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. OBJECTIVES AND METHODS: 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). CONCLUSION: 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.
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. OBJECTIVES AND METHODS: 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). CONCLUSION: 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.
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Authors: J A Ambrose; M A Tannenbaum; D Alexopoulos; C E Hjemdahl-Monsen; J Leavy; M Weiss; S Borrico; R Gorlin; V Fuster Journal: J Am Coll Cardiol Date: 1988-07 Impact factor: 24.094
Authors: E M Antman; R P Giugliano; C M Gibson; C H McCabe; P Coussement; N S Kleiman; A Vahanian; A A Adgey; I Menown; H J Rupprecht; R Van der Wieken; J Ducas; J Scherer; K Anderson; F Van de Werf; E Braunwald Journal: Circulation Date: 1999-06-01 Impact factor: 29.690
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Authors: Robert P Giugliano; Matthew T Roe; Robert A Harrington; C Michael Gibson; Uwe Zeymer; Frans Van de Werf; Kenneth W Baran; Hans Peter Hobbach; Lynn H Woodlief; Karen L Hannan; Sally Greenberg; Joanne Miller; Michael M Kitt; John Strony; Carolyn H McCabe; Eugene Braunwald; Robert M Califf Journal: J Am Coll Cardiol Date: 2003-04-16 Impact factor: 24.094
Authors: E M Antman; C M Gibson; J A de Lemos; R P Giugliano; C H McCabe; P Coussement; I Menown; C A Nienaber; T C Rehders; M J Frey; R Van der Wieken; D Andresen; J Scherer; K Anderson; F Van de Werf; E Braunwald Journal: Eur Heart J Date: 2000-12 Impact factor: 29.983
Authors: W C Little; M Constantinescu; R J Applegate; M A Kutcher; M T Burrows; F R Kahl; W P Santamore Journal: Circulation Date: 1988-11 Impact factor: 29.690
Authors: Stefan B Puchner; Maros Ferencik; Mihaly Karolyi; Synho Do; Pal Maurovich-Horvat; Hans-Ulrich Kauczor; Udo Hoffmann; Christopher L Schlett Journal: Int J Cardiovasc Imaging Date: 2013-08-30 Impact factor: 2.357
Authors: F Cademartiri; L La Grutta; R Malagò; F Alberghina; A Palumbo; M Belgrano; E Maffei; A Aldrovandi; F Pugliese; G Runza; A Weustink; W Bob Meeijboom; N R Mollet; M Midiri Journal: Radiol Med Date: 2009-04-15 Impact factor: 3.469
Authors: Aiden Jc O'Loughlin; Karen Byth; John K French; David Ab Richards; Annemarie Hennessy; A Robert Denniss; Pramesh Kovoor Journal: BMC Res Notes Date: 2011-03-07