Influence of cigarette smoking on rate of reopening of the infarct-related coronary artery after myocardial infarction: A multivariate analysis

Chillou, Christian de; Riff, Pascal; Sadoul, Nicolas; Éthevenot, Gérard; Feldmann, L.; Isaaz, Karl; Simon, Jean-Philippe; Boursier, Michel; Khalife, Khalifé; Thisse, J. Y.; Aliot, Étienne

doi:10.1016/0735-1097(96)00091-5

Cited by 51 publications

(22 citation statements)

References 28 publications

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“…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).…”

Section: Discussionsupporting

confidence: 93%

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

Keleş¹,

Yeter²,

Durmaz³

et al. 2010

Anadolu Kardiyol Derg

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Objective: Elevated homocysteine levels induce a hypercoagulable state and make the clot more resistant to fibrinolysis. In this prospective observational study, we investigated the influence of homocysteine levels on infarct-related artery (IRA) patency and flow as determined with regard to thrombolysis in myocardial infraction (TIMI) flow grade and corrected TIMI frame count (CTFC). Methods: Sixty-one patients who received fibrinolytic therapy for a first ST elevation myocardial infarction (STEMI) within 12 hours of chest pain were included. Coronary angiography was performed according to the Judkins technique within 72 hours after fibrinolytic therapy. Total plasma homocysteine level was determined by the high-performance liquid chromatography method with fluorescence detection. Statistical analysis was performed using Chi-square, Student's t and Pearson correlation tests. Logistic regression analysis was used to determine the predictors of IRA occlusion. Results: Of the 61 patients, 22 (36.1%) had an occluded IRA (group 1), 39 (63.9%) had a patent IRA (group 2). Mean plasma homocysteine levels were found to be significantly higher in the group 1 compared to the group 2 (18.5±9.6 μmol/L vs 14.3±5 μmol/L, p=0.04). In addition, we found a significant positive correlation between CTFC and plasma homocysteine levels (r=0.415; p<0.01). In multiple logistic regression analysis, high levels of plasma homocysteine (OR=1.2; 95% CI 1.1-1.25; p=0.03) and being a non-smoker (OR=5.9; 95% CI 1.1-31.6; p=0.03) were found to be significant independent predictors of having an occluded IRA. Conclusion: There is an inverse relation between plasma homocysteine levels and IRA patency and flow in patients receiving fibrinolytic therapy for STEMI. (Anadolu Kardiyol Derg 2010; 10: 410-5) Key words: Homocysteine, fibrinolytic therapy, infarct-related artery, logistic regression analysis ÖZET Amaç: Yüksek homosistein düzeyleri mevcut pıhtıyı fibrinolize daha dirençli hale getirmektedir. Bu prospektif gözlemsel çalışmada, homosistein düzey-lerinin, TIMI (thrombolysis in myocardial infarction) akım derecesi ve TIMI kare sayısına göre değerlendirilen enfarktüs ile ilişkili arter (EİA) açıklık ve akım hızı üzerine etkisini araştırdık. Yöntemler: ST yükselmeli miyokart enfarktüsü nedeniyle, göğüs ağrısının ilk 12 saati içinde fibrinolitik tedavi alan 61 hasta çalışmaya alındı. Fibrinolitik tedavi sonrası 72 saat içinde Judkins tekniği ile koroner anjiyografi yapıldı. Total plazma homosistein düzeyi flörosan saptama ile yüksek performanslı likit kromatografi metodu ile belirlendi. İstatistiksel analiz Ki-kare, Student t test, Pearson korelasyon testi kullanılarak yapıldı. EİA oklüzyonu öngördü-rücülerinin belirlemesinde lojistik regresyon analizi kullanıldı. Bulgular: Çalışmaya alınan 61 hastanın 22'sinde (%36.1) EİA tıkalı (grup 1), 39'unda (%63.9) EİA açık (grup 2) saptandı. Ortalama plazma homosistein düzeyleri grup 1 de grup 2 ile kıyaslandığında daha yüksekti (18.5±9.6 μmol/L'ye karşın 14.3±5 μmol/L, p=0.04). Ayrıca düzeltilmiş...

