Abstract – William Louch
Heart failure is a chronic disease characterized by a reduced ability of the heart to pump blood. The number of patients with heart failure is increasing, and less than 60% of patients survive for 5 years after diagnosis. Therefore, it’s important that new treatments are established, and we believe that these therapies should not only treat the disease symptoms, but also the root causes. In heart failure, the reduced pumping capacity of the heart results from decreased function of individual cardiac muscle cells. In each of these cells, contraction is triggered by Ca2+ being released from stores. We have seen that during heart failure, there is less release of Ca2+ and that its release is slower. This results in less powerful contraction of the cell, and the whole heart. Specifically, we have seen that these changes in Ca2+ release in part result from disrupted structure of the muscle cell. Normal muscle cells have tubules, called T-tubules, running through them in an organized pattern. This allows for Ca2+ release to be triggered uniformly across the cell. During heart failure, we have observed that these T-tubules are disrupted which impairs Ca2+ release. Our ongoing work is aimed at understanding how these changes in T-tubules come about. Our aim is to prevent or reverse T-tubule disruption in heart failure patients, to increase the power of the heartbeat and alleviate this disease.