Heart Attack In A Laboratory Dish

In a healthy cell, one of the components of the membrane, the phospholipids, are asymmetrically distributed across the two layers of the surrounding shell. During a (simulated) heart attack, however, and immediately after it, this asymmetrical distribution is partly lost. The researchers discovered that the absolute number of lipids increased in the outer layer of the membrane because they moved from the inner to the outer layer. This imbalance in phospholipid content probably plays a major role in the damage to the heart muscle cell and its death. It is possible that the quantity of calcium has something to do with changes in the original asymmetry, given that during a heart attack, the concentration of calcium ions in the heart muscle cell increases. The calcium ions can in turn produce the changes in the distribution of lipids.

Besides the blockage, the research team also studied the second phase of a heart attack, reperfusion, when the blood flow is restored. If this happens quickly enough, the tissue can be saved, but otherwise the asymmetrical distribution of the cell membrane phospholipids is lost and the imbalance in phospholipid content becomes more pronounced. Reactive oxygen causes damage to the fatty acid tails of the lipids. If it takes too long for the blood flow to be restored, or if it fails to do so at all, the muscle cell dies and scar tissue is formed.

The results of the research, financed by NWO, clarify why the heart muscle cells are damaged during a heart attack, but they do not yet make it possible to develop a treatment for the problem. This will require further research into just what happens in the lipids.