花生四烯酸5-脂氧合酶激活蛋白基因多态性与心肌梗死关系的研究

目的探讨在中国北方汉族人群中花生四烯酸5-脂氧合酶激活蛋白(ALOX5AP)基因单核苷酸多态性T(8733)C与心肌梗死的关系。方法采用PCR-重测序法对随机选取的无亲缘关系的48例中国北方汉族个体进行ALOX5AP基因单核苷酸多态性筛查,对经冠状动脉造影证实的125例心肌梗死患者和158例正常对照者,采用聚合酶链反应?限制性片段长度多态性(PCR-RFLP)方法检测ALOX5AP基因T(8733)C多态性基因型和等位基因分布情况。结果通过筛查发现7个多态。心肌梗死患者ALOX5AP基因T(8733)C3种基因型(TT型、TC型和CC型)及C等位基因分布频率分别为35.2%、48.8%、16.0%和40.4%,正常对照者分别为32.9%、50.0%、17.1%和42.1%,其差异均无统计学意义(P>0.05);按性别分层进行亚组分析,心肌梗死患者与正常对照者ALOX5AP T(8733)C多态的基因型和等位基因频率差异亦均无统计学意义。结论ALOX5AP基因T(8733)C多态性与中国北方汉族人群心肌梗死的发生可能无关。     

Platelet-activating factor-acetylhydrolase A379V (exon 11) gene polymorphism is an independent and functional risk factor for premature myocardial infarction

BACKGROUND: Oxidation of low density lipoproteins is an initial step of atherogenesis that generates pro-inflammatory phospholipids, including platelet-activating factor (PAF). PAF is degraded by PAF-acetylhydrolase (PAF-AH), which has been postulated to be a risk factor for myocardial infarction (MI). The role of PAF-AH for the onset of premature MI is unclear. METHODS: Polymorphisms located in putatively functional regions were investigated in a cohort of patients having premature MI onset prior to 46 years of age (n = 200) and a sex-age-matched control group (n = 200). The activity of PAF-AH and coronary angiograms were evaluated for the severity of coronary atherosclerosis. RESULTS: The V allele of A379V (exon 11) polymorphism on PAF-AH gene was more frequent in patients with premature MI (P = 0.001). This V allele polymorphism was also associated with a lower activity of plasma PAF-AH and a more complex coronary atherosclerosis (p Trends <0.05). Multiple logistic regression analysis showed that this polymorphism was an independent risk factor (Odds Ratio [OR] 1.66, 95% CI 1.14.1 to 5.80, P = 0.008) as well as smoking (OR 3.72, 95% CI 1.77 to 9.28, P = 0.001), diabetes mellitus (OR 2.25, 95% CI 1.40 to 5.32, P = 0.007) and hypertension (OR 1.88, 95% CI 1.25 to 5.36, P = 0.003) for the onset of premature MI. CONCLUSION: We conclude that a functional and significant association between the A379V polymorphism on exon 11 of PAF-AH gene and premature MI exists in this Taiwanese population. This polymorphism is significantly associated with the PAF-AH activity and the severity of coronary atherosclerosis.     

Circulating activated protein C is reduced in young survivors of myocardial infarction and inversely correlates with the severity of coronary lesions.

BACKGROUND: Cardiovascular risk factors for myocardial infarction (MI) are less frequent in younger than in older MI survivors. Therefore, the thrombotic component of MI may play a more important role at a young age. As activated protein C (APC) provides systemic anticoagulant and anti-inflammatory protection, a low plasma APC level may be an arterial thrombotic risk factor. AIM: To determine whether there is an association between reduced APC levels and early MI and severe coronary lesions. METHODS: APC was measured in 231 young MI survivors and 231 controls. RESULTS: Low APC levels were significantly associated with MI. Compared with the fourth quartile, the odds ratio (OR) for APC values in the first quartile was 3.7 [95% confidence interval (CI) = 2.1-6.4], and 3.2 (1.5-7.0) after adjustment for cardiovascular risk factors. Moreover, each decrease of 0.43 ng mL(-1) (1 SD) in APC increased the OR 1.7 times (1.4-2.2), and 1.5 times (1.2-1.9) after adjustment for cardiovascular risk factors. Low APC levels were also associated with the number of coronary arteries affected and with the severity of coronary lesions (P < 0.001). CONCLUSIONS: There is a significant association between low circulating APC levels and both early MI and the extent and severity of coronary atherosclerosis, which might be related to the anticoagulant and anti-inflammatory properties of APC.     

