EFFECT OF CIGARETTE-SMOKING ON CORONARY PATENCY AFTER THROMBOLYTIC THERAPY FOR MYOCARDIAL-INFARCTION

Citation
Ma. Gomez et al., EFFECT OF CIGARETTE-SMOKING ON CORONARY PATENCY AFTER THROMBOLYTIC THERAPY FOR MYOCARDIAL-INFARCTION, The American journal of cardiology, 72(5), 1993, pp. 373-378
Citations number
25
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
00029149
Volume
72
Issue
5
Year of publication
1993
Pages
373 - 378
Database
ISI
SICI code
0002-9149(1993)72:5<373:EOCOCP>2.0.ZU;2-M
Abstract
Smokers have been reported to have an improved short-term prognosis af ter myocardial infarction when compared with nonsmokers. This study ex amines the effect of smoking status on infarct-related artery patency, a determinant of outcome, following thrombolytic therapy for acute my ocardial infarction (AMI). To evaluate patency outcome by smoking stat us, the database of the Second Thrombolytic Trial of Eminase in Acute Myocardial Infarction was reviewed, and baseline characteristics were compared with infarct-related artery patency early (90 to 240 minutes) after thrombolysis in smokers versus nonsmokers. Smokers were younger (mean age 53 vs 59 years, p = 0.0001), more likely to be men (86 vs 7 3%, p = 0.008), normotensive (74 vs 58%, p = 0.004), to have an inferi or infarction (66 vs 51%, p = 0.007), and tended to have higher hemato crits and fibrinogen levels than nonsmokers. Smokers had a significant ly greater chance of achieving complete perfusion (Thrombolysis in Myo cardial Infarction trial grade 3) (66 vs 51% p = 0.007) than nonsmoker s, although the combination of grades 2 and 3 did not differ. After co rrecting for imbalances in baseline and angiographic variables multiva riate logistic regression identified smoking (odds ratio 1.8, p = 0.01 ) and infarct location (odds ratio 1.7, p = 0.03) as independent predi ctors of achieving grade 3 flow. The independent predictive component of smoking for achieving grade 3 patency after thrombolysis suggests t he hypothesis that more active thrombogenic mechanisms may be operativ e in smokers, leading to a larger thrombus component that is more susc eptible to lytic therapy.