title: Cardiac dysfunction and prolonged hemodynamic deterioration after implantable cardioverter-defibrillator shock in patients with systolic heart failure.
abstract: BACKGROUND
  We investigated the acute effects of implantable cardioverter-defibrillator shock on myocardium, cardiac function, and hemodynamics in relation to left ventricular systolic function.
  
  
  RESULTS
  We studied 50 patients who underwent implantable cardioverter-defibrillator implantation and defibrillation threshold (DFT) testing: 25 patients with left ventricular ejection fraction (LVEF) ≥ 45% and 25 patients with LVEF <45%. We measured cardiac biomarkers (creatine kinase, creatine kinase-MB, myoglobin, cardiac troponin T and I, and N-terminal probrain natriuretic peptide). Left ventricular relaxation was assessed by global longitudinal strain rate during the isovolumetric relaxation period using speckle-tracking echocardiography. Blood sampling and echocardiography were performed before, immediately after, and 5 minutes and 4 hours after DFT testing. Mean arterial pressure was measured directly during DFT testing. Cardiac biomarkers showed no significant changes in either group. LVEF was decreased until 5 minutes after DFT testing and had recovered to the baseline at 4 hours in the group with reduced LVEF (P<0.001), whereas LVEF reduction was not observed in the group with preserved LVEF (P=0.637). Global isovolumetric relaxation period was decreased until 5 minutes after DFT testing and had recovered to the baseline at 4 hours in both groups (preserved LVEF: 0.39 ± 0.14 versus 0.23 ± 0.13* versus 0.23 ± 0.13* versus 0.40 ± 0.13 s(-1), *P<0.001 versus baseline; reduced LVEF: 0.15 ± 0.05 versus 0.08 ± 0.04† versus 0.09 ± 0.04† versus 0.15 ± 0.05 s(-1), †P<0.001 versus baseline, repeated-measures ANOVA). Time to recovery of mean arterial pressure to the baseline was prolonged in the group with reduced LVEF (P<0.001).
  
  
  CONCLUSIONS
  Implantable cardioverter-defibrillator shock transiently impairs cardiac function and hemodynamics especially in patients with systolic dysfunction, although significant tissue injury is not observed.
authors: Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan. nori-t@fd5.so-net.ne.jp
authors: Norihisa
authors: N
authors: Toh
authors: Nobuhiro
authors: N
authors: Nishii
authors: Kazufumi
authors: K
authors: Nakamura
authors: Takeshi
authors: T
authors: Tada
authors: Hiroki
authors: H
authors: Oe
authors: Satoshi
authors: S
authors: Nagase
authors: Kunihisa
authors: K
authors: Kohno
authors: Hiroshi
authors: H
authors: Morita
authors: Kengo F
authors: KF
authors: Kusano
authors: Hiroshi
authors: H
authors: Ito
mesh_terms: D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form / Q000097:blood; D017147:Defibrillators, Implantable; D004452:Echocardiography; D005260:Female; D054143:Heart Failure, Systolic / Q000097:blood / Q000503:physiopathology* / Q000628:therapy*; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009211:Myoglobin / Q000097:blood; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D013318:Stroke Volume; D019210:Troponin I / Q000097:blood; D020107:Troponin T / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000209:etiology* / Q000503:physiopathology*
chemical_list: D015415:Biomarkers; D009211:Myoglobin; D010446:Peptide Fragments; D019210:Troponin I; D020107:Troponin T; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form