Fossa ovalis, patent foramen ovale, and cardiac masses

Key points

• Fossa ovalis is a depression on the right atrial side of interatrial septum. It is an embryonic remnant of a once patent channel between the right and left atria of the fetal heart, serving fetal circulatory system. In adults, this landmark is often used surgically for accessing the left atrium from right atrium for various surgical procedures.

• In about a quarter of the population, this channel fails to close leading to patent foramen ovale. This foramen is implicated in various pathologies like paradoxical thromboembolism leading to conditions like cryptogenic stroke. This patency may also be associated with atrial septal aneurysm, that increases the risk for associated pathologies. Patent foramen ovale can be diagnosed using transesophageal echocardiography with bubble study, and transthoracic echocardiography, among other radiological techniques. Management involves percutaneous closure of the foramen ovale using occluder devices.

• Cardiac masses can range from simple cardiac growths to benign cardiac tumors and malignant neoplasms. Management involves resection of most tumors depending on their size and severity of the associated symptoms.

Morphology

The fossa ovalis is a three-dimensional structure consisting of the septum itself and the annulus or limbus fossa ovalis, the raised edge around the perimeter of the fossa . The annulus gives the margins of the fossa a crater-like appearance. Although there is a wide variation in the location and geometry of the fossa ovalis, structurally, the fossa can vary from being smooth to a net-like formation. The fossa can also be patent or form a right-sided pouch (RSP) . The RSP may imitate a PFO channel. The shape of the fossa is oval in most people .

Anatomical relations

The septum that separates the right atrium from the left atrium has an oval thumbprint size depression called the fossa ovalis on the lower portion of its right atrial side. It has a prominent margin, the limbus fossa ovalis (border of the oval fossa). The fossa lies cephalad and left of the inferior vena cava, and the coronary sinus lies caudal and anterior to the fossa, whereas His bundle shares the same horizontal plane with the fossa ovalis ( Fig. 28.2 ). The depression in the fossa represents the residuum of the embryonic oval foramen and its valve—important components of the fetal circulation. The interatrial septum faces forward and to the right, corresponding to the location of left atrium that lies posteriorly and to the left of right atrium. The interatrial septum forms the anterior wall of the left atrium.

Surgically, the fossa ovalis, along with the midseptal region, represents the true interatrial septum and comprises only 20% of the entire interatrial septum. The fossa ovalis and this midseptal region are the only places where one can penetrate and create an interconnection between the two atria without exiting the heart .

Embryology

In the primitive atrium of the fetal heart, two partially muscular embryonic structures called septum primum and septum secundum fuse to form the interatrial septum ( Fig. 28.3 ).

The ostium primum in the septum primum serves the purpose of shunting oxygenated blood from the umbilical vein through inferior vena cava and right atrium directly to the left atrium, bypassing the pulmonary system and the nonfunctional fetal lungs. Oxygen-rich blood hence shunts directly into the systemic circulation, a process necessary for the normal expansion of left atrium and left ventricle.

During the 4th week of fetal life, as the septum primum grows, the evolving atrioventricular mesenchymal complex begins to fill the gap in the interatrial connection of ostium primum ( Fig. 28.3 A and B). At the same time, as the ostium primum is gradually disappearing, new tiny perforations are created in the central region of septum primum by programmed cell death; those coalesce to form a new foramen called the ostium secundum ( Fig. 28.3 C), which is purposed for continued right to left shunting of blood before ostium primum finally closes.

Around 5–6 weeks, a second ridge called septum secundum begins to grow craniocaudally and dorsoventrally, overlapping the ostium secundum ( Fig. 28.3 D and E). This muscular ridge leaves an opening near the floor of the right atrium, forming the foramen ovale.

The cranial part of the septum primum, initially attached to the roof of the left atrium, gradually disappears ( Fig. 28.3 E). The remaining part of the septum, attached to the fused endocardial cushions, forms the flap-like valve of the foramen ovale. This valve prevents the backflow of blood away from the left atrium by collapsing against the stiff septum secundum. This shunt continues for the rest of the fetal development during the intrauterine life.

Functional closure of the foramen ovale

After birth, as the lungs become functional with neonatal breathing, the pulmonary vasculature abruptly dilates. This, combined with the cessation of umbilical flow, reverses the pressure difference, significantly decreasing the pressure in right atrium compared to the left. Increased pressures in the left atrium push the flexible septum primum (valve of the foramen ovale) against the more rigid septum secundum, even during atrial diastole, thus leading to functional closure of the foramen ovale.

Anatomical closure of the foramen ovale

Anatomical closure is achieved at around 3rd month when tissue proliferation and adhesion of the septum primum to the left margin of the septum secundum are complete, obliterating the foramen ovale.

As a result, the interatrial septum becomes a complete partition between the atria in about 75% of humans, carrying the memory of fetal foramen ovale as a depression, called the fossa ovalis. The septum primum forms floor of the oval fossa. The inferior edge of the septum secundum forms a rounded fold, the border of the oval fossa (limbus fossa ovalis), which marks former boundary of the foramen ovale, giving it a crater-like appearance.

Vascular supply

Right and left coronary arteries give off right and left anterior and posterior atrial branches, which anastomose to form Kugel’s artery or the arteria anastomotica auricularis magna ( Fig. 28.4 ) which supplies the interatrial septum.

The midportion of the interatrial septum, together with the fossa ovalis, receives the least amount of vascular supply. The number and density of these vessel networks also decreases with age. In the antero-inferior part of the septum, a comparatively dense vascular network exists .

