Hypoplastic Left Heart Syndrome

Left heart syndrome (HLHS) is a rare congenital heart disease. This means that it existed at birth. It's the undeveloped left side of the heart, that is the side that transports oxygen-rich blood to other parts of the body. Diagnosis of HLHS may have various defects on the left side of the heart The most affected structures are the left ventricle, mitral valve, aorta and aortic valve. In a healthy heart, low oxygen or low saturated blood returns from the body to the right atrium and right ventricle.

Ventricular anomalies can be serious and even life-threatening. In the undeveloped left heart syndrome, the left ventricle including the aorta is underdeveloped. Infants born with this disease rarely survive for more than a few days. In other cases, only one room was fully developed. Survival is usually dependent on the presence of relevant compensatory abnormalities, such as the persistence of arterial catheter persistence or the presence of septal defects, which can occur under high pressure or from right to left or from the beneficial compensating heart Enable decompression. Inner shunt from left to right

My patient is a left heart dysplasia syndrome with his heart completely halfway. Usually, the left ventricle is strong and muscular, pumping blood throughout the body. His development is so bad that he underwent a series of operations that allowed all the work in the right ventricle.

An American woman's baby named "Baby Fae" left the first xenotransplanted baby suffering from cardiac hypoplasia, heart disease in 1984. The program was done by Leonardo L. Bailey of the University of Loma Linda Medical Center. Linda, California. Since body fluid based graft rejection is believed to be caused primarily by ABO blood group mismatch, Fae dies after 21 days and is thought to be inevitable due to rare O type sputum . Transplantation is temporary, but unfortunately it is impossible to find a suitable allograft substitute in time.

This case report explains a child suffering from protein-loss enteropathy (PLE) 4 years after orthotopic heart transplantation (OHT). He was born with left ventricular dysplasia syndrome and he received successful Norwood surgery, Hemi-Fontan palliative care, and Fontan palliative therapy at the age of 18 months. Fifteen months after Fontan's surgery, he developed a failure of PLE and Fontan requiring OHT. Four years after OHT, he developed severe tricuspid regurgitation and PLE. His PLE improved after exchanging the tricuspid valve. His tricuspid valve replacement surgery has been undertaken for two years, and his clinic still has no ascites or peripheral edema, and the serum albumin concentration is normal. His artificial tricuspid valve functioned normally. © 2011 Wiley Periodicals, Inc