Effect of cigarette smoking on outcome after thrombolytic therapy for myocardial infarction

Smoking is known to be a strong risk factor for premature atherosclerosis, myocardial infarction, and sudden cardiac death. Unexpectedly, in the reperfusion era, investigators have reported that patients who smoke have a more favorable prognosis after thrombolysis compared with non-smokers. Since sm...

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Veröffentlicht in:Circulation (New York, N.Y.) N.Y.), 1995-01, Vol.91 (2), p.298-303
Hauptverfasser: GRINES, C. L, TOPOL, E. J, O'NEILL, W. W, GEORGE, B. S, KEREIAKES, D, PHILLIPS, H. R, LEIMBERGER, J. D, WOODLIEF, L. H, CALIFF, R. M
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container_issue 2
container_start_page 298
container_title Circulation (New York, N.Y.)
container_volume 91
creator GRINES, C. L
TOPOL, E. J
O'NEILL, W. W
GEORGE, B. S
KEREIAKES, D
PHILLIPS, H. R
LEIMBERGER, J. D
WOODLIEF, L. H
CALIFF, R. M
description Smoking is known to be a strong risk factor for premature atherosclerosis, myocardial infarction, and sudden cardiac death. Unexpectedly, in the reperfusion era, investigators have reported that patients who smoke have a more favorable prognosis after thrombolysis compared with non-smokers. Since smoking is associated with a relatively hyper-coagulable state, we hypothesized that the coronary occlusion responsible for infarction may be primarily thrombotic, with improved outcome relating to enhanced patency or the absence of a residual stenosis after thrombolytic therapy. To examine this issue, we evaluated 1619 patients treated with TPA, urokinase, or both in six consecutive myocardial infarction trials, of whom 878 (54%) were currently smoking. Patients underwent 90-minute and predischarge catheterizations, which were quantified blinded to the patients' smoking status. As expected, baseline fibrinogen (2.8 [2.5,3.6] versus 2.7 [2.4,3.5] g/dL, P = .003) and hematocrit (44% [41%, 47%] versus 43% [40%, 45%], P = .0001) levels were greater in smokers. Although there were no differences between smokers and nonsmokers with regard to 90-minute patency (73% versus 74%), smokers were more likely to have TIMI-3 flow (41.1% versus 34.6%, P = .034), with a larger minimum lumen diameter of the infarct stenosis both acutely (0.82 [0.51, 1.11] versus 0.72 [0.43, 1.04] mm, P = .0432) and at follow-up (1.2 [0.8, 1.74] versus 1.0 [0.7, 1.5], P = .002). Although smokers tended to have reduced in-hospital mortality compared with nonsmokers in univariate analysis (4.0% versus 8.9%, P = .0001), after adjustment for baseline differences between smokers and nonsmokers in age (54 [47, 62] versus 60 [54, 68] years, P < .0001), inferior infarct location (60% versus 53%, P < .0001), three-vessel disease (16% versus 22%, P < .001), and baseline ejection fraction (53% [44%, 60%] versus 50% [42%, 58%], P = .0069), smoking history was of no independent prognostic significance. Therefore, smokers have a relatively hypercoagulable state, documented by increased hematocrit and fibrinogen levels. Quantitative coronary angiographic analysis suggests that the mechanism of infarction in smokers is more often thrombosis of a less critical atherosclerotic lesion compared with nonsmokers. Enhanced perfusion status, as well as favorable baseline clinical and angiographic characteristics, may be responsible for the more benign prognosis of current smokers.