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Section: Discussionsupporting

confidence: 93%

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

Keleş¹,

Yeter²,

Durmaz³

et al. 2010

Anadolu Kardiyol Derg

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“…19 Indeed, it has been provocatively suggested that thrombolytic therapy should be given only to smokers and that such alternative strategies as primary angioplasty be used in nonsmokers. 20 Our findings may account for these observations, because it might be anticipated that patients with impaired coronary endothelial cell tPA release would benefit most from thrombolytic therapy.…”

Section: Discussionmentioning

confidence: 59%

Impaired Coronary Tissue Plasminogen Activator Release Is Associated With Coronary Atherosclerosis and Cigarette Smoking

et al. 2001

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Background-The aim of the study was to establish the influence of proximal coronary artery atheroma and smoking habit on the stimulated release of tissue plasminogen activator (tPA) from the heart. Methods and Results-After diagnostic coronary angiography in 25 patients, the left anterior descending coronary artery (LAD) was instrumented, and the proximal LAD plaque volume was determined by use of intravascular ultrasound (IVUS). Blood flow and fibrinolytic responses to selective LAD infusion of saline, substance P (10 to 40 pmol/min; endothelium-dependent), and sodium nitroprusside (5 to 20 g/min; endothelium-independent) were measured by intracoronary IVUS and Doppler, combined with arterial and coronary sinus blood sampling. Mean plaque burden was 5.5Ϯ0.8 mm 3 /mm vessel (range 0.6 to 13.7 mm 3 /mm vessel). LAD blood flow increased with both substance P and sodium nitroprusside (PϽ0.001), although coronary sinus plasma tPA antigen and activity concentrations increased only during substance P infusion (PϽ0.006 for both). There was a strong inverse correlation between the LAD plaque burden and release of active tPA (rϭϪ0.61, Pϭ0.003). Cigarette smoking was associated with impaired coronary release of active tPA (current smokers, 31Ϯ23 IU/min; ex-smokers, 50Ϯ33 IU/min; nonsmokers 202Ϯ73 IU/min; PϽ0.05). Conclusions-We found that both the coronary atheromatous plaque burden and smoking habit are associated with a reduced acute local fibrinolytic capacity of the heart. These important findings provide evidence of a direct link between endogenous fibrinolysis, endothelial dysfunction, and atherothrombosis in the coronary circulation and may explain the greater efficacy of thrombolytic therapy for myocardial infarction in cigarette smokers.

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“…87 This may, in part, be explained by the finding that in current smokers the infarct related artery is more likely to become patent after thrombolytic therapy. 87 These observations are consistent with these findings on endothelial t-PA release because it might be anticipated that patients with impaired endothelial cell t-PA release would benefit most from thrombolytic therapy, whereas those with a normal endogenous fibrinolytic capacity are more likely to have coronary thrombus resistant to fibrinolysis.…”

Section: Smokingmentioning

confidence: 94%

“…Alternatively, hypertension and smoking may have different effects Figure 4. After myocardial infarction, smokers have a lower in-hospital mortality than nonsmokers (A) (data from Barbash et al 100 ), possibly because thrombolytic therapy is more effective in smokers (B) (data from de Chillou et al 87 ). Differences in the capacity for acute t-PA release in the coronary circulation (C) (data from Newby et al 53 ) may explain this observation.…”

Section: Hypertensionmentioning

confidence: 99%

“…49 This is consistent with the finding that serum cholesterol concentrations, unlike smoking status, do not influence the patency rate of the infarct related artery after thrombolytic therapy. 87 Moreover, hypercholesterolemia is particularly associated with vulnerable plaque rupture, whereas acute thrombosis develops in smokers even without plaque rupture. 76 It would therefore appear that, in contrast to smoking, hypercholesterolemia-associated plaque rupture is such a dramatic event that thrombosis occurs despite preserved local t-PA release.…”

Section: Hypercholesterolemiamentioning

confidence: 99%

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Stimulated Tissue Plasminogen Activator Release as a Marker of Endothelial Function in Humans

Oliver

Webb

Newby

2005

ATVB

118

117

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Stimulated Tissue Plasminogen Activator Release as a Marker of Endothelial Function in HumansJames J. Oliver, David J. Webb, David E. NewbyAbstract-The initiation, modulation, and resolution of thrombus associated with eroded or unstable coronary plaques are critically dependent on the efficacy of endogenous fibrinolysis. This is dependent on the cellular function of the surrounding endothelium and vascular wall. In particular, the acute release of tissue plasminogen activator from the endothelium makes an important contribution to the defense against intravascular thrombosis. Here, we describe the rationale and methodology for, and clinical relevance of, assessing acute endothelial tissue plasminogen activator release in humans. The investigation of endothelial fibrinolytic function has the potential to provide major new insights into the pathophysiology of cardiovascular disease, and to shape future therapeutic interventions.

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Influence of cigarette smoking on rate of reopening of the infarct-related coronary artery after myocardial infarction: A multivariate analysis

Cited by 51 publications

References 28 publications

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

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

Impaired Coronary Tissue Plasminogen Activator Release Is Associated With Coronary Atherosclerosis and Cigarette Smoking

Stimulated Tissue Plasminogen Activator Release as a Marker of Endothelial Function in Humans

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