Main points

• A cardiac outpouching (CO) is a protrusion in a heart chamber’s internal anatomical lining.

• Most CO are clinically insignificant, but some may be vital, requiring immediate surgery.

• The imaging findings of COs should be carefully evaluated along with the patient’s clinical history to determine the correct diagnosis and appropriate clinical management.

Acardiac outpouching (CO) is a protrusion in a heart chamber’s internal anatomical lining.^1,2 Although most COs are clinically insignificant, some may be vital, requiring immediate surgery. Moreover, identifying COs, which may be responsible for thromboembolic events, before performing invasive procedures is crucial. Therefore, the recognition and characterization of COs are of great importance.¹ Imaging findings of COs, such as location, morphology, size, and accompanying wall motion abnormalities, should be carefully evaluated along with the patient’s clinical history to determine the correct diagnosis and appropriate clinical management.² This article reviews the key cross-sectional imaging findings and differential diagnoses of COs (Figure 1). COs that occur as a result of surgery are outside the scope of this article.

Ventricular outpouchings

Ventricular true aneurysms (VTAs)

VTAs are usually wide-necked outpouchings, surrounded by dyskinetic and scarred myocardium. The presence of a smooth transition between the healthy myocardium and outpouching walls is a crucial finding for VTAs.^1,2,3 The walls of VTAs often exhibit late gadolinium elevation (LGE) on magnetic resonance imaging (MRI) caused by scarred myocardium. Moreover, this scarred myocardial tissue may contain fatty metaplasia and calcification.³ (Supplementary Figure 1). Because VTAs may contain thrombi, the presence of thrombus should be carefully examined when a VTA is detected (Figure 2, Supplementary Video 1). VTAs are often detected on the left ventricle (LV) but can also be seen on the right ventricle (RV). The etiopathogenesis of VTAs may include myocardial infarction (MI), myocarditis, Chagas disease, and trauma,^1,3,4 their medical management may consist of anticoagulation to prevent thromboembolism and afterload reduction. Surgical treatment may be considered for large VTAs, a VTA with an increased size during follow-up, angina, rupture, or heart failure.

Ventricular pseudoaneurysms (VPs)

VPs are often outpouchings in the posterior–inferior wall of the LV; they have a narrow neck and are surrounded by the pericardium as the result of a full-thickness myocardial tear or rupture (Figure 3, Supplementary Figure 2, Supplementary Video 2).³ The presence of an abrupt transition between the healthy myocardium and outpouching is a crucial imaging finding for VPs, unlike VTAs.^1,2,3 Moreover, VPs are often accompanied by hemorrhagic pericardial effusion, and focal LGE can be seen in the pericardium surrounding the VP. The etiopathogenesis of VPs may include MI, trauma, infection, and iatrogenic injury (Figure 4).^2,3 Untreated VPs have high mortality, and surgery is the treatment of choice in patients with VP.

Ventricular diverticulum (VD)

VD is an outpouching surrounded by healthy myocardial tissue. Therefore, VD exhibits synchronous contractility with the ventricles, and VD walls do not exhibit LGE on MRI, unlike VTAs and VPs.^1,5 Notably, VDs are often congenital, but they may rarely be acquired (Figure 5, Supplementary Figure 3). Although rare, VDs may be associated with ventricular thrombus, thromboembolism, and ventricular arrhythmias. Follow-up of patients is usually sufficient, and treatment should be based on complications (Supplementary Figure 4). Arrhythmogenic right ventricular cardiomyopathy (ARVC) can mimic VDs and is characterized by functional and wall motion abnormalities (akinesia, dyskinesia) of the RV and ventricular tachyarrhythmias. A corrugated pattern (accordion-like) can be seen on the RV-free wall caused by multiple outpouchings. Unlike VDs, outpouchings in ARVCs are akinetic or dyskinetic, and RV dysfunction is present (Supplementary Figure 5).⁶

Myocardial crypts (MCs) or clefts

MCs, also known as myocardial clefts, are narrow outpouchings of the ventricles, usually perpendicular to the interventricular septum. They are generally detected in the basal inferoseptal region of the LV and have uncertain clinical significance (Figure 6).¹ Patients with MCs are almost entirely asymptomatic and do not require treatment. MCs decrease in size or disappear during ventricular systole and do not cause wall motion defects. They are more common in patients with hypertrophic cardiomyopathy (HCM) than in healthy populations. In addition, MCs have been suggested as a predictor of gene carrier status in HCM, and when they are multiple, the patient should be examined for HCM.⁷

Ventricular herniation

Ventricular herniation may result from the outpouching of healthy ventricles caused by a congenital, traumatic, or iatrogenic pericardial defect (Figure 7, Supplementary Figure 6).^1,2,8 Although patients with ventricular herniation are almost completely asymptomatic, incarceration, cardiac valvular insufficiency, or coronary artery compression may rarely be detected. Surgery is preferred in cases that develop complications or are symptomatic.