Interleukin (IL)‐1β, IL‐1 receptor antagonist,IL‐6, IL‐8, IL‐10, and tumor necrosis factor α gene polymorphisms in patients with febrile seizures

Inflammation and genetics may play a role in the pathogenesis of febrile seizures (FSs). We aimed to test whether interleukin‐1β (IL‐1β), IL‐1 receptor antagonist (IL‐1 Ra), IL‐6 promoter, IL‐8, IL‐10, or tumor necrosis factor (TNF) gene polymorphisms could be used as markers of susceptibility to FSs. An association study was performed among a cohort of 104 patients with FSs and 143 normal control subjects. There was no significant difference between patients and controls in the distribution of allele frequencies of the IL‐1β promoter, IL‐1β exon 5, IL‐6 promoter, IL‐8, IL‐10, or TNF‐α gene polymorphisms. In contrast, the IL‐1 Ra‐I homozygote was more frequent in patients with FSs than in healthy controls (93.2% vs. 83.92%, χ²=4.51, P=0.034). In addition, individuals homozygous for the IL‐1 Ra‐I genotype were more than twice as likely to develop FSs than individuals heterozygous for the IL‐1 Ra‐I/II genotype (OR, 2.63, 95% CI: 1.08–6.39; χ²=4.55, P=0.033). We conclude that the IL‐1 Ra gene might be one of the useful markers for predicting susceptibility to FSs. J. Clin. Lab. Anal. 24:154–159, 2010. © 2010 Wiley‐Liss, Inc.     

Acute ST‐elevation myocardial infarction in a 24‐year‐old woman with atheromatous coronary artery disease

We report the case of a 24‐year‐old Torres Strait Islander woman who presented to a rural hospital ED with chest pain suspicious for myocardial ischaemia and was found to have an anterior ST‐elevation myocardial infarction. She was thrombolysed and transferred to a tertiary centre where subsequent angiography revealed atheromatous disease of the left anterior descending coronary artery. We believe this to be one of the youngest reported cases of myocardial infarction due to atheromatous coronary artery disease, and demonstrates important learning points regarding the demographics and risk factors of indigenous patients with chest pain.     

High platelet reactivity is associated with myocardial infarction in premenopausal women: a population‐based case–control study

Summary. Background: Platelets are involved in the occlusion of coronary arteries after rupture of an atherosclerotic plaque. Furthermore, activated platelets release large quantities of growth factors, chemokines and interleukines that regulate inflammatory reactions. Therefore, we hypothesized that high basal platelet reactivity may contribute to an increased risk of myocardial infarction (MI) in premenopausal women. Methods: We assessed the relation between high platelet reactivity and MI in a population‐based case–control study among premenopausal women (aged < 50 years). We used multivariable logistic regression to quantify the effect of high platelet reactivity, adjusted for potential confounders. Platelet reactivity was estimated by plasma levels of neutrophil activating peptide 2 (NAP‐2), CXC chemokine ligand (CXCL)4, soluble glycoprotein 1b (sGPIb) and soluble P‐selectin. Results: High platelet reactivity (i.e. levels ≥ 90th percentile control subjects) was associated with a 2‐ to 3‐fold increased incidence of MI: the adjusted odds ratios (ORs) were 3.0 [95% confidence interval (CI) 1.4–6.4] for NAP‐2, 2.2 (0.9–5.1) for CXCL4, 1.9 (0.7–4.6) for sP‐selectin and 2.5 (1.1–5.7) for sGPIb. The incidence of MI dose‐dependently increased when more markers were elevated. High platelet reactivity according to both NAP‐2 and sGPIb was associated with an up to tenfold increased incidence (9.9, 95% confidence interval 2.0–48.3). Conclusions: High basal platelet reactivity was associated with a 2‐ to 3‐fold higher incidence of MI compared with normal platelet reactivity in premenopausal women. Our results suggest that high basal platelet reactivity may contribute to a higher risk of MI.     

