Platelet activation and secretion associated with emotional stress

Platelets are believed to play a role in the pathogenesis of atherosclerosis and of the vascular obstruction that causes the acute complications of coronary artery disease. Since specific behavioral patterns appear to be related to the development of coronary artery disease and since emotional stress may predispose an individual to acute cardiovascular ischemia, it was hypothesized that platelet activation by catecholamines might be involved in these events. To study emotional stress, plasma samples were obtained from 61 senior medical residents immediately before they were to speak in public. There were significant increases in the plasma concentrations of the platelet-secreted proteins platelet factor 4 and beta-thromboglobulin and epinephrine and norepinephrine immediately before speaking, which demonstrates that platelet activation and secretion occur in association with this type of emotional stress. Four trials were carried out to study the mechanism for this observed platelet secretion: (1) phenoxybenzamine, (2) propranolol, (3) 650 mg aspirin, and (4) 80 mg aspirin were given several hours before the public speaking engagement. Neither phenoxybenzamine nor propranolol in doses that blocked the hemodynamic effects of alpha 1- and beta 1-adrenergic stimulation modified platelet secretion. Aspirin also did not block platelet secretion, which suggests that platelets were not being stimulated through a cyclooxygenase-dependent pathway. This study provides direct evidence of platelet secretion in vivo in association with emotional stress, and underscores the potential importance of platelet activation and secretion in the acute events that occur in patients with vascular disease.     

Enhanced platelet/endothelial activation in depressed patients with acute coronary syndromes: evidence from recent clinical trials.

Platelets play a key role in the progression of acute coronary syndromes (ACS). Clinical depression alone is also associated with enhanced platelet activation. The purpose of this study was to compare concentrations of established biomarkers of enhanced platelet/endothelial activation in clinically depressed versus non-depressed patients enrolled in recent clinical trials for ACS. Two hundred and eighty-one baseline plasma samples from patients with acute myocardial infarction (ASSENT-2; n = 41), with ACS (PRONTO; n = 126) and with clinical depression plus previous acute coronary syndrome within 6 months (SADHART; n = 64), and from normal healthy controls (n = 50) were analyzed. Blood was drawn before applying any therapeutic strategies including interventions, thrombolytics, infusions, and selective serotonin re-uptake inhibitors. Platelet factor 4, beta-thromboglobulin, platelet/endothelial cell adhesion molecule-1, P-selectin, thromboxane, prostacyclin, vascular cell adhesion molecule-1, and E-selectin were measured by enzyme-linked immunosorbent assay by a single core laboratory. Patients with ACS exhibited a higher degree of platelet activation than controls independently of the presence of depression. Plasma levels of P-selectin, thromboxane, prostacyclin, and vascular cell adhesion molecule-1 were the highest in the acute myocardial infarction group when compared with ACS despite the presence or absence of clinical depression. Surprisingly, patients with ACS and depression exhibited the highest levels of platelet factor 4, beta-thromboglobulin, and platelet/endothelial cell adhesion molecule-1 when compared with myocardial infarction or angina patients without clinical depression. E-selectin plasma level was constantly elevated compared with controls but did not differ among the groups dependent on the incidence of depression. The depressed plus ACS group had higher plasma levels of all biomarkers compared with the non-depressed patients. Retrospective analysis of the data from several clinical trials reveals that clinical depression is associated with enhanced activation of platelet/endothelial biomarkers even above the level expected in ACS. These findings may contribute to the unfavorable outcome associated with clinical depression in patients with ACS.     

