TY - JOUR
T1 - Cigarette smoking status and outcome among patients with acute coronary syndromes without persistent ST-segment elevation
T2 - Effect of inhibition of platelet glycoprotein IIb/IIIa with eptifibatide
AU - Hasdai, David
AU - Holmes, David R.
AU - Criger, Douglas A.
AU - Topol, Eric J.
AU - Califf, Robert M.
AU - Wilcox, Robert G.
AU - Paolasso, Ernesto
AU - Simoons, Maarten
AU - Deckers, Jaap
AU - Harrington, Robert A.
N1 - Funding Information:
From the Qeportment of Cardiology, Robm Medical Center, Petoh likvo; bAdult Cotheterwation Lob, Moyo Clime, Rochester; <Duke Clmical Research Inrhtute, Durham; Qepartment of Cordlology, Clevelond Clime Foundotlon; l Cord,ovosculor Medune, Queen’s Meo’~col Centre, Noninghom; ‘Ertudlos Cordiologxos Lotmoamer-~co, Rosorio; and gThoroxcentre, University Hospttol Rotterdom. Supported by COR Theropeuta, Inc (South Son Fronusco, ColtfJ ond Schermg Plough Research lnstltute (Kenifworth, NJ). Guest editor for this monuscnpt was Frank V. Aguirre, MD, Prome Cordrovosculor Consultants, Springfield, III Submitted March 30, 1999; accepted August 18, 1999. Reprmt requests: Dowd R. Holmes Jr, MD, Division of Internal Medicme and Cardiovascular Diseases, Mayo Clime, 200 First St SW, Rochester, MN 55905. E-mail. holmer.dovid@mayo.edu Copyright 0 2000 by Mosby, Inc 0002-8703/2000/f 12.00 + 0 4/I/103847
PY - 2000
Y1 - 2000
N2 - Background: Studies have shown that cigarette smokers constitute a substantial proportion of patients with acute coronary syndromes (ACS) and have platelet-rich coronary thrombi. We characterized the influence of smoking status on outcome of patients with ACS without persistent ST-segment elevation and tested the hypothesis that selective inhibition of the platelet glycoprotein IIb/IIIa receptor with eptifibatide would improve outcomes among cigarette smokers. Methods: The study population included patients enrolled in the PURSUIT trial (Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy) with known smoking status presenting with ischemic chest pain ≤24 hours and having either ischemic electrocardiographic changes without persistent ST-segment elevation or elevated creatine kinase MB levels. Patients were randomly assigned to receive a bolus and infusion of either eptifibatide or placebo in addition to standard therapy. The primary end point was a composite of death or nonfatal myocardial infarction within 30 days. Results: Of the 9406 patients with known smoking status, 2677 were current smokers, 3086 were former smokers, and 3643 were nonsmokers. Cigarette smokers had better 30-day outcomes (12.3%, 16.8%, and 15.4% for smokers, former smokers, and nonsmokers, respectively; P = .001). However, after adjusting for differences in baseline clinical variables, smoking status was not a predictor of 30-day outcome (P = .45). There was a reduction in the composite end point overall with eptifibatide compared with placebo (14.3% vs 15.7%, P = .054) but no interaction between smoking status and treatment strategy (P = .68). Conclusions: Among patients with ACS without persistent ST-segment elevation, cigarette smokers had better short-term outcomes because of their more favorable clinical profile. Although prior studies have suggested that smokers more commonly have platelet-rich thrombi than nonsmokers, eptifibatide did not result in more improvement in their outcome compared with former smokers or nonsmokers.
AB - Background: Studies have shown that cigarette smokers constitute a substantial proportion of patients with acute coronary syndromes (ACS) and have platelet-rich coronary thrombi. We characterized the influence of smoking status on outcome of patients with ACS without persistent ST-segment elevation and tested the hypothesis that selective inhibition of the platelet glycoprotein IIb/IIIa receptor with eptifibatide would improve outcomes among cigarette smokers. Methods: The study population included patients enrolled in the PURSUIT trial (Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy) with known smoking status presenting with ischemic chest pain ≤24 hours and having either ischemic electrocardiographic changes without persistent ST-segment elevation or elevated creatine kinase MB levels. Patients were randomly assigned to receive a bolus and infusion of either eptifibatide or placebo in addition to standard therapy. The primary end point was a composite of death or nonfatal myocardial infarction within 30 days. Results: Of the 9406 patients with known smoking status, 2677 were current smokers, 3086 were former smokers, and 3643 were nonsmokers. Cigarette smokers had better 30-day outcomes (12.3%, 16.8%, and 15.4% for smokers, former smokers, and nonsmokers, respectively; P = .001). However, after adjusting for differences in baseline clinical variables, smoking status was not a predictor of 30-day outcome (P = .45). There was a reduction in the composite end point overall with eptifibatide compared with placebo (14.3% vs 15.7%, P = .054) but no interaction between smoking status and treatment strategy (P = .68). Conclusions: Among patients with ACS without persistent ST-segment elevation, cigarette smokers had better short-term outcomes because of their more favorable clinical profile. Although prior studies have suggested that smokers more commonly have platelet-rich thrombi than nonsmokers, eptifibatide did not result in more improvement in their outcome compared with former smokers or nonsmokers.
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U2 - 10.1016/S0002-8703(00)90089-9
DO - 10.1016/S0002-8703(00)90089-9
M3 - Article
C2 - 10689260
AN - SCOPUS:0034015678
VL - 139
SP - 454
EP - 460
JO - American Heart Journal
JF - American Heart Journal
SN - 0002-8703
IS - 3
ER -