Sudden cardiac death resulting from an arrhythmia is a rare and difficult to study disorder. Now researchers at Johns Hopkins University have developed a computer model of the heart specifically mimicking what happens to it prior to and during sudden cardiac death. The biomolecular simulation is already pointing to drug targets that should be looked at as a potential preventive measure for the very serious arrhythmias that end up causing sudden cardiac death.
“For the first time, we have come up with a method for relating how distressed molecular mechanisms in heart disease determine the probability of arrhythmias in cardiac tissue,” said Raimond L. Winslow, professor of Biomedical Engineering at Hopkins and senior author of the study. “The importance of this is that we can now quantify precisely how these dysfunctions drive and influence the likelihood of arrhythmias. That is to say, we now have a way of identifying the most important controlling molecular factors associated with these arrhythmias.”
The simulation models the heart on the general level, as a whole organ, as well as on the cellular and molecular levels. Ion channels that move calcium received particular focus of attention, as they seem to play an important role in setting the rhythm of the heart. Within the simulation the researchers showed that cardiac cells overfilled with calcium, as happens often in heart disease patients, end up releasing the calcium and in the process generating electrical signals. If enough of the cells doing this generate a strong enough signal at the same time, it can be the trigger that starts an arrhythmia. This seems to be a clue of why sudden cardiac death is quite rare, as the chances of enough cells grouping together to produce a strong enough effect is small.
Study in PLOS Computational Biology: Estimating the probabilities of rare arrhythmic events in multiscale computational models of cardiac cells and tissue…
Via: Johns Hopkins…
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