The first anatomical description of lipomatous hypertrophy of the interatrial septum (HLSI) dates back to 1964, while the first in vivo diagnosis of this tumor was made in 1982 using echocardiography imaging [2,3].

The frequency of lepromatous hypertrophy of AIS has long been poorly known since most of the available data came from autopsy series. The autopsy incidence of lipomatous hypertrophy of the AIS is 1%, whereas recent echocardiographic data have reported that lipomatous hypertrophy of the interatrial septum has become a fairly common finding with a reported incidence of 1-8% of the general population [4,6] . This difference can be explained by the technological advances in modern imaging.  About 250 observations have been reported in the literature. It preferentially affects women in the elderly, obese, frequently suffering from atrial fibrillation or with a history of pulmonary disease [1,5] . According to the literature, a high incidence has been noticed in patients with metabolic disorders such as cerebrotendinous xanthomatosis or mediastino-abdominal lipomatosis and also in patients receiving long-term parenteral nutrition [3].

Histologically, the lipomatous hypertrophy of AIS is characterized by the presence of adipocytes, between which hypertrophied myocardial fibers are embedded. Occasionally, multivacuolar fat cells identical to fetal fat cells are found. The latter are considered by some authors to be the histological marker of this entity, as is the absence of a capsule distinguishing it from true cardiac lipomas [1]. Macroscopically, the tissue constituting this hypertrophy cannot be differentiated from the epicardial adipose tissue. It seems that a significant increase in epicardial fatty tissue is readily observed in these patients [2].

Anatomically, it is an accumulation of fatty tissue at the level of the interauricular septum sparing the foramen ovale responsible for a dumbbell or hourglass appearance. It is in continuity with the epicardial fat and can bulge laterally in one of the ear cavities, especially on the right, and then simulate a tumor [2].

The diagnosis of HLSI is most often fortuitous, with clinical signs absent or non-specific, as in our observation. Lipomatous hypertrophy of the AIS can, in very rare cases, become obstructive and invade the superior vena cava  [2]  .

Some series have reported ECG abnormalities, an alteration of the P wave is often noted, it can be negative, enlarged, hooked or biphasic. Other electrical abnormalities may be highlighted in the form of supraventricular arrhythmias (50% of cases) due to local irritation: atrial extrasystoles, paroxysmal supraventricular tachycardia, atrial tachycardia, atrial fibrillation or flutter  [1]. The frequency of these arrhythmias seems to be related to the extent of hypertrophy: a septal thickness greater than 30 mm is associated with an incidence of atrial arrhythmias of more than 60% in the Shirani and Roberts series [2,8].

In echocardiography (ETT and ETO), lipomatous hypertrophy results in a thickening of the AIS respecting the oval fossa (dumbbell appearance), almost pathognomonic when the thickness exceeds 20 mm, but it can vary depending on the series from 20 mm to 62 mm, with an average of 35 mm. It constitutes an unencapsulated hyperechoic mass, very little mobile, non-circulating, with a wide implantation base, which differentiates it from the myxoma, sometimes with linear echoes. It protrudes into the right atrium, no case of protrusion in the left atrium has been reported. Echocardiography cannot, however, differentiate between fatty tissue and connective tissue [2,4].

It is therefore necessary to confirm the fatty nature of the tumor by using chest CT or cardiac MRI. The CT scan can detect the presence of fat at the level of inter-atrial thickening (density ≤ 50 HU), within a mass with clear boundaries. MRI clarifies the ultrasound data, confirms the fatty content of the tumor process and thus limits the use of invasive methods (endomyocardial biopsy). It objectifies a well-limited and non-encapsulated lesion, respecting the oval fossa and the surrounding structures, appearing as a characteristic hypersignal on the T1-weighted sequences and as a T2-weighted hyposignal, especially after fat saturation. Typically, the thickening spares the oval pit giving a classic "hourglass" or "dumbbell" appearance [5]. Gadolinium injection does not enhance the tumor  [2] [1, 4] . Epicardial or mediastinal fat infiltration is often associated[5].

 The Pet Scanner can objectify a hypermetabolism thus causing the "hot spot" image of the interatrial septum in HLSA and lead us to a malignant nature of the mass [6,7].

The main differential diagnosis of lipomatous hypertrophy of AIS is lipoma. This benign tumor is rarer, only 70 observations have been reported in the literature, described in young patients, sometimes in the context of tuberous sclerosis of Bourneville. It is encapsulated and can affect epicardial, endocardial and pericardial fatty tissues. Their predictive site is the left ventricle and the right atrium but can also more rarely affect the right ventricle, the left atrium and the interventricular septum. The lipoma appears on echocardiography as a hypoechoic mass when it is pericardial and hyperechoic when it affects the heart chambers [2]. Their appearance in MRI and CT is characteristic. These are homogeneous, encapsulated, fat density masses, whose high signal on the T1 and T2 sequences collapses after fat saturation. They generally do not have significant contrast intake. Septa can be visualized. The presence of tissue components within the lipoma should suggest a well-differentiated liposarcoma (extremely rare)[5] . Microscopically, these are mature fat cells without fetal cells. These lipomas are most often asymptomatic and the surgical indication is very rare, reserved for large lipomas with pericardial development [1,5].

The prognosis for lipomatous hypertrophy of the AIS is good and surgical treatment is reserved only for rare cases of invasion of the superior vena cava with hemodynamic repercussions or malignant cardiac arrhythmias, which cannot be controlled under drug treatment [1,2].