In contrast to embryonic and neonatal cardiomyocytes, adult myocardial cells are terminally differentiated and have lost the ability to proliferate.

The product of a hypoxic myocardium can be hyperirritable myocardial cells.

It is interesting to note that most cardiac myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential.

Like a neuron, a given myocardial cell has a negative membrane potential when at rest.

The two bundle branches taper out to produce numerous Purkinje fibers, which stimulate individual groups of myocardial cells to contract.

This results in an accumulation of calcium in the myocardial cell via the sodium calcium exchanger.

There is evidence of myocyte (myocardial cell) degeneration and death seen in 50% of cases of fatty infiltration.

Increased EDV causes the stretching of the ventricular myocardial cells which in turn use more force when contracting.

During the process, myocardial cells are stretched and stressed to produce new contractile elements.

Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells.