primum to septum secundum creates a blind-ending pouch along the interatrial septum:

Left ASP: controversial association with AF, TIA, and migraine with aura (proposed mechanism: in situ thrombosis within the pouch).

Right ASP: no established clinical significance.

CT key distinction: If contrast is NOT seen crossing the interatrial septum from LA to RA, the finding is an ASP — not a PFO.

Patent Foramen Ovale (PFO) — CT distinction

On contrast-enhanced CT: direct visualization of contrast passing through the interatrial septum from LA to RA confirms a PFO. ASP shows a flap of tissue within the LA without contrast traversal. Clinical context and echocardiography remain the gold standard for PFO evaluation.

4 Ventricles

The ventricular outpouchings range from benign incidental findings (crypts, diverticula) to high-mortality conditions requiring urgent surgery (pseudoaneurysms). Four features drive classification:

LV / RV Crypt (Cleft)

• Slit-like invagination ≥50% of myocardial depth
• Does not protrude beyond the outer myocardial border
• Completely obliterates during systole
• No LGE on CMR — normal myocardium, no fibrosis
• Association with HCM: multiple crypts (>2) on long-axis CMR views are a specific finding in pre-hypertrophic HCM mutation carriers (sensitivity 51%, specificity 94%, PPV 100%)
• Most common location: basal-mid inferoseptal, followed by basal-mid anteroseptal and inferior walls

LV / RV Diverticulum

An outpouching of nonfibrotic myocardium that extends beyond the expected contour:

• Contractile during systole (normal wall motion) — this is the key feature distinguishing it from an aneurysm
• Normal wall thickness; no LGE
• Prevalence: 0.4–2.2% LV; 0.6% RV
• Usually incidental and asymptomatic in adults

Pediatric considerations: In neonates/young children, diverticula carry significant morbidity/mortality. Apical diverticula are associated with Cantrell syndrome (pentalogy: sternal, abdominal wall, diaphragm, and pericardial defects + congenital heart disease). Propensity to rupture if <8 years old.

Management: Surgery preferred in neonates and children. Asymptomatic adults with no arrhythmia can be observed.

True Ventricular Aneurysm

Acquired (post-MI — most common):

• Accounts for 80–90% of all LV aneurysms
• Prevalence after MI: 0.2–12%; higher morbidity and more frequent complications than pseudoaneurysm
• Location: apical, anterior, anterolateral (LAD territory)
• Thin walls (fibrous + residual myocardium), wide neck (>50% of aneurysm diameter)
• Akinetic or dyskinetic wall motion
• LGE present on CMR
• Epicardial fat separates the aneurysm wall from the pericardium
• Associated with: thrombosis (anticoagulation when thrombus detected), arrhythmia, heart failure

Other acquired causes: trauma, iatrogenic, Chagas disease, HCM (“burned out apex”), myocarditis, sarcoidosis

Congenital aneurysm: More commonly submitral location; rare; often incidentally discovered. Rupture risk up to 23%.

Management: Asymptomatic → medical management with imaging follow-up. Surgery for persistent angina, intractable arrhythmia, thromboembolism, or refractory heart failure.

LV Pseudoaneurysm

A contained myocardial rupture — the most feared ventricular outpouching:

• Most commonly a consequence of transmural MI with myocardial rupture; in the minority (0.2–0.5%) adjacent pericardium, hematoma, or scar tissue contains the rupture
• Other causes: mitral valve surgery (most common iatrogenic cause), trauma, endocarditis
• Location: inferior and inferolateral LV walls
• Neck: narrow — diameter ≤50% of the aneurysm diameter
• Wall is composed of fibrous tissue, pericardium, and organized hematoma (no normal myocardium)
• Myocardial cutoff sign (CT/CMR): abrupt thinning (>50% decrease in wall thickness) measured 1 cm from the aneurysm neck — sensitive and specific for pseudoaneurysm
• Pericardium forms the wall → no epicardial fat visible between the sac and pericardium (distinguish from true aneurysm where fat is present)
• LGE extends beyond the wall into the pericardium
• Up to 50% discovered incidentally

High rupture risk (30–45% within 1 year if untreated) → surgery is indicated. For small (<3 cm) asymptomatic pseudoaneurysms, conservative management with regular imaging is an option. Primary surgical repair, patch, or percutaneous closure preferred.

5 Arrhythmogenic cardiomyopathy (ACM)

A genetic cardiac disease resulting in fibrous or fibrofatty myocardial scar formation with associated malignant ventricular arrhythmias. Classically termed ARVC/D but now recognized to involve LV or both ventricles.

Prevalence: 1 in 1,000 to 1 in 5,000 persons. Presents with exercise-related palpitations, syncope, arrhythmia, and impaired cardiac function.