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L ; TOPOL, E. J ; O'NEILL, W. W ; GEORGE, B. S ; KEREIAKES, D ; PHILLIPS, H. R ; LEIMBERGER, J. D ; WOODLIEF, L. H ; CALIFF, R. M</creator><creatorcontrib>GRINES, C. L ; TOPOL, E. J ; O'NEILL, W. W ; GEORGE, B. S ; KEREIAKES, D ; PHILLIPS, H. R ; LEIMBERGER, J. D ; WOODLIEF, L. H ; CALIFF, R. M</creatorcontrib><description>Smoking is known to be a strong risk factor for premature atherosclerosis, myocardial infarction, and sudden cardiac death. Unexpectedly, in the reperfusion era, investigators have reported that patients who smoke have a more favorable prognosis after thrombolysis compared with non-smokers. Since smoking is associated with a relatively hyper-coagulable state, we hypothesized that the coronary occlusion responsible for infarction may be primarily thrombotic, with improved outcome relating to enhanced patency or the absence of a residual stenosis after thrombolytic therapy. To examine this issue, we evaluated 1619 patients treated with TPA, urokinase, or both in six consecutive myocardial infarction trials, of whom 878 (54%) were currently smoking. Patients underwent 90-minute and predischarge catheterizations, which were quantified blinded to the patients' smoking status. As expected, baseline fibrinogen (2.8 [2.5,3.6] versus 2.7 [2.4,3.5] g/dL, P = .003) and hematocrit (44% [41%, 47%] versus 43% [40%, 45%], P = .0001) levels were greater in smokers. Although there were no differences between smokers and nonsmokers with regard to 90-minute patency (73% versus 74%), smokers were more likely to have TIMI-3 flow (41.1% versus 34.6%, P = .034), with a larger minimum lumen diameter of the infarct stenosis both acutely (0.82 [0.51, 1.11] versus 0.72 [0.43, 1.04] mm, P = .0432) and at follow-up (1.2 [0.8, 1.74] versus 1.0 [0.7, 1.5], P = .002). 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Jan 15, 1995</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c524t-e9e3d4d1f70511913aa2d873ac4b432cc09357ab317d2f40d72971f4a294cc523</citedby><cites>FETCH-LOGICAL-c524t-e9e3d4d1f70511913aa2d873ac4b432cc09357ab317d2f40d72971f4a294cc523</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3688,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=3397972$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7805231$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GRINES, C. L</creatorcontrib><creatorcontrib>TOPOL, E. J</creatorcontrib><creatorcontrib>O'NEILL, W. W</creatorcontrib><creatorcontrib>GEORGE, B. S</creatorcontrib><creatorcontrib>KEREIAKES, D</creatorcontrib><creatorcontrib>PHILLIPS, H. R</creatorcontrib><creatorcontrib>LEIMBERGER, J. D</creatorcontrib><creatorcontrib>WOODLIEF, L. H</creatorcontrib><creatorcontrib>CALIFF, R. M</creatorcontrib><title>Effect of cigarette smoking on outcome after thrombolytic therapy for myocardial infarction</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Smoking is known to be a strong risk factor for premature atherosclerosis, myocardial infarction, and sudden cardiac death. Unexpectedly, in the reperfusion era, investigators have reported that patients who smoke have a more favorable prognosis after thrombolysis compared with non-smokers. Since smoking is associated with a relatively hyper-coagulable state, we hypothesized that the coronary occlusion responsible for infarction may be primarily thrombotic, with improved outcome relating to enhanced patency or the absence of a residual stenosis after thrombolytic therapy. To examine this issue, we evaluated 1619 patients treated with TPA, urokinase, or both in six consecutive myocardial infarction trials, of whom 878 (54%) were currently smoking. Patients underwent 90-minute and predischarge catheterizations, which were quantified blinded to the patients' smoking status. As expected, baseline fibrinogen (2.8 [2.5,3.6] versus 2.7 [2.4,3.5] g/dL, P = .003) and hematocrit (44% [41%, 47%] versus 43% [40%, 45%], P = .0001) levels were greater in smokers. 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Therefore, smokers have a relatively hypercoagulable state, documented by increased hematocrit and fibrinogen levels. Quantitative coronary angiographic analysis suggests that the mechanism of infarction in smokers is more often thrombosis of a less critical atherosclerotic lesion compared with nonsmokers. Enhanced perfusion status, as well as favorable baseline clinical and angiographic characteristics, may be responsible for the more benign prognosis of current smokers.