What is Heart Failure
Heart Failure (HF) is a complex, progressive clinical syndrome in which there is dyspnea or exertional limitation due to impairment of ventricular filling or ejection of blood, or a combination of both.
Once developed, HF results in significant morbidity and mortality, with a 1-year mortality rate of 7.2% and a 1-year hospitalization rate of 31.9% in patients with chronic HF.
In patients hospitalized for Acute Decompensated Heart Failure, these rates increase to 17.4% and 43.9%.
HF has traditionally been broadly subclassified according to the left ventricular ejection fraction (LVEF) into 3 categories:
Once developed, HF results in significant morbidity and mortality, with a 1-year mortality rate of 7.2% and a 1-year hospitalization rate of 31.9% in patients with chronic HF.
In patients hospitalized for Acute Decompensated Heart Failure, these rates increase to 17.4% and 43.9%.
HF has traditionally been broadly subclassified according to the left ventricular ejection fraction (LVEF) into 3 categories:
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heart failure with preserved ejection fraction (HFpEF) - LVEF ≥50%
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heart failure with midrange ejection fraction (HFmEF) - LVEF 41%-49%
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HF with reduced ejection fraction (HFrEF), in which the LVEF is ≤40%
Energy Dynamics of the Failing Heart
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.
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.
