The absence of pulmonary artery closure on palpation is the clinical manifestation of Ebstein syndrome. Ebstein syndrome, also known as Ebstein malformation, is a condition in which the tricuspid septal and/or posterior valves occasionally attach to the right ventricular wall near the apex along with the anterior valve downward about 0.5% to 1.0% of the time in precordial disease. This is a rare disease, first reported by Ebstein in 1866. This disease is also known as tricuspid inferior valve malformation. Occasionally, there is a family history, and the offspring of mothers taking lithium early in pregnancy are susceptible to this disease. In the functional right ventricle, systolic pressure may be normal, while diastolic pressure is often increased, similar to constrictive pericarditis. Both systolic and diastolic pressures are elevated in the atrial chambers. There may be a systolic pressure difference on both sides of the pulmonary valve and a diastolic pressure difference on both sides of the tricuspid valve. The former may be due to an overgrown tricuspid leaflet that partially obstructs the right ventricular outflow tract; the latter is due to a tricuspid valve malformation with narrowing of the tricuspid orifice. The onset of Ebstein’s syndrome can be early or late, and the symptoms can be mild or severe with a variety of signs. In severe malformations, cyanosis and congestive heart failure are evident from birth; in milder malformations, the most prominent symptoms of the malformation are cyanosis and congestive heart failure until adulthood. The main signs of Ebstein’s syndrome include: a bulging and quiet precordial region (no obvious precordial pulsation on visualization and no sense of pulmonary artery closure on palpation); a marked splitting of the first and second heart sounds, an enhanced third heart sound, and a fourth heart sound; the second component of the split first heart sound is often karate in nature, which is known as the sailsign; a soft A soft systolic murmur and a short mid-diastolic murmur may be present in the tricuspid region. The most characteristic signs for this malformation, according to Siber, are two groups: (1) cyanosis with a quiet precordial area; and (2) a quartet of first heart sounds, split second heart sounds, and augmented third or fourth heart sounds. Complications such as heart failure, arrhythmia, cerebral embolism and brain abscess can be combined. The pathologic changes without a sense of pulmonary closure on palpation are quite variable. The basic lesion is an abnormal development of the tricuspid valve leaflets and right ventricle with a downward shift of the diaphragmatic and posterior valve leaflets into the right ventricle, which attach to the right ventricular wall below the tricuspid valve annulus through the tendon papillary muscle. The tricuspid valve leaflets are enlarged or reduced in size, often thickening and shortening in deformity. The lesion most often involves the diaphragmatic leaflet, followed by the posterior leaflet, and the diaphragmatic and posterior leaflets may be partially absent. Lesions involving the anterior leaflet are rare. The anterior leaflet originates from the normal tricuspid annulus and may be enlarged like a sail, sometimes with many small holes, and attached to the ventricular wall by shortened and underdeveloped tendons and papillary muscles. The enlarged ventricle above the valve leaflet is called the atrialized ventricle and is similar in function to the right atrium; below the leaflet is the functional right ventricle. The right atrium is enlarged and the atrial wall is thickened by fibrosis.