ACM and outpouchings: Multiple small outpouchings of the RV free wall are a characteristic finding. As disease progresses, aneurysms multiply and take on a characteristic “accordion sign” — multiple small and large aneurysmal outpouchings creating a bellows-like appearance of the RV.

• RV inflow and outflow tracts most commonly involved early; RV apex (“triangle of dysplasia”) with late-stage disease
• Isolated LV involvement is exceptionally rare; usually seen with coexistent RV involvement

Diagnostic criteria (Table 5 in Hassani et al.):

The 2019 HRS guidelines include a weak (IIb) recommendation for antithrombotic therapy given increased thromboembolic risk from RV or LV aneurysms.

6 Transpericardial bulge or hernia

In constrictive pericarditis or pericardial absence, cardiac chambers can bulge or herniate through defects or between diseased segments:

• Constrictive pericarditis: thickened/calcified pericardium constricts ventricular relaxation; normal myocardium relaxes between areas of diseased pericardium, appearing as an outpouching. These segments have normal contraction, distinguishing them from aneurysms.
• Pericardial absence/defect: apical portions of RV, LV, and LAD can herniate through a defect — risk of strangulation and coronary artery compression.

Both CT and CMR can depict herniation; CMR better characterizes myocardial signal intensity and confirms absence of fibrosis (lack of LGE). Treatment is surgical (pericardial closure, enlargement, or pericardiectomy).

7 Interventricular septum

Outpouchings of the interventricular septum are called interventricular septal aneurysms (IVSAs), most commonly involving the membranous septum.

Membranous IVSA

The membranous septum is a thin, relatively straight fibrous septum between the basal ventricles, situated below the right and noncoronary aortic cusps:

• Mechanism: In developmental cases, a small embryologic VSD becomes covered by the septal leaflet of the tricuspid valve → creates an aneurysm-like protrusion into the RV (spontaneous closure)
• Prevalence: 19.0–22.4% in patients with open VSD; up to 25% in congenitally corrected transposition of the great arteries
• CT imaging: Best visualized with electrocardiographically gated CTA; CMR in coronal oblique and four-chamber views
• Complications: in-situ thrombosis → embolism; subpulmonic stenosis if large; associated aortic and tricuspid valve regurgitation
• Management: anticoagulation for thrombus; resection when embolism occurs despite anticoagulation, or when concurrent hemodynamic abnormality or heart disease is present

Muscular IVSA

Far rarer than membranous aneurysms; secondary to MI, trauma, or spontaneous closure of a pre-existing VSD by muscular and fibrous tissue:

• Appearance: finger-like, frond-like, or globular pouches in the interventricular septum
• Wall motion: akinetic or dyskinetic (distinguishes from a diverticulum)
• Complications: thrombosis, open VSD
• Management: in adults after MI, or if shunt present → surgical excision and closure

VSD Patch Aneurysm

After surgical VSD closure, various patch materials (pericardium, polytetrafluoroethylene) can develop aneurysmal dilatation. Perimembranous VSD patch aneurysm protrudes into the RV, rarely obstructing RV outflow. Best visualized on CT, CMR, and echocardiography.

8 Mitral-aortic intervalvular fibrosa

Pseudoaneurysms can develop in the fibrous cardiac skeleton at the mitral-aortic intervalvular fibrosa (MAIVF), also called the fibrous curtain or aortic-mitral fibrous continuity — the region between the anterior leaflet of the mitral valve and the noncoronary aortic cusp:

• Communication: connects to the LV outflow tract
• Causes: endocarditis (most common) or surgical trauma (aortic valve surgery)
• Presentation: signs of endocarditis (fever, embolic events, heart failure, stroke), or incidentally discovered (10%)
• Imaging: CTA better delineates extent and relationship to coronary arteries; CMR characterizes wall motion and fibrosis
• CT appearance: well-defined pouch below the aortic valve, between the aorta and anterior mitral valve leaflet
• Complications: fistulation to adjacent chambers, rupture, thrombosis, infection, compression of coronary arteries (left circumflex most common)
• Management: surgical resection even in asymptomatic cases; transcatheter closure when surgery not feasible

9 Mimics — Thebesian vessels and atrial veins

Thebesian vessels are a network of intramyocardial sinusoids and valveless veins that drain myocardial blood directly into the cardiac chambers. On CT they can enlarge and mimic cardiac outpouchings:

• Seen in the interatrial groove, interventricular septum, and along the LA
• Thebesian vessels near the interatrial groove may pass through superior interatrial muscle connections — the Bachmann bundle — and are more common
• Veins inferoposterior to the fossa ovalis, near the inferior cavoatrial junction, are less common but also seen
• Key distinguishing feature: tubular configuration and traceable connection to either atrium; lined by thickened muscle (Bachmann bundle) rather than cardiac chamber wall

Careful observation of tubular morphology and atrial connection distinguishes these from true outpouchings — an important distinction before reporting a false “diverticulum” or “aneurysm.”