Smoking status and outcome after primary coronary angioplasty for acute myocardial infarction

D. Hasdai, Amir Lerman, Charanjit Rihal, D. A. Criger, K. N. Garratt, A. Betriu, H. D. White, E. J. Topol, C. B. Granger, S. G. Ellis, R. M. Califf, David Holmes

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Background: Because of the increased propensity of intracoronary thrombi to form in cigarette smokers, percutaneous transluminal angioplasty (PTCA) for acute myocardial infarction (AMI) may be less effective in smokers. We sought to determine the impact of smoking status on outcome after PTCA for AMI. Methods Patients: enrolled in the GUSTO IIb Angioplasty Substudy were randomly assigned to receive PTCA or tissue-plasminogen activator (tPA) for AMI. The interaction of smoking status (nonsmokers = 344, former smokers = 294, current smokers = 490) and treatment strategy with the occurrence of death, nonfatal reinfarction, or nonfatal, disabling stroke at 30 days was analyzed. Procedural success (residual stenosis <50% and Thrombolysis in Myocardial Infarction [TIMI] flow grade 3) was also analyzed for patients who underwent PTCA (n = 444). Results: Among patients who underwent PTCA, nonsmokers had worse percent stenosis of the culprit lesion before reperfusion (P = .03) and more often had TIMI flow grade 0 (P < .05). Procedural success was more common in smokers (65.6%) than in former smokers (53.3%) and nonsmokers (52.4%; P = .02), reflecting a higher rate of postprocedure TIMI 3 flow. PTCA was associated with a better 30-day outcome than tPA for current smokers (odds ratio [95% confidence interval] = 0.41 [0.19 to 0.88]), with a similar trend for former smokers (0.73 [0.34 to 1.58]) and nonsmokers (0.77 [0.42 to 1.40]). At 6 months, smokers randomly assigned to PTCA also had fewer deaths and reinfarction (0.58 [0.31 to 1.07]). Conclusions: Although smoking status affects angiographic variables before and after PTCA for AMI, PTCA is associated with a better 30-day outcome than tPA regardless of smoking status and should be considered when readily available.

Original languageEnglish (US)
Pages (from-to)612-620
Number of pages9
JournalAmerican Heart Journal
Volume137
Issue number4 I
StatePublished - 1999

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Angioplasty
Smoking
Myocardial Infarction
Tissue Plasminogen Activator
Pathologic Constriction
Tobacco Products
Reperfusion
Thrombosis
Stroke
Odds Ratio
Confidence Intervals

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Hasdai, D., Lerman, A., Rihal, C., Criger, D. A., Garratt, K. N., Betriu, A., ... Holmes, D. (1999). Smoking status and outcome after primary coronary angioplasty for acute myocardial infarction. American Heart Journal, 137(4 I), 612-620.

Smoking status and outcome after primary coronary angioplasty for acute myocardial infarction. / Hasdai, D.; Lerman, Amir; Rihal, Charanjit; Criger, D. A.; Garratt, K. N.; Betriu, A.; White, H. D.; Topol, E. J.; Granger, C. B.; Ellis, S. G.; Califf, R. M.; Holmes, David.

In: American Heart Journal, Vol. 137, No. 4 I, 1999, p. 612-620.

Research output: Contribution to journalArticle

Hasdai, D, Lerman, A, Rihal, C, Criger, DA, Garratt, KN, Betriu, A, White, HD, Topol, EJ, Granger, CB, Ellis, SG, Califf, RM & Holmes, D 1999, 'Smoking status and outcome after primary coronary angioplasty for acute myocardial infarction', American Heart Journal, vol. 137, no. 4 I, pp. 612-620.
Hasdai D, Lerman A, Rihal C, Criger DA, Garratt KN, Betriu A et al. Smoking status and outcome after primary coronary angioplasty for acute myocardial infarction. American Heart Journal. 1999;137(4 I):612-620.
Hasdai, D. ; Lerman, Amir ; Rihal, Charanjit ; Criger, D. A. ; Garratt, K. N. ; Betriu, A. ; White, H. D. ; Topol, E. J. ; Granger, C. B. ; Ellis, S. G. ; Califf, R. M. ; Holmes, David. / Smoking status and outcome after primary coronary angioplasty for acute myocardial infarction. In: American Heart Journal. 1999 ; Vol. 137, No. 4 I. pp. 612-620.
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abstract = "Background: Because of the increased propensity of intracoronary thrombi to form in cigarette smokers, percutaneous transluminal angioplasty (PTCA) for acute myocardial infarction (AMI) may be less effective in smokers. We sought to determine the impact of smoking status on outcome after PTCA for AMI. Methods Patients: enrolled in the GUSTO IIb Angioplasty Substudy were randomly assigned to receive PTCA or tissue-plasminogen activator (tPA) for AMI. The interaction of smoking status (nonsmokers = 344, former smokers = 294, current smokers = 490) and treatment strategy with the occurrence of death, nonfatal reinfarction, or nonfatal, disabling stroke at 30 days was analyzed. Procedural success (residual stenosis <50{\%} and Thrombolysis in Myocardial Infarction [TIMI] flow grade 3) was also analyzed for patients who underwent PTCA (n = 444). Results: Among patients who underwent PTCA, nonsmokers had worse percent stenosis of the culprit lesion before reperfusion (P = .03) and more often had TIMI flow grade 0 (P < .05). Procedural success was more common in smokers (65.6{\%}) than in former smokers (53.3{\%}) and nonsmokers (52.4{\%}; P = .02), reflecting a higher rate of postprocedure TIMI 3 flow. PTCA was associated with a better 30-day outcome than tPA for current smokers (odds ratio [95{\%} confidence interval] = 0.41 [0.19 to 0.88]), with a similar trend for former smokers (0.73 [0.34 to 1.58]) and nonsmokers (0.77 [0.42 to 1.40]). At 6 months, smokers randomly assigned to PTCA also had fewer deaths and reinfarction (0.58 [0.31 to 1.07]). Conclusions: Although smoking status affects angiographic variables before and after PTCA for AMI, PTCA is associated with a better 30-day outcome than tPA regardless of smoking status and should be considered when readily available.",
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T1 - Smoking status and outcome after primary coronary angioplasty for acute myocardial infarction

