However, the muscles, usually those in the lower leg, become fatigued after running a long distance and lose their ability to absorb shock. As the bones now experience larger stresses, this increases the risk of fracture. Previous stress fractures have been identified as a risk factor. Along with history of stress fractures, a narrow tibial shaft, high degree of hip external rotation, osteopenia, osteoporosis, and pes cavus are common predisposing factors for stress fracturesCommon causes in sport that result in stress fractures include
Over training
Going back to competition too soon after an injury or illness
Going from one event to another without proper training for the second event
Starting initial training too quickly
Changing habits or the environment like training surface or shoes

Diagnosis
X-rays usually do not show evidence of new stress fractures, but can be used approximately three weeks after onset of pain when the bone begins to remodel. A CT scan, MRI, or 3-phase bone scan may be more effective for early diagnosis.MRI appears to be the most accurate diagnostic test.Tuning forks have been advocated as an inexpensive alternative for identifying the presence of stress fractures. The clinician places a vibrating tuning fork along the shaft of the suspected bone. If a stress fracture is present, the vibration would cause pain. This test has a low positive likelihood ratio and a high negative likelihood ratio meaning it should not be used as the only diagnostic method. Prevention
Altering the biomechanics of training and training schedules may reduce the prevalence of stress fractures.
Supravalvular aortic stenosis is a congenital obstructive narrowing of the aorta just above the aortic valve and is the least common type of aortic stenosis. It is often associated with other cardiovascular anomalies and is one of the characteristic findings of Williams syndrome. The diagnosis can be made by echocardiography or MRI. Genetics
Supravalvular aortic stenosis is associated with genetic damage at the Elastin gene locus on chromosome 7q11.23. Fluorescent in situ hybridisation techniques have revealed that 96% of patients with Williams syndrome, where supravalvular aortic stenosis is characteristic, have a hemizygous deletion of the Elastin gene. Further studies have shown that patients with less extensive deletions featuring the Elastin gene also tend to develop supravalvular aortic stenosis

Pathophysiology
Supravalvular aortic stenosis is due to diffuse or discrete narrowing of ascending aorta. The murmur associated with it is systolic murmur and is similar in character to valvular aortic stenosis murmur but commonly present at 1st Intercostal space (ICS) on the right. Individuals with this anomaly may have unequal carotid pulses, differential blood pressure in upper extremities and a palpable thrill in Suprasternal notch. Individuals with significant supravalvular AS chronically may develop left ventricular hypertrophy and also are at risk of developing coronary artery stenosis. With increased metabolic demands (e.g. exercise) such individuals may develop subendocardial or myocardial ischemia due to increased myocardial oxygen demand and seek medical help with symptoms of exercise induced angina. Diagnosis
Treatment


== References ==