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Coronary Angiography</subject><subject>Coronary heart disease</subject><subject>Heart</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Smoking</subject><subject>Thrombolytic Therapy</subject><subject>Treatment Outcome</subject><subject>Vascular Patency</subject><subject>Ventricular Function, Left</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkEFLJDEQhcOyouPsnj0JYZG9dZtK0pPJUQbdFYQF0dMeQk06ceN2d8YkfZh_b8TBg6fiUV-9ejxCzoC1ACu4ZNDakFoNLW-5Xn8hC-i4bGQn9FeyYIzpRgnOT8hpzs9VroTqjsmxWrOOC1iQv9feO1to9NSGJ0yuFEfzGP-H6YnGica52Dg6ir64RMu_FMdtHPYl2Cpcwt2e-pjouI8WUx9woGHymGwJcfpGjjwO2X0_zCV5vLl-2Pxu7v78ut1c3TW2Ri2N0070sgevWAegQSDyfq0EWrmVglvLtOgUbgWonnvJesW1Ai-Ra2mrhViSn---uxRfZpeLGUO2bhhwcnHORimmGe_WFfzxCXyOc5pqNsOBr4SW9fuSXL5DNsWck_Nml8KIaW-AmbfODQOzub03Ggw3tfN6cX6wnbej6z_4Q8l1f3HYY7Y4-ISTDfkDE0Irrbh4BUp0iZk</recordid><startdate>19950115</startdate><enddate>19950115</enddate><creator>GRINES, C. 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J</au><au>O'NEILL, W. W</au><au>GEORGE, B. S</au><au>KEREIAKES, D</au><au>PHILLIPS, H. R</au><au>LEIMBERGER, J. D</au><au>WOODLIEF, L. H</au><au>CALIFF, R. M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of cigarette smoking on outcome after thrombolytic therapy for myocardial infarction</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1995-01-15</date><risdate>1995</risdate><volume>91</volume><issue>2</issue><spage>298</spage><epage>303</epage><pages>298-303</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Smoking is known to be a strong risk factor for premature atherosclerosis, myocardial infarction, and sudden cardiac death. Unexpectedly, in the reperfusion era, investigators have reported that patients who smoke have a more favorable prognosis after thrombolysis compared with non-smokers. Since smoking is associated with a relatively hyper-coagulable state, we hypothesized that the coronary occlusion responsible for infarction may be primarily thrombotic, with improved outcome relating to enhanced patency or the absence of a residual stenosis after thrombolytic therapy. To examine this issue, we evaluated 1619 patients treated with TPA, urokinase, or both in six consecutive myocardial infarction trials, of whom 878 (54%) were currently smoking. Patients underwent 90-minute and predischarge catheterizations, which were quantified blinded to the patients' smoking status. As expected, baseline fibrinogen (2.8 [2.5,3.6] versus 2.7 [2.4,3.5] g/dL, P = .003) and hematocrit (44% [41%, 47%] versus 43% [40%, 45%], P = .0001) levels were greater in smokers. Although there were no differences between smokers and nonsmokers with regard to 90-minute patency (73% versus 74%), smokers were more likely to have TIMI-3 flow (41.1% versus 34.6%, P = .034), with a larger minimum lumen diameter of the infarct stenosis both acutely (0.82 [0.51, 1.11] versus 0.72 [0.43, 1.04] mm, P = .0432) and at follow-up (1.2 [0.8, 1.74] versus 1.0 [0.7, 1.5], P = .002). Although smokers tended to have reduced in-hospital mortality compared with nonsmokers in univariate analysis (4.0% versus 8.9%, P = .0001), after adjustment for baseline differences between smokers and nonsmokers in age (54 [47, 62] versus 60 [54, 68] years, P &lt; .0001), inferior infarct location (60% versus 53%, P &lt; .0001), three-vessel disease (16% versus 22%, P &lt; .001), and baseline ejection fraction (53% [44%, 60%] versus 50% [42%, 58%], P = .0069), smoking history was of no independent prognostic significance. Therefore, smokers have a relatively hypercoagulable state, documented by increased hematocrit and fibrinogen levels. Quantitative coronary angiographic analysis suggests that the mechanism of infarction in smokers is more often thrombosis of a less critical atherosclerotic lesion compared with nonsmokers. Enhanced perfusion status, as well as favorable baseline clinical and angiographic characteristics, may be responsible for the more benign prognosis of current smokers.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams &amp; Wilkins</pub><pmid>7805231</pmid><doi>10.1161/01.cir.91.2.298</doi><tpages>6</tpages></addata></record>
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source MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals
subjects Adolescent
Adult
Aged
Biological and medical sciences
Cardiology. Vascular system
Coronary Angiography
Coronary heart disease
Heart
Humans
Medical sciences
Middle Aged
Myocardial Infarction - drug therapy
Smoking
Thrombolytic Therapy
Treatment Outcome
Vascular Patency
Ventricular Function, Left
title Effect of cigarette smoking on outcome after thrombolytic therapy for myocardial infarction
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