急性冠状动脉综合征支架置入与血小板活化的临床研究

目的探讨急性冠状动脉综合征(acute coronary syndrome,ACS)患者行冠状动脉(冠脉)内支架置入术前、后血小板活化指标的变化。方法利用流式细胞术(flowcytometry,FCM)和单克隆抗体测定45例不稳定型心绞痛(unstable angina pectoris,UAP)与37例急性心肌梗死(acute myocardial in-farction,AMI)患者外周血中血小板膜糖蛋白CD62p,CD63和凝血酶敏感蛋白(thrombin-sensitive protein,TSP)的阳性表达率,并与45例冠脉造影正常者相对照。结果FCM可简单、迅速地检测血小板的活化功能。ACS患者支架置入后CD62p,CD63和TSP的阳性表达率均显著高于支架置入前;ACS组治疗前亦高于对照组。结论急性冠脉综合征伴随血小板活化,介入治疗进一步加强血小板的活化。     

Effect of mental stress on platelet function in normal subjects and in patients with coronary artery disease.

We studied the effect of emotional stress (mental arithmetic for 10 min) in 10 postinfarction patients and in 10 age-matched apparently healthy subjects as controls. Blood samples for platelet function studies and for the determination of epinephrine levels in serum were taken in basal conditions, at the end of mental stress and after 30 min of recovery. Patients were studied twice, in washout of medications and after oral administration of dipyridamole, 200 mg twice a day for 6 consecutive days. Mental stress induced in patients significant increments in different hemodynamic parameters (heart rate, systolic blood pressure and diastolic blood pressure) and in serum epinephrine levels. Concomitantly, the test produced a significant increase in platelet aggregation (induced by 3 microM ADP or 1 microgram/ml collagen), the formation of circulating platelet aggregates and an increase in plasma thromboxane B2 levels. Hemodynamic parameters and platelet function tests returned to baseline values after 30 min. Similar activation of hemodynamic parameters, similar increase in epinephrine levels and lower increase in platelet function by emotional stress were observed in control subjects. Treatment of patients with dipyridamole had no effect on stress-induced increase in hemodynamic parameters and epinephrine levels, but decreased stress-related platelet activation. These data can contribute to a better understanding of the complex relationships between psychosocial factors, the hemostatic system and vascular disease.     

Inhibition of platelet aggregation by nitric oxide donors improves with rest

It has been suggested that the platelets of patients with acute coronary syndromes (ACS) exist in a more activated state than those of patients with stable coronary heart disease (CHD) or healthy individuals. “Platelet nitrate responsiveness” (PNR) has been suggested as a measure of platelet activation, and has been shown to be reduced in both ACS and stable CHD. We examined the effect of a short period of undisturbed supine rest, an intervention aimed at reducing levels of “stress”, on PNR. In 8 healthy subjects we found that 45?minutes of rest led to a highly significant reduction in platelet aggregation and increase in PNR. Our finding supports the hypothesis that stress contributes to platelet activation as reflected in reduced PNR, which may contribute to the link between acute stress and cardiovascular events. It also emphasises that standardisation of sampling conditions in vitally important in studies utilizing PNR.     

Inhibition of platelet aggregation by nitric oxide donors improves with rest

It has been suggested that the platelets of patients with acute coronary syndromes (ACS) exist in a more activated state than those of patients with stable coronary heart disease (CHD) or healthy individuals. "Platelet nitrate responsiveness" (PNR) has been suggested as a measure of platelet activation, and has been shown to be reduced in both ACS and stable CHD. We examined the effect of a short period of undisturbed supine rest, an intervention aimed at reducing levels of "stress", on PNR. In 8 healthy subjects we found that 45 minutes of rest led to a highly significant reduction in platelet aggregation and increase in PNR. Our finding supports the hypothesis that stress contributes to platelet activation as reflected in reduced PNR, which may contribute to the link between acute stress and cardiovascular events. It also emphasises that standardisation of sampling conditions in vitally important in studies utilizing PNR.     

