Heart failure is a progressively debilitating disease that impacts 5.7 million US adults.1 Past treatment approaches have focused on symptom management, but researchers now say it is likely that the function of cardiomyocytes can be rescued from their ‘metabolically stunned’ state.2 Since the heart maintains specialized cellular processes that demand high but varying levels of energy, and because it stores only a small amount of energy substrate, the focus of current research is on developing treatment strategies for meeting those fluctuating workload demands.3
Patients with heart failure have decreased ATP production in heart cells as well as other abnormalities in cardiac metabolism.4-5 Innovative therapies consider energy deficiency as both cause and effect at the level of gene expression.3 The electron transport and phosphorylation apparatus is now thought to be where mitochondrial defects are found. Reduced ATP production is caused by progressively reduced mitochondrial respiratory pathway activity, which reduces pump function, stimulating soaring energy demand as functionality decreases.5
Preclinical models of therapies targeting the mitochondria have produced encouraging results, as have iron and exercise therapies that target mitochondrial biology.6 Mitochondrial biogenesis means stimulating the production of new mitochondria through transcription of peroxisome proliferator–activated receptor gamma co-activator (PGC1?) in order to maintain the volume and flow of the mitochondrial network.2
Which nutrients are supported by the research? A review of 14 randomized controlled trials on the efficacy of CoQ10 found that patients had a lower mortality rate and improved exercise capacity compared to study participants receiving a placebo.7 Supplementing with CoQ10 daily can improve a patient’s New York Heart Association Class rating.8-9 Another review found that heart failure patients can benefit from receiving nutraceuticals such as hawthorn, beet nitrates, l-carnitine, and vitamin D.10
Research into supporting mitochondrial health for cardiometabolic patients and patients with migraines, fatigue, and other conditions continues to grow. Learn the latest interventions at IFM’s Energy Advanced Practice Module.
- Mozzafarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics—2016 update: a report from the American Heart Association. 2016;133(4):e38-e360. doi:10.1161/CIR.0000000000000350.
- Bayeva M, Gheorghiade M, Ardehali H. Mitochondria as a therapeutic target in heart failure. J Am Coll Cardiol. 2013;61(6):599-610. doi:1016/j.jacc.2012.08.1021.
- Huss JM, Kelly DP. Mitochondrial energy metabolism in heart failure: a question of balance. J Clin Invest. 2005;115(3):547-555. doi:1172/JCI24405.
- Doenst T, Nguyen TD, Abel ED. Cardiac metabolism in heart failure: implications beyond ATP production. Circ Res. 2013;113(6):709-724. doi:1161/CIRCRESAHA.113.300376.
- Rosca MG, Hoppel CL. Mitochondrial dysfunction in heart failure. Heart Fail Rev. 2013;18(5):607-622. doi:1007/s10741-012-9340-0.
- von Hardenberg A, Maack C. Mitochondrial therapies in heart failure. Handb Exp Pharmacol. 2017;243:491-514. doi:1007/164_2016_123.
- Lei L, Liu Y. Efficacy of coenzyme Q10 in patients with cardiac failure: a meta-analysis of clinical trials. BMC Cardiovasc Disord. 2017;17(1):196. doi:1186/s12872-017-0628-9.
- Rosenfeldt F, Hilton D, Pepe S, Krum H. Systematic review of effect of coenzyme Q10 in physical exercise, hypertension and heart failure. 2003;18(1-4):91-100.
- Madmani ME, Yusuf Solaiman A, Tamr Agha K, et al. Coenzyme Q10 for heart failure. Cochrane Database Syst Rev. 2014;(6):CD008684. doi:1002/14651858.CD008684.pub2.
- Cicero AFG, Colletti A. Nutraceuticals and dietary supplements to improve quality of life and outcomes in heart failure patients. Curr Pharm Des. 2017;23(8):1265-1272. doi:2174/1381612823666170124120518.