Regulatory mechanisms of C4b‐binding protein (C4BP)α and β expression in rat hepatocytes by lipopolysaccharide and interleukin‐6

Summary. Background: C4b‐binding protein (C4BP), a multimeric protein structurally composed of α chains (C4BPα) and a β chain (C4BPβ), regulates the anticoagulant activity of protein S (PS). Patients with sepsis have increased levels of plasma C4BP, which appears to be induced by interleukin (IL)‐6. However, it is not fully understood how lipopolysaccharide (LPS) and IL‐6 affect the plasma C4BP antigen level and C4BPα and C4BPβ expression in hepatocytes. Objectives: To assess the effect of LPS and IL‐6 on plasma C4BP, PS–C4BP complex levels, PS activity, and C4BP expression by rat liver in vivo and on C4BP expression by isolated rat hepatocytes in vitro. Results: Plasma C4BP antigen level transiently decreased from 2 to 12 h after LPS (2 mg kg^?1) injection, and then it abruptly increased up to 24 h after LPS injection. Plasma C4BP antigen level increased until 8 h after IL‐6 (10 μg kg^?1) injection, and then gradually decreased up to 24 h after IL‐6 injection. LPS significantly decreased the protein and mRNA expression of both C4BPα and C4BPβ in rat hepatocytes, and this effect was inhibited by NFκB and MEK/ERK inhibitors. IL‐6 mediated increase in C4BPβ expression in rat hepatocytes, which leads to increased plasma PS–C4BP complex level and to decreased plasma PS activity, was inhibited by inhibition of STAT‐3. Conclusion: LPS decreases both C4BPα and C4BPβ expression via the NFκB and MEK/ERK pathways, whereas IL‐6 specifically increases C4BPβ expression via the STAT‐3 pathway, causing an increase in plasma PS–C4BP complex, and thus decreasing the anticoagulant activity of PS.     

Identification of residual ischemia,infarction, and microvascular impairment in revascularized myocardial infarction using 64‐slice MDCT

This study aimed to assess the potential of 64‐slice MDCT in characterizing revascularized infarcted myocardium at the cellular and microvascular levels. Pigs (n = 7) underwent 2 h left anterior descending coronary artery occlusion/reperfusion. In acute (2–4 h) and subacute (1 week) infarction, first‐pass perfusion (FPP) (1 ml/kg of 300 mg/ml Omnipaque) was performed using a cine (rotation time 60 s/bpm) non‐ECG gated sequence (mAS/kV = 100/120). Delayed contrast enhanced images (DE) (mAS/kV = 650/120) were acquired every 2 min for 10 min to determine the kinetics of Omnipaque and to define infarcted myocardium and microvascular impairment (representing microvascular obstruction and/or no‐ or low‐reflow phenomenon). Maximum upslope, maximum attenuation and time to the peak were measured from FPP plots. 2,3,5‐Triphenyltetrazolium‐chloride (TTC) was used to define true infarction in the excised hearts. Hyperenhanced myocardium on DE was measured and compared with TTC. The contrast media caused minor beam hardening and X‐ray scatter on FPP. The above‐mentioned perfusion parameters significantly differed between remote and acute infarction. Infarcted myocardium showed two patterns of enhancement on DE, hyperenhanced rim representing the perfused infarction and hypoenhanced core representing a microvascular impaired region, with significantly different attenuation. The extent of infarction on DE‐MDCT decreased over the course of 1 week and did not differ from TTC. Post‐processed FPP semi‐quantitative images showed a decline in myocardial blood volume and flow in acute revascularized infarction. In conclusion, modern MDCT has the potential to identify residual ischemia on FPP and microvascular impairment and infarction on DE images. Copyright © 2008 John Wiley & Sons, Ltd.     

Increase in plasma plasminogen activators inhibitor type 1 concentration after fibrinolytic treatment in patients with acute myocardial infarction is associated with 4G/5G polymorphism of PAI-1 gene

BACKGROUND: Preliminary data suggest that plasma concentration of plasminogen activators inhibitor type 1 (PAI-1) is genetically determined and may be related to differential regulation of plasma PAI-1 concentration at baseline and after stimulation. AIM: This study aimed to evaluate whether increase in the plasma PAI-1 antigen concentration or activity after fibrinolytic therapy in patients with acute myocardial infarction is associated with the -675 4G/5G genetic polymorphism in the promoter region of PAI-1 gene. RESULTS & CONCLUSIONS: Our study revealed that a rebound effect is observed in PAI-1 activity (ActPAI-1) and PAI-1 antigen (AgPAI-1) concentration after standard streptokinase treatment with maximal values of 3 h (t3) after the completion of streptokinase infusion. Both ActPAI-1 and AgPAI-1 were significantly higher at t3 compared to the levels before fibrinolytic treatment: 37.3 (20.0-67.7) vs. 10.0 (3.6-26.0) IU L(-1); P = 0.00001 and 29.9 (15.6-42.3) vs. 20.9 (13.0-30.2) ng mL(-1); P = 0.001, respectively. The stratification of the patients by genotype revealed that carriers of the 4G allele had higher concentrations of PAI-1 antigen 3 h after streptokinase infusion: 30.9 vs. 13.8 ng mL(-1); P = 0.019. No significant association between PAI-1 activity and genotype was found. In conclusion, the rebound effect in serum PAI-1 concentration observed after streptokinase treatment may be related to the 4G/5G polymorphism in the PAI-1 gene promoter.     