Biomarkers in cardiovascular disease: integrating pathophysiology into clinical practice

Biomarkers play an important role in the diagnosis, prognostic assessment, and management of patients with suspected acute coronary syndromes (ACS). Specific biomarkers identify different components of the pathophysiology of ACS: troponins are prototype markers of myocyte necrosis, natriuretic peptides reflect neurohormonal activation and hemodynamic stress, soluble CD40 ligand is an indicator of platelet activation, and C-reactive protein, myeloperoxidase, and monocyte chemoattractant protein-1 reflect various inflammatory processes. When combined, multiple biomarkers reflecting different pathophysiologic processes appear to enhance risk stratification, as compared with using individual markers alone. Advances in proteomic technology promise to identify additional novel biomarkers that facilitate diagnosis, risk stratification, and selection of therapies in ACS. In the future, it is hoped that multiple biomarker panels will form the basis of an individualized approach to the treatment of ACS, in which therapy is tailored to individual biomarker profiles.     

Frequency of distress and fear of dying during acute coronary syndromes and consequences for adaptation

Experiencing an acute coronary syndrome (ACS) may provoke a range of negative emotional responses, including acute distress and fear of dying. The frequency of these emotional states has rarely been assessed. This study examined the presence and severity of the fear of dying and acute distress in 184 patients with ACS and analyzed its correlates and consequences. Intense distress and fear of dying was reported by 40 patients (21.7%) and moderate fear and distress by 95 patients (51.6%). Intense distress and fear was associated with female gender (odds ratio [OR] 2.49, 95% confidence interval [CI] 1.07 to 2.49), lower levels of education (OR 2.44, 95% CI 1.02 to 5.87), greater chest pain (OR 5.33, 95% CI 1.40 to 20.4), and emotional upset in the 2 hours before onset of ACS (OR 2.70, 95% CI 1.13 to 6.45). Having no acute distress or fear was more common in patients who exercised regularly (OR 3.32, 95% CI 1.35 to 8.18) and who did not initially attribute the chest pain to cardiac causes (OR 2.67, 95% CI 1.10 to 6.47). No association was found with cardiovascular disease history, objective measures of clinical severity, or with clinical presentation of ACS. Acute distress and fear of dying predicted greater depression and anxiety 1 week after ACS (p=0.006), and elevated levels of depression at 3 months (p=0.009), after adjustment for age, gender, and negative affect. In conclusion, distress and fear during the initial stages of an ACS may trigger subsequent depression and anxiety, thereby promoting poorer prognosis and greater morbidity with time.     

Platelet activation in patients after an acute coronary syndrome: results from the TIMI-12 trial. Thrombolysis in Myocardial Infarction

This study was designed to determine the magnitude and time course of platelet activation during therapy of acute coronary syndromes with an oral platelet antagonist. BACKGROUND: Platelet activation and aggregation are central to the pathogenesis of the acute coronary syndromes (ACS). However, few data are available on levels of platelet activation over time in patients with ACS, especially in the setting of chronic glycoprotein (GP) IIb/IIIa inhibition. METHODS: The Thrombolysis in Myocardial Infarction (TIMI) 12 trial was a phase II, double-blind trial evaluating the effects of sibrafiban, an oral, selective antagonist of the platelet glycoprotein IIb/IIIa receptor in patients stabilized after an ACS. A subset of 90 of the 329 patients in the study had measurement of platelet activation as assessed by the expression of platelet associated P-Selectin on days 0, 7 and 28. Platelet activation was measured in blood samples that were fixed either immediately (spontaneous activation) or after 5 minute incubation with 0, 1 microM or 5 microM ADP in order to assess platelet responsiveness to very low or moderate stimulation. RESULTS: At baseline there was a significant elevation of spontaneous platelet activation as compared to samples obtained from normal donors or from patients who did not have acute coronary syndromes (ACS patients 27.6+/-18.7%, Normal controls 8.5+/-4.4%, Patient controls 10.9+/-7.1%, p < 0.005 for both). In addition, there was a significant decrease in the levels of platelet activation with time during the 28 days of treatment with sibrafiban. Nevertheless, even on day 28, the TIMI-12 patients continued to show elevated platelet activation in comparison to the control groups (p < 0.05 for both). CONCLUSIONS: These results suggest that platelets remain activated long after clinical stabilization post ACS. Although platelet activation decreased after one month of oral GPIIb/IIIa inhibition, levels remained higher than normal, suggesting the need for long-term antiplatelet therapy following ACS.     

