Contractility is a Key Driver of Cardiac Output1
HFrEF occurs when the heart is unable to maintain sufficient cardiac output to accommodate the body’s metabolic requirements and venous return.1
Heart muscle function is dependent on the key contractile proteins of the sarcomere, actin and myosin. Directly affecting these contractile proteins is referred to as myotropy.2
Fluxes in intracellular Ca2+ reveal myosin binding sites on the actin filament2
Myosin acts as a molecular motor that converts energy stored as ATP into a contractile force2
Myosin and actin bind to create a crossbridge. Crossbridge cycling allows many myosin heads to work together to cause the sarcomere to contract2,3
Take a closer look at the role of contractility in cardiac function
In HFrEF, abnormalities in crossbridge cycling result in fewer myosin heads interacting with actin, which diminishes the force of contraction4,5
In HFrEF hearts, contractility drives performance4,6,7
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ATP, adenosine triphosphate; HFrEF, heart failure with reduced ejection fraction.
1. Kemp CD, et al. Cardiovasc Pathol. 2012;21:365‑371. 2. Psotka MA, et al. J Am Coll Cardiol. 2019;73:2345‑2353. 3. Spudich JA. Biophys J. 2014;106:1236‑1249. 4. Hartupee J, et al. Nat Rev Cardiol. 2017;14:30‑38. 5. Mann DL, et al. Heart failure and cor pulmonale. In: Longo DL, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. McGraw‑Hill; 2012:1901‑1915. 6. Malik FI, et al. J Mol Cell Cardiol. 2011;51:454‑461. 7. Fearnley CJ, et al. Cold Spring Harb Perspect Biol. 2011;3:a004242. doi:10.1101/cshperspect.a004242.