title: Both systolic and diastolic dysfunction characterize nonischemic inhibition of myocardial energy metabolism: an experimental strain rate echocardiographic study.
abstract: BACKGROUND
  Ischemia is primarily a metabolic event. However, regional functional changes can be affected by structural alterations. We developed an experimental model of sole myocardial energy metabolism inhibition and characterized the resulting regional dysfunction.
  
  
  METHODS
  In 12 pigs, we regionally inhibited creatine kinase (CK) and, consequently, myocyte high-energy phosphate transfer by intracoronary administration of iodoacetamide. Myocardial biopsies for CK activity and structural analyses and strain rate (SR) echocardiography scans were obtained at baseline and 60 minutes after iodoacetamide administration. Plasma levels of the CK isoenzyme MB and troponin I were assessed to determine possible myocardial damage.
  
  
  RESULTS
  CK activity in the iodoacetamide-perfused myocardium decreased to 0.5% of the original value and was accompanied by a reduction in peak systolic SR ( P < .0001), end-systolic strain ( P < .0001), and peak SRs of myocardial early and late filling waves ( P < .0001). Microscopy showed contracture without sarcomere disruption. Plasma levels of CK isoenzyme MB and troponin I did not change.
  
  
  CONCLUSIONS
  Regional inhibition of myocyte energetics leads to both systolic and diastolic dysfunction by SR echocardiography, but the presence of a residual phosphotransfer protects microstructural integrity.
authors.affiliation: Department of Internal Medicine, Division of Cardiovascular Diseases , Mayo Clinic, Rochester, MN 55905, USA.
authors.forename: Josef
authors.initials: J
authors.lastname: Korinek
authors.forename: Peter C
authors.initials: PC
authors.lastname: Anagnostopoulos
authors.forename: Cristina
authors.initials: C
authors.lastname: Pislaru
authors.forename: Petras
authors.initials: P
authors.lastname: Dzeja
authors.forename: James B
authors.initials: JB
authors.lastname: Seward
authors.forename: Andre
authors.initials: A
authors.lastname: Terzic
authors.forename: Marek
authors.initials: M
authors.lastname: Belohlavek
mesh_terms: D000818:Animals; D003402:Creatine Kinase / Q000037:antagonists & inhibitors; D003971:Diastole / Q000187:drug effects / Q000502:physiology; D004452:Echocardiography; D004734:Energy Metabolism / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007460:Iodoacetamide / Q000494:pharmacology; D023421:Models, Animal; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging* / Q000503:physiopathology; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D013552:Swine; D013599:Systole / Q000187:drug effects / Q000502:physiology; D018754:Ventricular Dysfunction / Q000000981:diagnostic imaging* / Q000201:enzymology / Q000378:metabolism
chemical_list: D004791:Enzyme Inhibitors; D003402:Creatine Kinase; D007460:Iodoacetamide