Platelet function in clopidogrel-treated patients with acute coronary syndrome.

Percutaneous coronary intervention (PCI) in patients presenting with acute coronary syndrome (ACS) is associated with increased risk of thrombotic complications. ACS enhances platelet activation; whether pretreatment with clopidogrel is sufficient to suppress platelet function in patients with ACS is not known. This study assessed platelet function in patients with and without ACS prior to PCI and after pretreatment with a single dose of 600 mg clopidogrel. Blood samples of 402 patients prior to PCI with (n = 119) or without (n = 283) ACS were collected at least 2 h after 600 mg clopidogrel administration. Maximal platelet aggregation in response to ADP (5 and 20 micromol/l), collagen (4 microg/ml) and TRAP (25 micromol/l) was measured with optical aggregometry. Surface expression of glycoprotein IIb/IIIa and P-selectin was assessed with flow cytometry at baseline and after stimulation with 5 and 20 micromol/l ADP. Agonist-induced platelet aggregation did not differ significantly between patients with and without ACS (P > or = 0.15). Parameters of platelet activation (glycoprotein IIb/IIIa and P-selectin surface expression) were significantly higher in ACS patients at baseline and after 5 and 20 micromol/l ADP stimulation (P < 0.0001). Patients with ACS continue to exhibit increased platelet activation after pretreatment with 600 mg clopidogrel. This finding supports the need for additional platelet function inhibition during PCI in patients with ACS.     

氯吡格雷在急性冠状动脉综合征中的抗炎作用

目的:观察氯吡格雷在急性冠状动脉综合征(ACS)中的抗炎作用。方法:入选健康对照组30例、稳定型心绞痛(SAP)组40例、ACS患者66例,后者按照治疗方案不同随机、单盲分为氯吡格雷加阿司匹林组(A组)和阿司匹林(B组),观察疗程1周。所有受检者测定入院时血浆高敏C反应蛋白(hs-CRP)和P选择素(Ps)水平,ACS患者治疗1周后复查hs-CRP和Ps。观察各组hs-CRP和Ps的基线状态及治疗后变化情况。结果:药物干预前ACSA、B组患者hs-CRP和Ps较SAP组和健康对照组明显升高(P<0.01)。而SAP组与健康对照组之间,A组和B组之间hs-CRP和Ps差异无统计学意义(P>0.05),干预1周后A组比B组hsCRP和Ps显著降低(P<0.01)。结论:ACS存在明显的炎症过程;氯吡格雷可以下调ACS患者的炎症因子,具有抗炎作用。     