Successful reperfusion for acute ST elevation myocardial infarction is associated with a decrease in WBC count

BACKGROUND: Elevated white blood cell (WBC) count on admission in patients with ST segment elevation myocardial infarction (STEMI) has been associated with an adverse prognosis. Whether successful reperfusion by primary percutaneous coronary intervention (PCI) is associated with a decrease in WBC count is unknown. METHODS: In this subanalysis of the On-TIME trial, WBC count was measured on admission and 6 h and 24 h after primary PCI for STEMI (n = 364). Angiographic measurements of reperfusion, including TIMI-flow and myocardial blush grade, were compared with changes in WBC count. RESULTS: Restoration of TIMI 3 flow by primary PCI was associated with a significant decrease in median WBC count (11.5 (9.7-14.2), 10.7 (9.0-12.5), 9.9 (8.5-11.5) at baseline, 6 h and 24 h), whereas after unsuccessful PCI (TIMI < 3 flow) WBC count remained elevated (12.5 (9.5-14.6), 12.1 (9.9-14.4), and 11.4 (9.2-15.2)). Improved myocardial blush was also related to a decrease in WBC count. After multivariate analysis, improved myocardial perfusion (TIMI 3 flow and myocardial blush grade 3) was an independent predictor of a decrease of WBC count after PCI. CONCLUSION: Impaired myocardial reperfusion after primary PCI for STEMI is associated with persistent WBC elevation.     

The minor allele of GP6 T13254C is associated with decreased platelet activation and a reduced risk of recurrent cardiovascular events and mortality: results from the SMILE–Platelets project

Summary. Background: Contradictory results have been published on the effects of T13254C (rs1613662), which distinguishes the two major isoforms of GP6, the gene encoding the platelet receptor glycoprotein VI, on platelet function and the risk of cardiovascular disease. Methods: We performed a population‐based case–control study, the Study of Myocardial Infarctions in Leiden, among 547 male patients with a first myocardial infarction (MI) and 646 control subjects, as well as a prospective cohort study in which the same MI patients were followed for recurrent events (fatal and non‐fatal MI and unstable angina) and mortality (median follow‐up of 12 years). P‐selectin expression by platelets induced by crosslinked collagen‐related peptide (CRP‐XL) was measured by whole blood flow cytometry in 274 MI patients. Results: T13254C was not associated with a first MI, but seemed to be associated with a reduced incidence of recurrent events [per‐allele hazard ratio 0.77, 95% confidence interval (CI) 0.56–1.06] and mortality (hazard ratio 0.57, 95% CI 0.37–0.89). Pooling with the Heart and Estrogen/Progestin Replacement Study revealed hazard ratios of 0.81 (95% CI 0.66–0.99) and 0.73 (95% CI 0.55–0.96). The minor C‐allele was also strongly associated with a reduced percentage of P‐selectin‐expressing platelets. The reduction per C‐allele was 23% (95% CI 18–28%). In an independent study of 219 healthy volunteers, the per‐allele reduction of CRP‐XL‐induced aggregation was 10% (95% CI 2–18%). Conclusion: The minor allele of GP6 T13254C that reduced platelet activation and aggregation also seemed to be associated with a reduced incidence of recurrent cardiovascular events and mortality, but was not associated with first MI.     

The CD14++CD16+ monocyte subset and monocyte‐platelet interactions in patients with ST‐elevation myocardial infarction

