Protecting the aged heart during cardiac surgery: The potential benefits of del Nido cardioplegia
Received 5 January 2010; received in revised form 15 February 2010; accepted 2 June 2010. published online 26 July 2010. Corrected Proof
Objective
Aged hearts are more vulnerable than mature hearts to reperfusion injury during cardiac surgery because of altered cardiomyocyte Ca2+ homeostasis. Inasmuch as immature cardiomyocytes have similar properties, a specialized cardioplegic solution (del Nido cardioplegia) designed to protect children's hearts may also be beneficial for elderly patients. Our objective was to evaluate the ability of del Nido cardioplegic solution, containing lidocaine and less Ca2+ than our standard cardioplegic solution, to protect aged cardiomyocytes during cardioplegic arrest and reperfusion.
Methods
We used our novel isolated cell model of cardioplegic arrest and reperfusion to compare the effect of del Nido cardioplegic solution with that of our standard cardioplegic solution on intracellular Ca2+ concentration, contractions, and membrane potential in cardiomyocytes from senescent rat hearts.
Results
The incidence of spontaneous contractions during cardioplegic arrest was lower with del Nido cardioplegia (3/11 vs 9/11 cells; P < .05) than with standard cardioplegia, and contractions could not be induced by field stimulation of cardiomyocytes arrested with del Nido cardioplegia (0/11 vs 9/11 cells; P < .05). Intracellular diastolic Ca2+ levels were lower during arrest with del Nido cardioplegia (57.10 ± 3.06 vs 76.19 ± 3.45 nmol/L; P < .05). During early reperfusion, a potentially injurious rapid recovery of intracellular Ca2+ associated with hypercontraction in cardiomyocytes arrested with standard cardioplegic solution was avoided in cells treated with del Nido cardioplegia (81.42 ± 2.99 vs 103.15 ± 4.25 nM; P < .05).
Conclusions
Del Nido cardioplegic solution has the potential to provide superior myocardial protection in senescent hearts by preventing electromechanical activity during cardioplegic arrest and Ca2+-induced hypercontraction during early reperfusion.
aIWK Health Centre, Dalhousie University, Halifax, Nova Scotia, Canada
bDepartment of Surgery, Dalhousie University, Halifax, Nova Scotia, Canada
cDepartment of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia, Canada
dDepartment of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada
eDepartment of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada
fDepartment of Medicine, Division of Geriatric Medicine, Dalhousie University, Halifax, Nova Scotia, Canada
Address for reprints: Stacy O'Blenes, IWK Children's Heart Centre, IWK Health Centre, 5850/5980 University Ave, PO Box 9700, Halifax, NS, Canada B3K 6R8.
This work was supported by a Seed Grant from the Dalhousie University Department of Surgery.
ABSTRACT