老年急性冠状动脉综合征患者血小板P选择素、血管性血友病因子的变化及氯吡格雷干预的临床研究

目的观察老年急性冠状动脉综合征(ACS)患者血小板P选择素和血管性血友病因子(vWF)的变化,及抗血小板聚集药物氯吡格雷干预后的临床相关研究,探讨它们在ACS发病机制中的作用和相互联系。方法选取60例老年ACS患者,其中急性心肌梗死(AMI)患者30例,不稳定型心绞痛(UAP)患者30例,另设对照组30例。随机将UAP分为常规治疗组和氯吡格雷(75mg/d)组,AMI组应用抗血小板聚集药物(氯吡格雷300mg+阿司匹林)联合治疗,采用全血法流式细胞术及血浆酶联免疫吸附法测定各组治疗前后血小板P选择素、vWF水平变化,同时探讨P选择素与vWF的相关关系。结果老年ACS患者P选择素、vWF水平[AMI组P选择素(9.74±1.97)%,vWF(272.24±28.62)%;UAP组P选择素(8.87±1.78)%,vWF(215.81±22.01)%]显著高于正常对照组[P选择素(2.27±1.30)%,vWF(112.45±13.22)%](P<0.001)。常规治疗组和氯吡格雷组均可降低UAP患者P选择素与vWF水平[常规治疗组P选择素治疗前(8.60±1.39)%,治疗后(5.60±2.18)%,降低(2.97±1.82)%,vWF治疗前(217.52±25.68)%,治疗后(170.17±20.88)%,降低(47.34±24.31)%;氯吡格雷组P选择素治疗前(9.15±2.11)%,治疗后(4.24±1.73)%,降低(4.89±2.02)%,vWF治疗前(214.10±18.35)%,治疗后(151.72±12.66)%,降低(62.38±21.58)%],但氯吡格雷组较常规治疗组降低的程度更明显(P<0.05),AMI组联合治疗后P选择素与vWF水平均低于治疗前[P选择素(2.27±1.30)%,vWF(112.45±13.22)%](P<0.001),但仍高于对照组(P<0.001)。老年ACS患者P选择素水平与vWF水平成正相关(r=0.365,P<0.05)。结论P选择素、vWF与ACS的发病过程有关,可能是老年ACS不稳定斑块的识别和预测指标。     

急性冠脉综合征患者冠脉血小板微粒水平

目的利用流式细胞法检测急性冠脉综合征(ACS)患者冠状动脉血中血小板微粒(PMPs)水平,探索其与冠心病发生发展的关系及其机制。方法入选患者共92例分为4组,其中ST段抬高型急性心肌梗死(STEAMI)组28例,非ST段抬高型急性冠脉综合征(NSTE-ACS)组24例,稳定型心绞痛(SA)组20例,正常对照组20例。冠脉造影术中取冠脉内血液3 ml,离心制得贫血小板血浆,依次加入CD61荧光抗体及0.82μm标准微球,流式细胞仪测定PMPs的相对水平。结果 STEAMI组、NSTEACS组PMPs水平(分别为8.9%±3.3%,7.8%±2.4%)均高于正常组(4.7%±2.9%);STEAMI组、NSTE-ACS组也均高于SA组(5.9%±2.6%,P均0.05)。STEAMI组和NSTE-ACS组组间比较、SA组和冠脉正常组组间比较,差异无统计学意义(P均0.05)。结论 ACS患者冠脉血中的PMPs水平明显升高,稳定性心绞痛患者PMPs无明显升高,提示PMPs与冠心病发生发展有关。其机制可能通过PMPs与血小板的相互激活,导致动脉粥样硬化进程的加速。检测PMPs水平可能有助于高危ACS患者的早期诊断。     

Cardiovascular stress responsivity, body mass and abdominal adiposity

OBJECTIVE: To assess the relationship between adiposity and cardiovascular stress reactivity and recovery in middle-aged men and women, and investigate the influence of impaired poststress cardiovascular recovery on changes in body mass index (BMI) and waist-hip ratio over 3 y. PARTICIPANTS: In total, 225 healthy men and women aged 47-59 y were recruited from the British civil service. METHODS: Laboratory mental stress testing was carried out, with blood pressure (BP), cardiac output and total peripheral resistance being measured at baseline, during moderately challenging tasks, and during recovery 40-45 min poststress. Weight, height, waist and hip circumference were assessed at the time of mental stress testing and 3 y later. RESULTS: Behavioural tasks elicited increases in BP sustained by a combination of cardiac activation and raised peripheral resistance. BMI and waist/hip ratio were associated cross-sectionally with impaired poststress recovery of systolic pressure, diastolic pressure and cardiac index independently of age, gender, socioeconomic status, smoking, alcohol consumption and baseline cardiovascular activity. Increases in waist-hip ratio over 3 y were predicted both by impaired poststress recovery of systolic pressure and cardiac index in men, independently of baseline adiposity and other covariates. No associations between subjective stress and BMI or waist-hip ratio were observed. CONCLUSIONS: Disturbances of cardiovascular responsivity to psychological stress, manifest through impaired poststress recovery, were associated cross-sectionally with BMI, and longitudinally with central adiposity in men. Stress-related cardiovascular dysregulation may contribute to obesity risk.     

