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Project

Dissecting the molecular mechanisms underlying triggered activities and arrhythmogenic substrates in the infarct border zone using living myocardial slices

Heart rhythm disturbances arising from abnormal electrical pulses after a heart attack are major causes of death, as the heart beats too slow, too fast or irregular. A heart attack occurs when blood flow decreases or stops to a part of the heart, causing damage to the cardiac muscle. The region next to the damaged tissue is called the border zone and has been implicated as the region where rhythm disturbances initiate. This region features presence of cardiac fibrosis interspersed with surviving heart muscle cells. During fibrosis, heart muscle cells are replaced by deposits that stiffen the heart and by other groups of cells, such as cardiac fibroblasts and immune cells. In this region, the surviving viable heart muscle cells may have different structural and electrical properties. Cardiac fibroblasts, which normally support the healthy heart muscle, can become malignantly after cardiac injury. They have the capacity to directly couple to heart muscle cells via small connecting channels and thereby influence the electrical properties of the cardiac muscle. In this project, I will use thin sections of living heart muscle to investigate the underlying mechanisms of rhythm disturbances after a heart attack in a multicellular environment and correlate findings to the whole heart observations. This will provide new insights and will thereby contribute to the development of new therapies.
 

Date:1 Nov 2019 →  31 May 2022
Keywords:Cardiac myocytes, infarct border zone, arrhythmia, triggered activities, cardiac fibroblasts, organotypic cardiac tissue slices, optical mapping
Disciplines:Cardiology, Cell physiology, Pathophysiology, Electrophysiology