Lower cardiac mortality in smokers following thrombolysis for acute myocardial infarction may be related to more effective fibrinolysis

Abstract

Smokers have unexplained lower cardiac mortality than non-smokers in the short term following acute myocardial infarction (AMI). We hypothesized that smokers may have enhanced systemic fibrinolysis following thrombolysis. We studied 185 consecutive patients receiving thrombolysis for first AMI. Cardiac mortality at 36 days after thrombolysis was 11.9% (22 deaths). Factors associated with cardiac mortality were: smoking (current 3.4% mortality, previous 11.4%, never 24.2%) (p < 0.001); post-thrombolysis plasma fibrinogen at 60 min (p < 0.05); diabetes (p < 0.005); age (p < 0.01); time to thrombolysis (p < 0.05); and ECG evidence of reperfusion (p < 0.05). In logistic regression analysis, smokers were at significantly lower risk of cardiac death compared with non-smokers: unadjusted odds ratio (OR) 0.3 (95% CI 0.2-0.7) (p < 0.01). This was independent of age, diabetes, ECG evidence of reperfusion and pain to treatment time: OR 0.4 (95% CI 0.3-0.9) (p < 0.05). Smoking was not an independent prognostic factor after adjustment for post-thrombolysis plasma fibrinogen OR 0.5 (95% CI 0.4-1.1) (p = 0.1), although its insignificance may be due to lack of numbers. In non-smokers, there was a subgroup with persistent ST elevation, high post-thrombolysis fibrinogen and 40% short-term mortality. No similar high-risk sub-group was observed in smokers. Smoking was associated with lower mortality in patients receiving thrombolysis for first AMI, and post-thrombolysis fibrinogen concentrations were associated with this beneficial effect. Although patient numbers are small, and the hypothesis should be tested further in a larger group, the higher likelihood of incomplete reperfusion and of incomplete fibrinolysis in non-smokers supports the hypothesis that smokers may have enhanced systemic fibrinolysis following thrombolysis in AMI.

Relation of homocysteine levels with patency and flow rate of infarct related artery in patients receiving fibrinolytic therapy

“…Actually, this finding is consistent with the data in literature (20)(21)(22). Smoking is associated with a hypercoagulable state, particularly higher fibrinogen, compared to non-smokers (23).…”

Smoking Paradox in Patients Hospitalized With Coronary Artery Disease or Acute Ischemic Stroke

“…Smoking has been associated with increased hematocrit, platelet activation and aggregation, vasoconstriction, increased circulating levels of fibrinogen, thrombin generation, impaired endogenous fibrinolytic capacity, and increased response to clopidogrel. 7,[35][36][37][38] As a result, the pathogenesis of vascular occlusions in smokers may be more because of changes in thrombogenicity than in atherosclerotic plaque rupture or morphology. This may be particularly true in those patients with fewer clinically manifest traditional atherosclerosis risk factors, whereas in nonsmokers, occlusion may be more frequently because of rupture or ulceration of atheromatous plaque with formation of platelet-rich clot.…”

“…2 However, some studies have shown that smokers with myocardial infarction (MI) or AIS have lower case fatality than nonsmokers, including subgroups that undergo treatment with thrombolysis. [3][4][5][6][7][8] This phenomenon was described as the smoker's paradox and was first introduced into scientific discourse >25 years ago. [9][10][11][12] The smoker's paradox is one of several reported paradoxes in the cardiovascular literature that include the obesity paradox and the sex paradox.…”

Effect of Smoking Status on Outcome after Acute Ischemic Stroke

“…Interestingly, several cardiac studies have revealed that smokers who receive fibrinolytics have better short-term survival after an acute myocardial infarction than nonsmokers exposed to the same treatment [28,29,30,31,32], and a recent analysis of the National Institute of Neurological Disorders and Stroke rt-PA database similarly suggested that smokers who received intravenous thrombolysis following acute ischemic stroke experienced better early outcomes and longer survival through 1 year after treatment than nonsmokers [33]. Against the backdrop of our findings in this study in which smokers fared more poorly than nonsmokers among a cohort of patients, the overwhelming majority of whom were not thrombolysed, the benefits of thrombolysis in smokers may be even more substantial than is currently realized.…”