Plasma Concentrations of Platelet Factor 4 in Acute Myocardial Infarction

The aim was to investigate whether in the acute stage of myocardial infarction (MI) platelet activation, as measured by plasma platelet factor 4 (PF-4), excluding that in ischaemic heart disease (IHD) is taking place. Over a period of 4 d the plasma levels of PF-4 were determined on 44 consecutive patients admitted to a coronary care unit with suspected MI. 21 of them had a definite acute MI (group 1), and 13 had evidence of IHD but no MI (group 2). In the remaining 10 subjects there was no evidence of either MI or IHD. On the first day the mean plasma PF-4 concentrations in group 1 and 2 patients were 11.8 ± 1.1 and 15.0 ± 2.3 ng/ml, respectively; the difference between means was not statistically significant. A peak mean PF-4 for group 1 patients (17.5 ± 4.6 ng/ml) was recorded on the second day of study. The corresponding value for group 2 patients was lower, but not significantly so. In the latter subjects no peak PF-4 was recorded. During the last 2 d of study the plasma PF-4 concentrations tended to decrease, but the means for the 2 groups did not differ statistically. Thus, at no point in time was there a significant difference between the PF-4 values for MI and IHD patients present.     

ADP-induced Platelet Aggregation and Metoprolol Treatment of Myocardial Infarction Patients

ABSTRACT The effect of metoprolol on platelet aggregation was investigated in a group of postmyocardial infarction (MI) patients. The study was double-blind and included 63 subjects; 30 patients were maintained on metoprolol and 33 received placebo treatment. Adenosine diphosphate (ADP)-induced platelet aggregation was carried out in each subject close to 4 weeks after the acute MI. It was demonstrated that metoprolol as compared to placebo did not influence ADP-induced platelet aggregation in the present clinical setting.     

Platelet Function and Plasma Free Fatty Acids during Acute Myocardial Infarction and Severe Angina Pectoris

The relationship between platelet function and plasma free fatty acid concentration has been studied serially during the initial 24 h in 11 patients suffering from acute myocardial infarction and in 5 patients with severe angina pectoris. Similar results were obtained in the 2 groups. Plasma free fatty acid concentration was initially high, and decreased significantly. The distribution of plasma free fatty acids remained unchanged. Platelet concentration was constant, whereas the percentage of reversible venous platelet aggregates initially was higher than in 11 healthy persons matched for age and sex. Platelet aggregates decreased transiently at 16 h. Venous reversible platelet aggregates correlated significantly with concentration of plasma free fatty acid, thus establishing a possible link between a change in lipid metabolism and platelet function. Plasma concentration of platelet factor 4 increased slightly but significantly during the initial hours. This may indicate an increased platelet release reaction.     

Platelet Number and Volume during Myocardial Infarction in Relation to Infarct Size

ABSTRACT Platelet number and mean platelet volume (MPV) were measured in 100 patients with acute chest pain, 41 with acute myocardial infarction (AMI), 33 with angina pectoris (AP) and 26 with non-coronary event (NCE), and compared with 21 controls. We found no significant difference in platelet count on admission in the patient groups, but it was lower compared with controls. There were no significant differences in MPV between the patient groups nor between patients and controls. Thirty patients with AMI were followed for 10 days and showed an initial 12% fall in platelet count followed by a 36% increase. Initially there was an increase in MPV (2%) followed by a fall (8%). The fall in platelet count and increase in MPV correlated with infarct size (maximum activity of lactate dehydrogenase (LDH)) and might reflect consumption of platelets. The precise role of platelets in the process of infarction is still unknown.     

