Failure to produce an adequate amount of energy causes mechanical failure of the heart.

When heart muscle cells are put under stress, for example by high blood pressure or by oxygen deprivation (such as occurs during a heart attack), they switch from using fatty acids as their source of energy to using glucose.

The well-oxygenated heart consumes several different substrates and converts them to a common form of chemical energy that fuels myocardial contraction and is required for viability.

The mechanisms underlying the development of HF are multiple, complex, and not well understood, primarily because HF is not a disease, but a manifestation of diverse cardiac and noncardiac abnormalities.

Adequate amounts of ATP must be generated to support the heart’s contractile demands and maintain viability for the other cells in the body. Abnormalities in cardiac metabolism, such as a lack of ATP-ADP metabolism, cause mechanical failure of the heart.

Dysfunctional mitochondria produce less cellular energy (ATP) and produce increased levels of reactive oxygen species (ROS), both of which lead to oxidative stress and ultimately to HF.

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