Nerve supply

Angiotensinergic (renin–angiotensin–aldosterone dependent) innervation dominates the right atrium, which might also be a source of angiotensin II. It modulates autonomic nervous function in the heart thereby facilitating presynaptic noradrenaline release. Vagal efferents and noncatecholaminergic afferents comprise the peripheral nerve fibers, a small amount of whose impact is sympathetic.

Use of fossa ovalis as a surgical plane

For most surgical procedures that require access from the right atrium to the left heart chambers, the (limbus) fossa ovalis represents the most direct anatomical landmark and avenue of access ( Fig. 28.5 ). Situations requiring such access include hemodynamic assessment of the mitral valve, catheter-based mitral valve repair, paravalvular leak closure, and percutaneous balloon valvuloplasty. Left atrial appendix closure, pulmonary vein isolation, and radiofrequency catheter ablation also make use of the true interatrial septum formed by the fossa ovalis for transseptal puncture. In the presence of a prosthetic aortic valve, the fossa ovalis provides an alternate access to the left ventricle besides the retrograde route through the aortic valve. PFO and ASD repair also makes use of the same fossa landmark for access.

Change of morphology of fossa ovalis in certain conditions

Patent foramen ovale

Incidence and morphology

In about 25%–35% of the population, the fetal foramen ovale fails to close, leaving a patency between the right and left atria known as the “patent foramen ovale.” It is not a true defect of the interatrial septum like the atrial septal defects, rather a variant of fossa ovalis occurring due to the failure of successful fusion of the septum primum and secundum . There is variation in the location and size of the fossa ovalis from heart to heart ; therefore, a corresponding variation is seen in the corresponding characteristics of the patent foramen ovale. In most cases, the height of the curvilinear, oblong tunnel-like patent foramen ovale ranges anywhere between 1 and 6 mm and width between 5 and 13 mm along the curve of the muscular rim formed by septum secundum, with a diameter of 1–10 mm. The size tends to increase with increasing age .

Antero-superiorly, the right atrial entrance of patent foramen ovale is bordered by the muscular rim of the fossa, whereas the thin flap valve forms the posterior border. A crescentic free edge of the embryonic septum primum forms the left atrial entrance . This entrance is in proximity to the left atrial antero-superior wall and is of surgical importance while advancing a catheter due to the risk of exiting the heart as this part of the left atrial wall is exceptionally thin ( Fig. 28.6 ).

Clinical pathology

Patent foramen ovale, atrial septal aneurysm, paradoxical embolism, and cryptogenic stroke

Paradoxical embolism

Patent foramen ovale (PFO), although benign on its own, is usually too small to be hemodynamically significant. However, even a small patent foramen can provide a channel for thrombi, fat particles, and gas bubbles to enter the systemic circulation, bypassing the pulmonary arterial circuit. This right to left shunting of the embolus via PFO, called “paradoxical embolism” ( Figs. 28.7 and 28.8 ), has been long associated with cryptogenic stroke, especially in a younger population without risk factors for ischemic stroke. In fact, out of all individuals who suffer cryptogenic stroke, nearly half harbor a PFO .

Atrial septal aneurysm

Atrial septal aneurysm (ASA), although rarely an isolated abnormality, is frequently associated (50%–89%) with PFO . Presenting on echocardiography as a focal bulge of the IAS with displacement toward the left or right atrium , atrial septal aneurysm has been implicated as a source of cardiogenic emboli from thrombi formed by the stagnation of blood in the depth of its recess . Atrial septal aneurysm has also been known to develop fibrosis of its wall. An associated preexisting ASD can provide the patent connection permitting left atrial to right atrial intracardiac shunting, with all of its associated consequences. Elevated intracardiac pressures secondary to cardiac pathologies (and increased left atrial pressures) are likely to be involved in the formation of ASA .

A Chiari network, a fine, net-like latticework of residual atrial tissue, can serve as a nidus for thrombi to form, potentially leading to paradoxical embolization via a patent foramen ovale (see Fig. 28.9 ).

One can easily picture how an ASA full of thrombus, oscillating (hypermobile) right and left during the cardiac cycle, could easily displace systemic emboli, resulting in initially cryptogenic stroke ( Fig. 28.10 ).

Other than associated ASA, certain morphologic features of the PFO confer high risk for causing pathology. These include large size (≥ 2 mm in height) and long tunnel (≥ 10 mm in length) of the PFO, prominent Eustachian valve, and large right-to-left shunt seen on echocardiography at rest and during Valsalva maneuver . Also included in the list is low-angle PFO (≤ 10 degree of PFO angle from the inferior vena cava longitudinal orientation) .

It is absolutely essential that individuals with otherwise unexplained embolic stroke undergo an echocardiogram with bubble study. The origin of the embolic material may often be ascertained by this simple, noninvasive study.

Decompression sickness and gas embolism

Decompression sickness (DCS) is caused by the supersaturation of blood and tissues with dissolved gases caused by breathing under high pressure, with subsequent evolution of gas bubbles as the pressure decreases when a diver rises toward the surface. These gas bubbles embolize from a pulmonary or intravascular origin into the arterial circulation, causing occlusion of a distal systemic arterial locus, leading to symptomology of cutis marmorata and vestibular and neurological DCS . PFO has been implicated to provide a channel for gas embolism to move from venous to arterial circulation via paradoxical embolism, especially in unprovoked and “undeserved” decompression sickness, where diving has been done within accepted safety limits .

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