title: Left ventricular remodeling and systolic deterioration in acute myocardial infarction: findings from the Stent-PAMI Study.
abstract: BACKGROUND
  Left ventricular systolic deterioration (LVSD) develops in some patients despite successful percutaneous intervention and medical therapy for myocardial infarction (MI). We sought to determine predictors of LVSD by comparing demographic, procedural, angiographic variables, and 6-month major adverse cardiac events (MACE) in patients with and without LVSD after MI.
  
  
  METHODS
  We performed a posthoc analysis of patients prospectively enrolled in the Stent-PAMI trial if they had successful percutaneous intervention for MI (<50% residual stenosis and TIMI-3 grade flow), normal left ventricular systolic function on index ventriculogram, and protocol driven coronary angiography with ventriculography at 6 months. We defined LVSD as an absolute decrease in ejection fraction > or =15% compared to baseline value.
  
  
  RESULTS
  Of the 900 patients enrolled in Stent-PAMI, 187 patients met the inclusion criteria. LVSD developed in 30 patients (16%) and occurred independent of demographic, procedural, angiographic variables, and 6-month MACE. Multivariate predictors of LVSD were higher baseline ejection fraction (P = 0.0065, OR 1.09; 95% CI = 1.02-1.16) and peak creatine phosphokinase (CPK) level (P = 0.0022, OR 1.04; 95% CI = 1.02-1.07).
  
  
  CONCLUSIONS
  LVSD occurs in a minority of patients despite successful mechanical reperfusion and occurred independent of procedural, angiographic variables, target vessel revascularization, reinfarction, and combined MACE. Infarct size (determined by peak CPK) and high baseline ejection fraction predicted development of LVSD at 6 months. LVSD in this population likely occurred by negative left ventricular remodeling.
authors.affiliation: William Beaumont Hospital, Royal Oak, MI 48073, USA. smattichak@beaumont.edu
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Mattichak
authors.forename: Kishore J
authors.initials: KJ
authors.lastname: Harjai
authors.forename: Jacob R
authors.initials: JR
authors.lastname: Dutcher
authors.forename: Judith A
authors.initials: JA
authors.lastname: Boura
authors.forename: Gregg
authors.initials: G
authors.lastname: Stone
authors.forename: David
authors.initials: D
authors.lastname: Cox
authors.forename: Bruce R
authors.initials: BR
authors.lastname: Brodie
authors.forename: William W
authors.initials: WW
authors.lastname: O'Neill
authors.forename: Cindy L
authors.initials: CL
authors.lastname: Grines
mesh_terms: D003402:Creatine Kinase / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology* / Q000628:therapy; D011446:Prospective Studies; D016032:Randomized Controlled Trials as Topic; D013318:Stroke Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D003402:Creatine Kinase