应用血栓弹力图评估ACS患者替格瑞洛与氯吡格雷抗血小板的疗效

目的通过血栓弹力图(TEG)检测血小板聚集率,观察接受双联抗血小板药物治疗的急性冠状动脉综合征(ACS)患者应用替格瑞洛或氯吡格雷的抗血小板疗效。方法选取清华大学第一附属医院心脏中心住院的84例急性冠状动脉综合征患者,随机分为两组,氯吡格雷组(n=42)与替格瑞洛组(n=42),通过TEG检测方法比较两组患者服用氯吡格雷和替格瑞洛后的血小板抑制率情况。结果氯吡格雷组中11例出现氯吡格雷抵抗,发生率为26.19%,替格瑞洛组中1例患者出现替格瑞洛抵抗,发生率为2.38%,两组发生率的比较差异有统计学意义(χ2=9.722,P=0.002);氯吡格雷组中有1例(2.38%)发生阿司匹林抵抗;替格瑞洛组中有2例(4.76%)发生阿司匹林抵抗,两者发生率比较差异无显著统计学意义(χ2=0.346,P=0.557)。结论接受标准抗血小板治疗的部分急性冠状动脉综合征患者存在抗血小板抵抗,TEG监测结果显示,替格瑞洛的抗血小板聚集效果明显优于氯吡格雷。     

CD62p、CD63、C-RP在急性冠状动脉综合征中的作用

目的　研究血小板活化和炎症反应在急性冠状动脉综合征 (ACS)中的作用。方法　采用全血流式细胞术测定 ACS患者 5 0例和正常对照组 30例血小板胞浆内α-颗粒上的膜糖蛋白 (CD6 2 p)、溶酶体膜糖蛋白 (CD6 3) ,用速率散射比浊法测定血浆 C-反应蛋白 (C- Rective Protein,C- RP)。结果　 ACS组血小板表面活性标志蛋白 CD6 2 p(11.2 1± 0 .84 ) %、CD6 3(4 .17± 0 .4 5 ) %和 C- RP(19.16± 2 .5 8) m g/ L均明显高于对照组 (3.31± 0 .6 2 ) %、(1.5 2±0 .4 1) %和 (5 .12± 1.4 3) m g/ L(P<0 .0 1) ;CD6 2 p、CD6 3与 C- RP呈显著正相关 (相关系数分别为 0 .4 2 8和 0 .4 6 9,均 P<0 .0 1)。结论　 ACS患者存在血小板活性增强和炎症反应 ,这些变化与 ACS的病理过程有关。     

氧化型低密度脂蛋白对急性冠状动脉综合征患者血小板聚集率的影响

目的检测急性冠状动脉综合征(ACS)患者血浆氧化型低密度脂蛋白(ox-LDL)和血小板聚集率的变化并探讨ox-LDL对ACS患者血小板聚集率的影响。方法收集经冠状动脉造影确诊的48例稳定型心绞痛(SA)患者,59例不稳定型心绞痛(UA)患者以及51例急性心肌梗死(AMI)患者外周血标本,同时收集同期住院且冠状动脉造影正常的60例患者外周血标本作为对照组,通过ELISA检测血浆ox-LDL的表达水平,通过血小板聚集仪检测血小板聚集率的变化,通过体外实验加入ox-LDL检测ox-LDL对ACS患者血小板聚集率的影响。结果与对照组相比,UA组和AMI组血浆ox-LDL和血小板聚集率显著升高(P0.05),而SA组与对照组及UA组与AMI组相比血浆ox-LDL和血小板聚集率并无显著性变化(P0.05),同时ACS患者(UA和AMI)血浆ox-LDL水平与血小板聚集率呈明显正相关(r=0.651,P0.01),体外实验进一步证实ox-LDL可明显提高生理激动剂二磷酸腺苷(ADP)诱导的ACS患者血小板聚集率(P0.01)。结论 ACS患者血浆ox-LDL水平升高与血小板高聚集状态密切相关,高水平的ox-LDL可能是ACS患者血栓形成的重要危险因素,因此检测ox-LDL水平对ACS患者预后判断有重要价值。     

