Final answer:
Turner Syndrome and Noonan Syndrome both involve congenital heart defects, but Noonan Syndrome with Multiple Lentigines particularly results in cardiac hypertrophy due to PTPN11 gene mutations affecting endocardial cells.
Step-by-step explanation:
Cardiac Findings in Turner Syndrome vs. Noonan Syndrome
When comparing cardiac findings between Turner Syndrome and Noonan Syndrome, it’s important to note that both conditions are associated with a variety of heart defects. Turner Syndrome often involves congenital cardiac issues such as bicuspid aortic valves, coarctation of the aorta, and sometimes even hypertension or aortic dissection. Noonan Syndrome, on the other hand, includes congenital heart defects as well, such as pulmonary valve stenosis, hypertrophic cardiomyopathy, and atrial septal defects. In particular, Noonan Syndrome with Multiple Lentigines (NSML) has been associated with cardiac hypertrophy due to mutations in the PTPN11 gene.
Recent research has uncovered that these mutations lead to hypertrophy through abnormal cell communication, specifically affecting endocardial cells rather than myocardial cells. This discovery is crucial as it offers potential targets for the treatment of NSML and increases our understanding of the causes behind other, more common cardiac disorders.