Interventricular septal aneurysm (IVSAs)

IVSAs are characterized by an outpouching of the interventricular septum to either side. They have two forms, membranous or muscular (Figures 8 and Figure 9), and are often seen in the membranous region and are usually congenital. Rarely, IVSAs may occur secondary to trauma, ischemia, surgery, or infection.^9,10 Although IVSAs are often detected incidentally, they carry risks such as rupture, thrombosis, arrhythmias, right ventricular outflow obstruction, paradoxical thromboembolism, and infective endocarditis. Moreover, IVSAs may be associated with congenital cardiac anomalies, such as transposition of the great arteries and ventricular septal defects.^1,5,9,10 Although anticoagulation is recommended in asymptomatic cases of IVSAs, surgical treatment is considered in symptomatic patients and those who develop complications. In the differential diagnosis for muscular IVSA, MCs should be considered. Although muscular IVSA indents toward the right ventricle, MCs terminate in the myocardium and do not indent the RV.^1,5,9

Mitral-aortic intervalvular fibrosa pseudoaneurysm (MAIVF)

The fibrous connection between the mitral and aortic valve is known as the MAIVF. Pseudoaneurysm formation may rarely occur in the MAIVF as a result of infective endocarditis, surgery, or trauma (Figure 10). An MAIVF pseudoaneurysm may cause thromboembolism, septic embolism, mitral valve dysfunction, and rupture. Rarely, it can cause the compression of adjacent structures, including the coronary arteries.¹¹ Surgery is the preferred treatment because of the high risk of serious complications.

Atrial outpouchings

Atrial septal aneurysm

Atrial or interatrial septal aneurysms (ASAs) are characterized as outpouchings (with a protrusion >11 mm to either side in adults) of the interatrial septum beyond the interatrial septal plane (Figure 11, Supplementary Video 3).^12,13 They are often congenital, and patients with ASAs are usually asymptomatic. Atrial septal aneurysms are divided into different subgroups according to their dynamic protrusion into the right and left atrium (LA) on echocardiography.¹² They can be associated with patent foramen ovale (PFO), atrial septal defect, stroke, and thromboembolism.¹³ Therefore, when ASAs are detected, accompanying findings should be carefully examined. Treatment is not recommended in patients with ASAs unless complications occur.

Atrial septal pouch (ASP)

ASPs are characterized by a well-defined pouch along the interatrial septum and can occur on either the left side (40.8%), right side (5.1%), or both (3.7%). ASPs can cause thrombus formation, and arrhythmogenic focus can be detected in ASPs (Figure 12).¹⁴ Left-sided ASPs have been associated with thromboembolism, stroke, PFO, and atrial fibrillation. Treatment is not recommended in patients with ASPs unless complications develop.^12,14

Accessory appendage (AA) and diverticulum of the left atrium

AAs and diverticula of the LA are common outpouchings of the LA, and both are considered anatomical variants.^1,13 Although AAs are characterized by outpouchings with trabeculated contours and a small base, LA diverticula are characterized by outpouchings with smooth contours and a broad base (Figure 13). Both are usually located in the anterior upper wall of the LA and can be associated with thromboembolism, stroke, and arrhythmia.^1,2,13 The presence of these outpouchings should be examined before invasive procedures (such as radiofrequency ablation) to prevent complications, such as wall penetration and atrioesophageal fistula.^1,3

Diverticulum, aneurysm, and pseudoaneurysm of the right atrium (RA)

Diverticula, aneurysms, and pseudoaneurysms of the RA are unusual outpouchings and may present similar clinical and radiological findings. These are characterized by outpouchings that originate from the RA appendage (Figure 14). Distinguishing between diverticula, aneurysms, and pseudoaneurysms definitively without surgery is often impossible. These RA outpouchings are usually congenital and detected incidentally, but they may present various clinical symptoms.^1,2,13 The subthebesian sinus, also known as subeustachian or Keith sinus, is an outpouching of the RA wall below the coronary sinus ostium. It is an anatomical variant that should not be misdiagnosed as a diverticulum or aneurysm (Figure 15).¹⁵ Right atrial diverticula, aneurysms, and pseudoaneurysms may cause fatal complications, such as pulmonary thromboembolism, arrhythmias, and sudden cardiac death. Although follow-up and anticoagulation are recommended in patients with RA outpouchings who are asymptomatic, surgery is preferred in patients who are symptomatic.^13,15

Ventricular and atrial outpouchings and differential diagnoses are summarized in Table 1.

Conclusion

Radiologists should be familiar with COs on cross-sectional imaging, as the timely characterization of COs is essential to ensure optimal clinical management and therapeutic approaches.

Supplementary Video 1 link: https://www.youtube.com/shorts/__i8Rb8vV7E

Supplementary Video 1. Balanced steady-state free precession cine magnetic resonance imaging revealing left ventricular apical dyskinesia and dilation with a wide neck, compatible with a true ventricular aneurysm.

Supplementary Video 2 link: https://www.youtube.com/shorts/Hq-ur3V5rYk

Supplementary Video 2. Balanced steady-state free precession cine magnetic resonance imaging demonstrating a large outpouching in the basal part of the left ventricle with a narrow neck and abrupt transition between the healthy and thinned myocardium, consistent with a left ventricular pseudoaneurysm.

Supplementary Video 3 link: https://www.youtube.com/watch?v=5K9JkTEPlj4

Supplementary Video 3. Cardiac computed tomography images demonstrating the bidirectional abnormal motion and bowing of the interatrial septum during different cardiac phases, consistent with atrial septal aneurysm.

Supplementary Video 4 link: https://www.youtube.com/shorts/n6jV56LQ0mQ

Supplementary Video 4. Cine cardiac magnetic resonance imaging depicting both the right and left ventricles forming separate apices, consistent with a butterfly apex. Butterfly apex is an anatomic variation that is not to be confused with pathological conditions.

Conflict of interest disclosure

The authors declared no conflicts of interest.