Expression of platelet collagen receptor glycoprotein VI is associated with acute coronary syndrome.

AIMS: Platelet collagen receptor glycoprotein VI (GPVI) is critical for the formation of arterial thrombosis. In this observational study, we examined the platelet surface expression of GPVI in patients with symptomatic coronary artery disease (CAD). METHODS AND RESULTS: We evaluated a consecutive cohort of 367 patients with symptomatic CAD, who underwent coronary angiography. The surface expression of platelet activation markers (GPVI, CD62P, and CD42b) was determined by flow cytometry. Patients with acute coronary syndrome (ACS) showed a significantly enhanced GPVI expression on admission when compared with patients with stable angina pectoris (SAP) (ACS: 21.4+/-9.7; SAP: 18.6+/-7.1 mean fluorescence intensity+/-SD; P=0.004). The expression of GPVI correlated with CD62P (r=0.702; P=0.001). Logistic regression analysis demonstrated that on admission, elevated platelet GPVI expression was associated with ACS, independent of markers of myocardial necrosis such as troponin and creatine kinase. CONCLUSION: Platelet GPVI surface expression is elevated in patients with ACS and is associated with imminent acute coronary events. The determination of the platelet-specific thrombotic marker GPVI may help to identify patients at risk before myocardial ischaemia is evident.     

Platelet glycoprotein VI: a novel marker for acute coronary syndrome

The platelet collagen receptor glycoprotein (GP) VI is critical for the formation of arterial thrombosis. GPVI platelet surface expression was examined in patients with stable angina and in patients with acute coronary syndrome (ACS). Surface expression of platelet activation markers such as P-selectin, GPIbalpha, and platelet GPVI was determined by flow cytometry. Patients with ACS showed a significantly enhanced GPVI expression compared with patients with stable angina and healthy controls. The expression of GPVI correlated well with CD62P. Elevated platelet GPVI expression was associated with ACS independent of markers of myocardial necrosis such as troponin and creatine kinase. In ACS, platelet surface GPVI expression was already elevated several hours before troponin and creatine kinase indicated myocardial injury. We conclude that the determination of the platelet-specific thrombotic marker GPVI may help to identify patients at risk before myocardial ischemia is evident.     

Increased rate of formation of small-sized platelet aggregates in patients with acute coronary syndromes

Coronary thrombosis has been implicated in the pathogenesis of acute coronary syndromes, and platelet activation plays a pivotal role in the pathogenesis of coronary thrombus. A new platelet aggregometer using a laserlight scattering beam was trialled for assessment of platelet aggregation. Platelet aggregability, especially small-sized platelet aggregates, was investigated on admission using the laser-light scattering method and again after treatment in 23 patients with acute coronary syndromes. The platelet aggregability in 14 patients with stable exertional angina and in 14 control subjects was also examined. On admission, the number of small- and medium-sized platelet aggregates in the acute coronary syndromes group was significantly greater than in the stable exertional angina group or control group. However, the number of large-sized platelet aggregates on admission was not increased in the acute coronary syndromes group. Furthermore, the number of small- and medium-sized platelet aggregates decreased significantly after treatment in the acute coronary syndromes group. The increased number of small-sized platelet aggregates may sensitively reflect attacks of thrombosis in patients suffering acute coronary syndromes.