title: Protecting the aged heart during cardiac surgery: use of del Nido cardioplegia provides superior functional recovery in isolated hearts.
abstract: OBJECTIVE
  Aged hearts are particularly vulnerable to ischemia-reperfusion injury. Our objective was to determine if del Nido cardioplegia, which contains lidocaine, less blood, and less calcium than our standard cardioplegia, provides superior protection for aged hearts. We also sought to determine if the lidocaine in del Nido cardioplegia is adequate to prevent Na(+) influx via the window current.
  
  
  METHODS
  Sodium channel kinetics were measured in rat cardiomyocytes with and without lidocaine. Recovery after 60 minutes of cardioplegic arrest was assessed in isolated working senescent rat hearts. Del Nido cardioplegia was delivered as a single dose (n = 8) because it is used clinically, and standard cardioplegia was delivered as an induction dose with re-dosing every 20 minutes (n = 8). After 20 minutes of reperfusion, hearts were switched to working mode for 60 minutes. Flows were indexed to ventricular dry weight. Troponin release was assayed.
  
  
  RESULTS
  Sodium channel kinetics indicated that the lidocaine concentration in del Nido cardioplegia minimizes the potential for Na+ influx via the window current. Spontaneous contractions occurred in fewer hearts arrested with del Nido cardioplegia (88% vs 13%; P = .01), and troponin release was reduced (0.24 vs 0.89 ng/mL; P = .017). Cardiac output was approximately 90% of baseline in the del Nido group compared with approximately 50% in the standard group (173 ± 14 vs 86 ± 22 mL · min(-1) · g(-1); P = .0008). Stroke work was higher in the del Nido group (93 ± 6 vs 41 ± 10 mL · mm Hg · g(-1); P = .0002).
  
  
  CONCLUSIONS
  Del Nido cardioplegia prevents spontaneous contractions during arrest, reduces troponin release, and results in superior myocardial function in isolated aged hearts. Del Nido cardioplegia has the potential to provide superior myocardial protection for older patients undergoing cardiac surgery.
authors: Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia, Canada.
authors: Arun
authors: A
authors: Govindapillai
authors: Rui
authors: R
authors: Hua
authors: Robert
authors: R
authors: Rose
authors: Camille Hancock
authors: CH
authors: Friesen
authors: Stacy B
authors: SB
authors: O'Blenes
mesh_terms: D000367:Age Factors; D000375:Aging; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D002302:Cardiac Output / Q000187:drug effects; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D002314:Cardioplegic Solutions / Q000008:administration & dosage*; D006324:Heart Arrest, Induced / Q000379:methods*; D066298:In Vitro Techniques; D007700:Kinetics; D008012:Lidocaine / Q000008:administration & dosage*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism; D010477:Perfusion; D051381:Rats; D011916:Rats, Inbred F344; D020127:Recovery of Function; D012964:Sodium / Q000378:metabolism; D026941:Sodium Channel Blockers / Q000008:administration & dosage*; D015222:Sodium Channels / Q000187:drug effects / Q000378:metabolism; D014336:Troponin / Q000378:metabolism
chemical_list: D015415:Biomarkers; D002314:Cardioplegic Solutions; D026941:Sodium Channel Blockers; D015222:Sodium Channels; D014336:Troponin; D008012:Lidocaine; D012964:Sodium
keywords: 31.4; 31.7; 38.1; I(Na); sodium current