title: Predictive value of the index of microcirculatory resistance in patients with ST-segment elevation myocardial infarction.
abstract: OBJECTIVE
  The objective of this study is to evaluate the predictive value of the index of microcirculatory resistance (IMR) in patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI).
  
  
  BACKGROUND
  Despite adequate epicardial artery reperfusion, a number of patients with STEMI have a poor prognosis because of microvascular damage. Assessing the status of the microvasculature in this setting remains challenging.
  
  
  METHODS
  In 29 patients after primary PCI for STEMI, IMR was measured with a pressure sensor/thermistor-tipped guidewire. The Thrombolysis In Myocardial Infarction (TIMI) myocardial perfusion grade, TIMI frame count, coronary flow reserve, and ST-segment resolution were also recorded.
  
  
  RESULTS
  The IMR correlated significantly with the peak creatinine kinase (CK) (R = 0.61, p = 0.0005) while the other measures of microvascular dysfunction did not. In patients with an IMR greater than the median value of 32 U, the peak CK was significantly higher compared with those having values <or=32 U (3,128 +/- 1,634 ng/ml vs. 1,201 +/- 911 ng/ml, p = 0.002). The IMR correlated significantly with 3-month echocardiographic wall motion score (WMS) (R = 0.59, p = 0.002) while the other measures of microvascular function did not. The WMS at 3-month follow-up was significantly worse in the group with an IMR >32 U compared with <or=32 U (28 +/- 7 vs. 20 +/- 4, p = 0.001). On multivariate analysis, IMR was the strongest predictor of peak CK and 3-month WMS. The IMR was the only significant predictor of recovery of left ventricular function on the basis of the percent change in WMS (R = 0.50, p < 0.01).
  
  
  CONCLUSIONS
  Compared to standard measures, IMR appears to be a better predictor of microvascular damage after STEMI, both acutely and in short term follow-up.
authors.affiliation: Division of Cardiovascular Medicine, Stanford University Medical Center, Stanford, California 94305, USA. wfearon@stanford.edu
authors.forename: William F
authors.initials: WF
authors.lastname: Fearon
authors.forename: Maulik
authors.initials: M
authors.lastname: Shah
authors.forename: Martin
authors.initials: M
authors.lastname: Ng
authors.forename: Todd
authors.initials: T
authors.lastname: Brinton
authors.forename: Andrew
authors.initials: A
authors.lastname: Wilson
authors.forename: Jennifer A
authors.initials: JA
authors.lastname: Tremmel
authors.forename: Ingela
authors.initials: I
authors.lastname: Schnittger
authors.forename: David P
authors.initials: DP
authors.lastname: Lee
authors.forename: Randall H
authors.initials: RH
authors.lastname: Vagelos
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Fitzgerald
authors.forename: Paul G
authors.initials: PG
authors.lastname: Yock
authors.forename: Alan C
authors.initials: AC
authors.lastname: Yeung
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D003326:Coronary Circulation / Q000502:physiology*; D003402:Creatine Kinase / Q000378:metabolism; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008833:Microcirculation / Q000502:physiology; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology* / Q000628:therapy; D009206:Myocardium / Q000473:pathology; D011379:Prognosis; D014655:Vascular Resistance; D016277:Ventricular Function, Left
chemical_list: D003402:Creatine Kinase