AU - Hasdai, D.

AU - Lerman, Amir

AU - Rihal, Charanjit

AU - Criger, D. A.

AU - Garratt, K. N.

AU - Betriu, A.

AU - White, H. D.

AU - Topol, E. J.

AU - Granger, C. B.

AU - Ellis, S. G.

AU - Califf, R. M.

AU - Holmes, David

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N2 - Background: Because of the increased propensity of intracoronary thrombi to form in cigarette smokers, percutaneous transluminal angioplasty (PTCA) for acute myocardial infarction (AMI) may be less effective in smokers. We sought to determine the impact of smoking status on outcome after PTCA for AMI. Methods Patients: enrolled in the GUSTO IIb Angioplasty Substudy were randomly assigned to receive PTCA or tissue-plasminogen activator (tPA) for AMI. The interaction of smoking status (nonsmokers = 344, former smokers = 294, current smokers = 490) and treatment strategy with the occurrence of death, nonfatal reinfarction, or nonfatal, disabling stroke at 30 days was analyzed. Procedural success (residual stenosis <50% and Thrombolysis in Myocardial Infarction [TIMI] flow grade 3) was also analyzed for patients who underwent PTCA (n = 444). Results: Among patients who underwent PTCA, nonsmokers had worse percent stenosis of the culprit lesion before reperfusion (P = .03) and more often had TIMI flow grade 0 (P < .05). Procedural success was more common in smokers (65.6%) than in former smokers (53.3%) and nonsmokers (52.4%; P = .02), reflecting a higher rate of postprocedure TIMI 3 flow. PTCA was associated with a better 30-day outcome than tPA for current smokers (odds ratio [95% confidence interval] = 0.41 [0.19 to 0.88]), with a similar trend for former smokers (0.73 [0.34 to 1.58]) and nonsmokers (0.77 [0.42 to 1.40]). At 6 months, smokers randomly assigned to PTCA also had fewer deaths and reinfarction (0.58 [0.31 to 1.07]). Conclusions: Although smoking status affects angiographic variables before and after PTCA for AMI, PTCA is associated with a better 30-day outcome than tPA regardless of smoking status and should be considered when readily available.

AB - Background: Because of the increased propensity of intracoronary thrombi to form in cigarette smokers, percutaneous transluminal angioplasty (PTCA) for acute myocardial infarction (AMI) may be less effective in smokers. We sought to determine the impact of smoking status on outcome after PTCA for AMI. Methods Patients: enrolled in the GUSTO IIb Angioplasty Substudy were randomly assigned to receive PTCA or tissue-plasminogen activator (tPA) for AMI. The interaction of smoking status (nonsmokers = 344, former smokers = 294, current smokers = 490) and treatment strategy with the occurrence of death, nonfatal reinfarction, or nonfatal, disabling stroke at 30 days was analyzed. Procedural success (residual stenosis <50% and Thrombolysis in Myocardial Infarction [TIMI] flow grade 3) was also analyzed for patients who underwent PTCA (n = 444). Results: Among patients who underwent PTCA, nonsmokers had worse percent stenosis of the culprit lesion before reperfusion (P = .03) and more often had TIMI flow grade 0 (P < .05). Procedural success was more common in smokers (65.6%) than in former smokers (53.3%) and nonsmokers (52.4%; P = .02), reflecting a higher rate of postprocedure TIMI 3 flow. PTCA was associated with a better 30-day outcome than tPA for current smokers (odds ratio [95% confidence interval] = 0.41 [0.19 to 0.88]), with a similar trend for former smokers (0.73 [0.34 to 1.58]) and nonsmokers (0.77 [0.42 to 1.40]). At 6 months, smokers randomly assigned to PTCA also had fewer deaths and reinfarction (0.58 [0.31 to 1.07]). Conclusions: Although smoking status affects angiographic variables before and after PTCA for AMI, PTCA is associated with a better 30-day outcome than tPA regardless of smoking status and should be considered when readily available.

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