title: Non-uniform recovery of left ventricular transmural mechanics in ST-segment elevation myocardial infarction.
abstract: BACKGROUND
  After a transient ischemic episode, the subendocardial region is more severely injured than outer subepicardial layers and may regain a proportionately greater degree of mechanical function in the longitudinal direction. We sought to explore left ventricular (LV) transmural mechanics in patients with ST-segment elevation myocardial infarction (STEMI) for determining the mechanism underlying recovery of global LV function after primary percutaneous coronary intervention (PCI).
  
  
  METHODS
  A total of 42 patients (62 +/- 11 years old, 71% male) with a first STEMI underwent serial assessments of LV longitudinal, circumferential and radial strains (LS, CS and RS) by selective tracking of subendocardial and subepicardial regions within 48 hours and a median of 5 months after PCI. LV mechanical parameters were compared with sixteen age and gender matched normal controls.
  
  
  RESULTS
  In comparison with controls, endocardial and epicardial LS were markedly attenuated at 48 hours following PCI (P < 0.001). An improvement in LV ejection fraction (EF > 5%) following PCI was seen in 24 (57%) patients and was associated with improvement in endocardial and epicardial LS (P < 0.001 and P = 0.003, respectively) and endocardial CS (P = 0.01). Radial strain and wall motion score index, however, remained persistently abnormal. The change in endocardial LS (OR 1.2, 95% CI 1.03 to 1.42, P = 0.01) and the change in epicardial LS (OR 1.2, 95% 1.03 to 1.46, P = 0.02) were significantly associated with the improvement in LVEF, independent of the location of STEMI and the presence of underlying multivessel disease.
  
  
  CONCLUSIONS
  In patients with STEMI treated by PCI, the recovery of LV subendocardial shortening strain seen in the longitudinal direction underlies the improvement in LV global function despite persistent abnormalities in radial mechanics and wall motion score index.
authors.affiliation: Division of Cardiovascular Diseases, Mayo Clinic Arizona 13400 East Shea Blvd, Scottsdale, AZ 85259, USA.
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Caracciolo
authors.forename: Mackram F
authors.initials: MF
authors.lastname: Eleid
authors.forename: Haruhiko
authors.initials: H
authors.lastname: Abe
authors.forename: Nisha
authors.initials: N
authors.lastname: Bhatia
authors.forename: F David
authors.initials: FD
authors.lastname: Fortuin
authors.forename: Susan
authors.initials: S
authors.lastname: Wilansky
authors.forename: Scipione
authors.initials: S
authors.lastname: Carerj
authors.forename: Partho P
authors.initials: PP
authors.lastname: Sengupta
mesh_terms: D004452:Echocardiography / Q000379:methods*; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology; D011379:Prognosis; D012372:ROC Curve; D020127:Recovery of Function; D012189:Retrospective Studies; D013318:Stroke Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology*