In-hospital mortality of habitual cigarette smokers after acute myocardial infarction. The 'smoker's paradox' in a countrywide study

Andrikopoulos, George; Richter, Dimitri; Dilaveris, Polychronis; Pipilis, Athanasios; Zaharoulis, A; Gialafos, John; Toutouzas, Pavlos; Chimonas, Elias

doi:10.1053/euhj.2000.2315

Cited by 128 publications

(87 citation statements)

References 36 publications

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“…This fact, although known and reported in the literature as the "smoker's paradox", does not hold after a strict analysis in regard to its favorable influence in patients with acute myocardial infarction when considered with other variables, mainly age 32 . In our sample, similarly to the report by Grines et al 33 , the lower mortality among smokers disappeared in the context of multivariate analysis.…”

Section: Discussionmentioning

confidence: 88%

Acute myocardial infarction: predictors of mortality at a public hospital in the city of Fortaleza, Ceará state

Dg¹,

Pj²,

Jn³

et al. 2003

Arq. Bras. Cardiol.

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OBJECTIVE: To identify the clinical and demographic predictors of in-hospital mortality in acute myocardial infarction with elevation of the ST segment in a public hospital, in the city of Fortaleza, Ceará state, Brazil. METHODS: A retrospective study of 373 patients experiencing their first episode of acute myocardial infarction was carried out. Of the study patients, 289 were discharged from the hospital (group A) and 84 died (group B). Both groups were analyzed regarding: sex; age; time elapsed from the beginning of the symptoms of myocardial infarction to assistance at the hospital; use of streptokinase; risk factors for atherosclerosis; electrocardiographic location of myocardial infarct; and Killip functional class. RESULTS: In a univariate analysis, group B had a greater proportion of the following parameters as compared with group A: non-Killip I functional class; diabetes; age >70 years; infarction of the inferior wall associated with right ventricular impairment; time between symptom onset and treatment at the hospital >12 h; anteroseptal or extensive anterior infarction; no use of streptokinase; and no tobacco use. In a multivariate logistic regression analysis, only non-Killip I functional class, diabetes, and age >70 years persisted as independent factors for death. CONCLUSION: Non-Killip I functional class, diabetes, and age >70 years were independent predictors of mortality in acute myocardial infarction with elevation of the ST segment

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Section: Discussionmentioning

confidence: 88%

Acute myocardial infarction: predictors of mortality at a public hospital in the city of Fortaleza, Ceará state

Dg¹,

Pj²,

Jn³

et al. 2003

Arq. Bras. Cardiol.

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“…90,91 28), comparing dual antiplatelet therapy consisting of aspirin and clopidogrel versus aspirin alone, showed that clopidogrel therapy may be more effective in current smokers compared with nonsmokers. [92][93][94] These findings have been suggested to reflect a smoker's paradox.…”

Section: Smoker's Paradoxmentioning

confidence: 99%

Mechanisms of Coronary Thrombosis in Cigarette Smoke Exposure

Barua

Ambrose

2013

ATVB

193

126

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Abstract-Acute rupture or erosion of a coronary atheromatous plaque and subsequent coronary artery thrombosis cause the majority of sudden cardiac deaths and myocardial infarctions. Cigarette smoking is a major risk factor for acute coronary thrombosis. Indeed, a majority of sudden cardiac deaths attributable to acute thrombosis are in cigarette smokers. Both active and passive cigarette smoke exposure seem to increase the risk of coronary thrombosis and myocardial infarctions. Cigarette smoke exposure seems to alter the hemostatic process via multiple mechanisms, which include alteration of the function of endothelial cells, platelets, fibrinogen, and coagulation factors. This creates an imbalance of antithrombotic/ prothrombotic factors and profibrinolytic/antifibrinolytic factors that support the initiation and propagation of thrombosis.

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“…[4][5][6][7] Some investigators have shown that cigarette smokers, suffering an acute myocardial infarction, tend to be younger with less diffuse coronary artery disease and fewer comorbidities compared to nonsmokers and these differences have been invoked to explain many of the differences in early mortality. [6][7][8] On the other hand, there is now increasing evidence that acute coronary syndrome (ACS) is an inflammatory condition. [9][10][11] It is likely that smoking induces inflammation, an atherogenic lipid profile, and a propensity to thrombosis, thereby promoting the development of coronary atherothrombosis.…”

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confidence: 99%

<b>The Etiology of ‘Smoker’s Paradox’ in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>

Katayama¹,

Iwasaki²,

Sakoda³

et al. 2008

Int. Heart J.

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SUMMARYDespite increased risk for coronary artery disease and acute myocardial infarction (AMI), prior studies have found that smokers with AMI have lower mortality rates than nonsmokers, a phenomenon often termed 'smoker's paradox'. The present study was designed to examine the etiology of 'smoker's paradox', especially with respect to the association with inflammation.The subjects included 528 consecutive AMI patients who were admitted within 24 hours of onset and underwent successful coronary intervention. Of the 528 subjects, 232 (44%) were smokers.The cardiac mortality rates over a 6 month period was significantly lower in the smoking group than the nonsmoking group (3% versus 9%, P = 0.01). There were significantly more male patients in the smoking group, and the smoking group was significantly younger than the nonsmoking group (P < 0.0001). The value of high sensitivity C-reactive protein (hs-CRP) on admission and 24 hours after onset, and serum amyloid A protein (SAA) were significantly higher, and acute phase BNP was significantly lower (hs-CRP on admission 1.36 ± 1.03 mg/dL versus 0.75 ± 0.82 mg/dL, P = 0.02, hs-CRP at 24 hours 3.86 ± 4.32 mg/dL versus 2.90 ± 3.46 mg/dL, P = 0.008, SAA; 288 ± 392 µg/dL versus 176 ± 206 µg/dL, P < 0.05, BNP; 248 ± 342 pg/mL versus 444 ± 496 pg/mL, P = 0.0002) in the smoking group than in the nonsmoking group. The early ST-segment resolution rate was higher in the smoking group compared with the nonsmoking group (80% versus 66%, P = 0.003).The reason why smokers with AMI have lower mortality rates than nonsmokers, the so-called 'smoker's paradox', is believed to be because smoking induces inflammation and smokers may have less damage to microvascular function after primary percutaneous coronary intervention. (Int Heart J 2008; 49: 13-24) Key words: Myocardial infarction, Smoking, Inflammation EVEN though many epidemiologic studies have shown that cigarette smoking is associated with higher rates of myocardial infarction and death from coronary From the

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In-hospital mortality of habitual cigarette smokers after acute myocardial infarction. The 'smoker's paradox' in a countrywide study

Cited by 128 publications

References 36 publications

Acute myocardial infarction: predictors of mortality at a public hospital in the city of Fortaleza, Ceará state

Acute myocardial infarction: predictors of mortality at a public hospital in the city of Fortaleza, Ceará state

Mechanisms of Coronary Thrombosis in Cigarette Smoke Exposure

<b>The Etiology of ‘Smoker’s Paradox’ in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>

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In-hospital mortality of habitual cigarette smokers after acute myocardial infarction. The 'smoker's paradox' in a countrywide study

Cited by 128 publications

References 36 publications

Acute myocardial infarction: predictors of mortality at a public hospital in the city of Fortaleza, Ceará state

Acute myocardial infarction: predictors of mortality at a public hospital in the city of Fortaleza, Ceará state

Mechanisms of Coronary Thrombosis in Cigarette Smoke Exposure

<b>The Etiology of &lsquo;Smoker&rsquo;s Paradox&rsquo; in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>

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<b>The Etiology of ‘Smoker’s Paradox’ in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>