title: Distance from the coronary ostium to the culprit lesion in acute ST-elevation myocardial infarction and its implications regarding the potential prevention of proximal plaque rupture.
abstract: BACKGROUND
  Shorter distances from the coronary ostia to culprit lesions have been associated with a higher incidence of adverse outcomes in ST elevation acute myocardial infarction (STEMI). As drug-eluting stents are associated with low rates of restenosis and formation of a stable intima, we sought to develop a mathematical model to estimate how far down the coronary artery a drug-eluting stent would have to be placed to theoretically mitigate the risk of proximal plaque rupture.
  
  
  OBJECTIVE
  Distances from the ostia to the end of the culprit lesions were planimetered in 1,914 patients from the TIMI 14, INTEGRITI, FASTER and ENTIRE/TIMI 23 trials.
  
  
  RESULTS
  The first 60 mm of the coronary artery contained 75% of STEMI culprit lesions. The median distance from the vessel ostium to the end of the culprit lesion was 43 mm (mean 50 +/- 34) and the relative distance from the vessel ostium to the end of the lesion was 29% (mean 33 +/- 17%) of the total culprit artery length. Diabetes was the only baseline clinical characteristic associated with a longer absolute distance to the end of the culprit lesion (46 mm vs. 43 mm, p = 0.03) as well as relative to total artery length (31% vs. 29%, p = 0.04). Median distances from the artery ostium to the end of the culprit lesion were shortest among the left anterior descending culprits (40 mm), followed by circumflex lesions (43 mm) and then right coronary artery lesions (47 mm, 3-way p < 0.0001).
  
  
  CONCLUSIONS
  The majority of culprit lesions in STEMI are contained within the proximal 30% of the major epicardial coronary arteries, but the distance varies depending upon which epicardial artery is involved. Cumulative distribution functions are presented to allow estimation of the percent of culprit lesions lying proximal to any given distance from the ostium to model the feasibility of prophylactic drug-eluting stenting to minimize the risk of subsequent proximal plaque rupture.
authors.affiliation: TIMI Study Group, Department of Medicine, Brigham & Women's Hospital and Harvard Medical School, 350 Longwood Avenue, Boston, MA 02115, USA. mgibson@perfuse.org
authors.forename: C Michael
authors.initials: CM
authors.lastname: Gibson
authors.forename: Ajay J
authors.initials: AJ
authors.lastname: Kirtane
authors.forename: Sabina A
authors.initials: SA
authors.lastname: Murphy
authors.forename: Juhana
authors.initials: J
authors.lastname: Karha
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Cannon
authors.forename: Robert P
authors.initials: RP
authors.lastname: Giugliano
authors.forename: Mathew T
authors.initials: MT
authors.lastname: Roe
authors.forename: Robert A
authors.initials: RA
authors.lastname: Harrington
authors.forename: E Magnus
authors.initials: EM
authors.lastname: Ohman
authors.forename: Elliott M
authors.initials: EM
authors.lastname: Antman
mesh_terms: D000368:Aged; D016503:Drug Delivery Systems; D004562:Electrocardiography; D004867:Equipment Design; D005260:Female; D006342:Heart Rupture, Post-Infarction / Q000517:prevention & control*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology* / Q000628:therapy*; D015607:Stents