Heart failure refers to the clinical signs – such as fluid accumulation in the lungs or abdomen – that occur when the heart can no longer adequately compensate for changes associated with the heart disease.
When heart failure develops, current nutritional recommendations focus on correcting nutrient deficiencies, managing clinical signs, and maintaining adequate caloric and protein intake to preserve lean body mass and avoid cachexia.
At the cellular level, heart failure could be called an energy crisis. The mitochondria become dysfunctional, energy metabolism is inefficient, and cardiac contractility diminishes.2
Learn more about the bioenergetic changes in heart failure that provide opportunities for new nutritional approaches to cardiac health.
Image courtesy of Rebecca L. Stepien, DVM, MS, DACVIM (Cardiology), University of Wisconsin, USA
The clinical signs of heart failure are hard to miss: lethargy, tachypnea, a cough, or a fluid-filled abdomen. At this late stage of heart disease, ACVIM guidelines make several nutritional recommendations.1
But changes at the cellular level are not so easy to see.
Compromised cardiac energy metabolism is a key aspect of heart failure.2-5
In general, energy metabolism in cardiac mitochondria has three components:2-5
In heart failure, studies show that changes can occur in any, or all three, areas of energy metabolism.2
When cardiac function declines, any one area of altered energy metabolism leads to negative impacts on every other aspect of ATP production.
Ultimately, the failing heart has an energy crisis.2, 6, 7
Studies show that mitochondria in the failing heart change the substrates used to produce energy. The overall process of mitochondrial energy production becomes less efficient.
Purina scientists applied advanced metabolomics and transcriptomics to mitral valve and myocardial tissue to better understand underlying changes in dogs with early stage myxomatous mitral valve disease (MMVD).8
Omics studies, in both people and animals, have shown that gene expression and metabolite profiles associated with energy metabolism differ significantly between healthy hearts and those with heart failure.8–10
Purina scientists found more than 1,000 gene transcripts were differentially expressed between healthy dogs and those with MMVD.
The genes expressed in MMVD dogs were associated with altered pathways in:
Similar to findings in studies of human heart failure, these changes suggest that MMVD dogs also make a metabolic shift away from using long-chain fatty acids as a primary energy source and there is less efficient use of energy overall.
These omics study insights, and emerging research in therapeutic nutrition,12 suggest that providing alternate sources of energy metabolism may lead to better management, treatment, or even prevention of heart diseases.