Major advances in treatment have improved the survival of hearts in the first year after transplantation. However, the function of these transplants progressively decreases with time. The cause of this chronic failure is a gradual narrowing of the coronary arteries that provide the heart with oxygen. This process has some similarities to atherosclerosis that causes heart attacks. The two diseases share some of the same risks, including high lipids in the circulation. Some of these risk factors are enhanced by immunosuppressive drugs that are used to prevent rejection of the transplant. Recently, it has been found that fat (adipose tissue) produces a molecule called adiponectin that decreases the risk of atherosclerosis. Adiponectin is a natural anti-inflammatory molecule. We hypothesize that adiponectin levels decreased in cardiac transplant patients due to surgery, immunosuppression and rejection. We will measure the levels of adiponectin at regular intervals after transplantation and determine whether these measurements predict rejection. We will also determine whether certain patients, who are genetically prone to making high levels of adiponectin, are protected from rejection. Finally, we will determine whether adiponectin can be detected in tissue biopsies from heart transplants. These studies are important for three reasons. First, if measuring levels of adiponectin in blood can predict which patients are likely to reject their transplants, then a simple blood test can be used to identify patients who need more preventive treatment. Second, if adiponectin is protective for the graft, then treatment can be given to increase adiponectin levels. Third, if adiponectin can be detected in tissue biopsies from heart transplants, then it may be useful in diagnosing rejection.