Summary. Aim: Monocytes contribute to both myocardial damage and repair by virtue of subset heterogeneity. The dynamics and functional characteristics of the three human monocyte subsets, including the unique CD14++CD16+ subset, and their contributions to monocyte platelet aggregates (MPAs) following ST‐elevation myocardial infarction (STEMI) are unknown. We aimed to examine dynamic changes and relation to left ventricular ejection fraction (LVEF) of the three human monocyte subsets and their aggregates with platelets following STEMI. Methods: Three monocyte subsets, CD14++CD16?CCR2+ (‘classical’, Mon1), CD14++CD16+CCR2+ (‘intermediate’, Mon2) and CD14+CD16++CCR2? (‘non‐classical’, Mon3), and their contribution to MPAs were analyzed by flow cytometry in 50 patients with STEMI, 40 patients with stable coronary artery disease (CAD) and 40 healthy volunteers. Study parameters were measured within 24 h of primary percutaneous coronary intervention (PCI) (day1) and on days 3, 7 and 30. Monocyte activation was assessed by measuring the nuclear factor κB (NFκB) pathway. LVEF was assessed 6 weeks after STEMI. Correlations between monocyte subsets/MPAs and plasma cytokines and troponin were assessed. Results: We observed marked differences in subset dynamics, with a prominent increase in Mon2 (P < 0.0001) but no changes in Mon3. Significant increases in Mon2 CD14 (P = 0.002) and CCR2 (P < 0.0001) expression, and reduction in CD16 expression (P = 0.001) were seen. NFκB pathway activity increased most prominently in Mon2 (P = 0.007). Mon2 count correlated with peak troponin (r = 0.31, P = 0.04) and plasma interleukin (IL)‐6 (r = 0.65, P < 0.0001) and IL‐10 (r = 0.34, P = 0.017). Mon1 correlated with IL‐6 (r = 0.55, P < 0.0001). Reduced Mon2 expression of CD16 on day 1 was independently predictive of higher LVEF (β = ?0.37, P = 0.013). The increase in MPA count following STEMI persisted at 1 month. Conclusion: The Mon2 ‘intermediate’ subset has unique dynamic and functional characteristics following STEMI and significant correlations with troponin, plasma cytokines and convalescent left ventricular function. The persistent increase in MPA count 30 days after STEMI may affect monocyte subset functional activity.     

Novel mutations in leukotriene C4 synthase and risk of cardiovascular disease based on genotypes from 50 000 individuals

Summary. Background: Atherosclerosis is an inflammatory condition where cysteinyl leukotrienes have been identified to play an important role. Furthermore, cysteinyl leukotrienes may also affect thrombus formation. Using prospective, cross‐sectional and case‐control designs, we tested the hypothesis that hitherto unknown genetic variation, likely to affect the function of leukotriene C₄ synthase, is associated with risk of venous thromboembolism, ischemic stroke and myocardial infarction. Methods and Results: Resequencing the gene coding for leukotriene C₄ synthase in an extreme risk population with more than 1500 individuals revealed 17 new mutations, of which four are likely to change protein function (211G>A (minor allele frequency, 0.0001), IVS3 + 1G>A (0.002), 374G>A (0.0006) and 451_453+10del (0.0007)). Based on genotyping 50 000 individuals, age and sex adjusted odds ratios for venous thromboembolism were 2.0 (95% CI, 1.3–3.5) for IVS3+1G>A heterozygotes vs. wild type, and 1.9 (1.5–2.7) for any mutation heterozygote vs. wild type. Corresponding values were 2.0 (1.3–3.2) and 1.5 (1.1–2.1) for ischemic stroke, and 1.0 (0.8–1.3) and 1.2 (1.0–1.4) for myocardial infarction. Conclusions: Four novel mutations that are likely to change the function of leukotriene C₄ synthase were associated with increased risk of venous thromboembolism and ischemic stroke. These findings need confirmation in other independent studies. In addition, the mechanism behind these findings deserves further investigation.     

Elevated levels of PAI‐1 activity and t‐PA antigen are associated with newly diagnosed abnormal glucose regulation in patients with ST‐elevation myocardial infarction

Summary. Background: Both Type 2 diabetes and cardiovascular disease have been associated with enhanced coagulation and suppressed fibrinolysis. Objectives: To investigate a possible relationship between selected hemostatic variables and abnormal glucose regulation (AGR) in patients with acute ST‐elevation myocardial infarction (STEMI) without known diabetes and to study changes in selected hemostatic variables from baseline to follow‐up in STEMI patients with or without AGR. Methods: Plasminogen activator inhibitor‐1 (PAI‐1) activity, tissue plasminogen activator (t‐PA) antigen, prothrombin fragment 1+2 (F₁₊₂) and von Willebrand factor (vWF) were measured in fasting blood samples from 199 STEMI patients 16.5 h (median time) after admission and 3 months later. All patients were classified into normal glucose regulation (NGR) or AGR based on an oral glucose tolerance test at follow‐up, according to the WHO criteria. Results: High PAI‐1 activity (≥ 75th percentile) measured in‐hospital was associated with AGR (n = 49) with an adjusted odds ratio of 2.2 (95% confidence interval, 1.1, 4.4). In addition, high levels of t‐PA antigen (≥ 75th percentile) were associated with AGR (adjusted odds ratio, 3.5; 95% confidence inteval, 1.5, 8.2), but only in men. Changes in the levels of F₁₊₂ were significantly more pronounced in patients with AGR compared with NGR (adjusted P = 0.04). Conclusion: Elevated levels of PAI‐1 activity and t‐PA antigen measured in‐hospital in STEMI patients were associated with AGR classified at 3‐month follow‐up. Additionally, changes in the levels of F₁₊₂ were more pronounced in patients with AGR compared with NGR. The data suggest an enhanced prothrombotic state after an acute STEMI in patients with AGR without known diabetes.     

