Our patient is a 41 years old male, born and living in Cairo, working as a constructor worker and has 3 children the older of which is 13 years old. He was admitted to the internal medicine department by fever and shortness of breath for about 1 week associated with weakness of his right upper limb for 12 h before his presentation which made him sought medical advice. He was not known to be hypertensive nor diabetic.He was a heavy Cigarette and Shesha smoker for about 17 years .He denied history of any substance abuse. He has no family history of any cardiac disease O/E: The patient appeared pale, toxic, orthopenic, a little confused however he was oriented to time, place and persons.There was mild weakness of his right upper limb with intact sensation. BP: 100/70 bilaterally, HR: 110, regular, of average volume, peripherally felt, Temp: 38.8 °C, RR: 20/min. Bilateral fine basal rales on deep inspiration, Normal abdominal examination. Cardiac examination: The cardiac impulse was hyperdynamic at the 5th intercostal space just outside the mid-clavicular line with no palpable thrill. Auscultation revealed S3 gallop apically with grade III–IV pan systolic murmur radiating to the anterior axillary line. Hgb: 11.2,WBC’s: 13,000, Platelet count: 270,000. Total billirubin: 1.1, BUN: 17, Creat: 1.4, Na: 135, K: 3.9, SGOT: 45, SGPT: 37. Left atrial dissection (LAD) is a rare complication and the literature reveals only a small number of cases. LAD is by Gallego et al. as a gap from the mitral or tricuspid annular area to interatrial septum or left atrial wall, creating a new chamber with or without communications into the true left or right atrium. The most common etiology of LAD is mitral valve surgery. Debridement of much calcified valves annulus, improper suturing of the annulus to the prosthetic cuff, excessive traction on sutures in the posterior annulus, and the hemodynamic influence of the paraprosthetic leak extended the dissection into the left atrial wall, developing a false cavity. Also left atrial thrombectomy can be associated with injury to the left atrial endocardium as a mechanism of primary tear.A rare case of left atrial dissection as a consequence of infectious endocarditis was reported. They present a patient with infectious endocarditis with involvement of mitral and aortic valves; in whom the trans-esophageal echocardiography was able to visualize the left atrial dissection. The LA has a venous component that receives the PVs, a fingerlike atrial appendage, and shares the septum with the right atrium. The major part of the atrium, including the septal component, is relatively smooth-walled whereas the appendage is rough with pectinate muscles. The smoothest parts are the superior and posterior walls that make up the pulmonary venous component, and the vestibule. Seemingly uniform, the walls are composed of one to three or more overlapping layers of differently aligned myocardial fibers, with marked regional variations in thickness. Why the posterior wall of the left atrium:A sagittal section through the left atrium of a cadaver shows the proximity of the esophagus to the posterior wall of the left atrium The wall is particularly thin at the level of the superior pulmonary veins. Clinical presentation may be the appearance of a new systolic murmur, associated with or without symptoms of heart failure and low-output manifestations, hours to days after the operation but there were patients in whom clinical onset occurs years after surgery. Rarely, LAD can be an incidental finding on TEE in an asymptomatic patient. LA dissection typically appears as a hypoechoic space from the mitral/tricuspid origin extending along the interatrial septum or LA wall. M-mode is excellent at distinguishing subtle movement of the intima or the endocardium in relation to the cardiac cycle. Similar to what is seen in aortic dissections, the false cavity is compressed during systole as the LA is being filled. Other entities that should be considered when an LA mass is visualized are: Thrombi most common left atrial myxoma, cysts, coronary aneurysms. Pericardial blood impinging on the LA wall may mimic these findings. Color flow Doppler can be used to examine the endocardium for a tear and point of communication with the chamber. Pulsed wave Doppler can also be used to identify flow across a tear. TEE is the diagnostic modality of choice for LAD. No definitive criteria exist to help guide management of LAD. Prompt surgical repair is usually required because of coexistent significant mitral regurgitation, intra-cardiac shunt, mycotic aneurysm, pseudo aneurysm or fistulous communication. However, in the absence of these findings, surgery may not always be necessary and occasionally successful repair has been performed years after diagnosis.