Lusitropy refers to the ability of the myocardium to relax following excitation contraction coupling. The removal of calcium to the endoplasmic reticulum (SR) promotes relaxation. The sarcoplasmic reticulum calcium ATPase (SERCA), NA/CA exchanger (NCX) and sarcolema CA-ATPase account for 90% removal of calcium. In essence, lusitropy is diastolic function as inotropy (or contractility) is systolic function.
Factors that produce positive lusitropy are: beta adrenergic agonists phosphorylate phospholamban via cAMP, reducing calcium available for binding with troponin. Phospholamban is antagonist of SERCA in the non phosphorylated state
Factors that produce negative lusitrophy are: high calcium, impaired sarcoplasmic reticulum calcium ATPase (SERCA). Increase affinity of troponin C, alkalosis that increases calcium sensitivity
Why is this important? Lusitropy along with ventricular hypertrophy, can cause diastolic dysfunction causing increase end diastolic pressure, wedge pressure, PA presure, edema. The volume loop is smaller, may be moved to the left, and may be moved up due to decrease compliance.
References
- A M Katz Influence of altered inotropy and lusitropy on ventricular pressure-volume loops. J. Am. Coll. Cardiol.: 1988, 11(2);438-45 PubMed Link
Other References
- Ventricular Diastolic Dysfunction, Accessed 3/5/15. Link
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