Folate, homocysteine levels, methylenetetrahydrofolate reductase (MTHFR) 677C → T variant, and the risk of myocardial infarction in young women: effect of female hormones on homocysteine levels

Summary.  In young women data are limited about the association between myocardial infarction (MI) and hyperhomocysteinemia, low folate or methylenetetrahydrofolate reductase ( MTHFR ) genotypes. The effect of oral contraceptive (OC) use on plasma homocysteine levels is not clear. We assessed the association between hyperhomocysteinemia, low folate, MTHFR 677TT mutation and risk of MI, and we investigated the effect of OC use on homocysteine levels in controls. In 181 patients with a first MI and 601 controls 18–49 years of age from a population-based case–control study, non-fasting blood samples were available. The homozygote mutant allele (TT) was detected in 12% of the patients and in 10% of controls. The odds ratio (OR) for MI in TT patients compared with the wild-type (CC) controls was 1.3 [95% confidence interval (CI) 0.8, 2.3]. For all MTHFR genotypes combined, the OR for MI in the lowest quartile of folate (<5.4 nmol L⁻¹) compared with the highest quartile (>10.4 nmol L⁻¹) was 3.0 (95% CI 1.7, 5.1). A 2-fold increased risk of MI was found in women with the TT genotype who had folate levels below the median of 7.4 nmol L⁻¹ compared with CC genotype and folate levels above the median (OR = 2.0; 95% CI 1.0, 3.7). Mean homocysteine levels were 12.2 µmol L⁻¹ in OC users and 12.3 µmol L⁻¹ in non-users. Only at the 97.5 percentile (cut-off 21.0 µmol L⁻¹) was the adjusted OR for higher vs. lower homocysteine levels increased by 2.8-fold (95% CI 1.2, 6.8). Low folate is a risk factor for MI, particularly in women with the MTHFR 677TT genotype. Homocysteine levels were not influenced by OC use.     

Serum brain‐derived neurotrophic factor and platelet activation evaluated by soluble P‐selectin and soluble CD‐40‐ligand in patients with acute myocardial infarction

Little is known about the role of neurotrophins (NT) under adult vascular homeostasis in normal and pathological conditions. The NT family, including nerve growth factor and brain‐derived neurotrophic factor (BDNF) are expressed in atherosclerotic vessels. Previous studies demonstrated that plasma BDNF levels were increased in the coronary circulation in patients with unstable angina. However, the role of BDNF during the onset and evolution of unstable angina remains to be elucidated. The objective of this study was to evaluate the relationship between BDNF, functional parameters and biological markers associated with inflammatory processes and platelet activation. BDNF serum levels were assessed in patients with acute myocardial infarction (MI) (n = 20) or stable angina pectoris (SAP) (n = 20) who underwent coronary angiography. Serum levels of IL‐6, MCP1, sVCAM, soluble CD‐40‐ligand (sCD40L) and soluble P‐selectin (sP‐selectin) were measured simultaneously by flux cytometry. Median BDNF levels were higher in the MI than in the SAP group (1730 vs. 877 pg/mL, respectively; P = 0.025). In MI patients, we observed a significant correlation between BDNF and sP‐selectin (r = 0.58, P = 0.023), although we found a non‐significant trend between BDNF and sCD40L (r = +0.35, P = 0.144). By contrast, no such correlation was observed in SAP patients (r = ?0.22, P = 0.425). No difference was observed between the two groups regarding baseline demographics, risk factors, biological data and angiographic findings. The study suggests that BDNF serum levels in MI patients could be related to platelet activation and the inflammatory response. Further studies are needed to investigate the role of NT in the setting of acute MI.