When people have myocardial infarctions (heart attacks) the cardiomyocytes (heart muscle cells) can suffer hypoxia (lack of oxygen) and so apoptosis (the death of cells) can occur. The (very complicatedly named) effects can be mitigated through a process called angiogenesis. This is where new blood vessels are created rapidly in order to perforate some living tissue and in this case combat the hypoxia. Now when it comes to treating and intervening in patients with growing areas of dead cells (the infarct) in the heart, fitting a catheter is the most reliable cure. Cell based therapies or those that provide angiogenic assistance could be used to treat the growing risk of a heart attack but no clinical trials have proven them to be a success. It can be seen as worrying that in the last sixty years (the Nobel prize for cardiac catheters was awarded in 1956) there have been no more advancements or great innovations.
The main problem is that what cells and sections need to recover in an infarcted heart is still a mystery. The current target for various therapies is the interface between the liquid carrying (called perfused) and dry (non-perfused) sections of the heart. These work as described above by triggering enhanced vessel growth to increase oxygenation, reduce hypoxia and hopefully combat apoptosis. Unfortunately the physiological interaction between wet, dry and dead cells is not an easy thing to understand. Being able to specifically analyse which cells still have a chance of being saved is essential to developing an effective treatment for the developing heart attack.
A highly detailed study has been performed on mouse hearts as well as a dissection of a patient who had suffered a lethal heart attack which confirmed the suggested idea that heart cells could survive inside the heart valves even if they had been engulfed by the dead and dying cells. Evidence was also found for the idea that a circulatory system, independent of the heart’s circulation, developed from the left ventricle due to angiogenesis.