ADP-induced Platelet Aggregation in Young Female Survivors of Acute Myocardial Infarction and Their Female Controls

ABSTRACT Adenosine diphosphate (ADP)-induced platelet aggregation was studied in 35 young female survivors of acute myocardial infarction (AMI) 14–46 (median 30) months after the infarction. The results were compared to those obtained for 35 control females of comparable age. Five different final ADP concentrations (0.2–1.0 μM) were employed, and the object was to assess the slope for the primary wave of aggregation as well as the threshold ADP concentration for secondary aggregation. The results showed that AMI patients and control subjects did not differ with respect to the primary wave of aggregation. However, secondary platelet aggregation was recorded to a significantly higher extent (p<0.02) in AMI patients than in their controls. The results therefore support the concept that enhanced platelet reactivity is present in patients with documented ischemic heart disease.     

血小板活化因子和P-选择素在脑梗死中的意义

血小板活化因子广泛存在于人体各种组织，参与多种生理和病理学过程。P-选择素是血小板活化的标志物，在脑缺血再灌注过程中起重要作用。文章对二者在脑梗死中的意义做了综述。     

Platelet Counts in Myocardial Infarction,Angina Pectoris and Peripheral Artery Disease

ABSTRACT Serial determinations of peripheral venous platelet counts were performed in 43 consecutive patients with acute chest pain. On admission, patients with acute myocardial infarction (AMI) had a significantly lower mean platelet count (p<0.05) than patients without AMI, whereas hematocrit was higher (p<0.025). Thereafter a further reduction was seen with steadily reduced platelet counts by about 20%, both in comparison with healthy controls (p<0.001) (n=113) and patients with peripheral artery disease (PAD) without heart symptoms (p<0.005) (n=54). The platelet number increased one week after admission and even thrombocytosis was observed. The changes in platelet number during AMI seem to parallel the changes in platelet function. Patients with PAD had normal mean platelet counts. Female patients as well as healthy subjects had significantly higher values than men (p<0.01).     

A Syndrome of Factor VII Deficiency and Abnormal Platelet Release Reaction

A 15-year-old girl with severe factor VII deficiency and chronic arthropathy showed an excessively prolonged bleeding time. Further studies demonstrated low platelet adhesiveness and abnormal platelet aggregation with ADP, collagen and epinephrine. Release of ¹⁴C-serotonin was deficient after aggregation with ADP and epinephrine, but was normal with thrombin. Transfusion of plasma or prothrombin complex concentrate resulted in a partial or complete correction of the bleeding time, respectively, but had no effect on in vitro platelet function tests. Both parents and the only sister had factor VII activities of 42 % - 72 % and factor VII antigen levels of 45 % - 66 % of normal and may thus be heterozygotes with respect to factor VII deficiency. All three had normal bleeding times in spite of abnormal in vitro platelet functions. The observations are interpreted to mean that in this family with factor VII deficiency and abnormal platelet release reaction the platelet abnormality as such was not sufficiently severe to prolong the bleeding time unless the factor VII activity was also very low.     

西洛他唑联合替格瑞洛对急性心肌梗死病人支架植入后冠状动脉再狭窄的防治效果及血小板功能的影响

目的观察西洛他唑联合替格瑞洛对急性心肌梗死(AMI)病人支架植入后冠状动脉再狭窄的防治效果及对血小板功能的影响。方法将90例择期行冠状动脉支架置入术的AMI病人随机分为研究组与对照组,各45例。两组术前均给予替格瑞洛,对照组术后给予替格瑞洛与阿司匹林,研究组术后给予替格瑞洛与西洛他唑,连续应用1年。血栓弹力图(TEG)凝血分析仪检测两组术后1 d、15 d、30 d二磷酸腺苷(ADP)诱导的血小板抑制率及最大聚集率(MPAR);随访统计术后1年期间出血事件、主要心血管事件及支架内狭窄发生情况。结果两组术后不同时刻ADP途径诱导的血小板抑制率比较差异无统计学意义(P>0.05);两组术后1 d ADP途径诱导的MPAR比较差异无统计学意义(P>0.05),而研究组术后15 d、30 d MPAR均高于对照组(P<0.05);两组术后15 d、30 d ADP途径诱导的血小板抑制率均高于术后1 d(P<0.05),MPAR低于术后1 d(P<0.05),而术后15 d与30 d比较差异均无统计学意义(P>0.05);两组主要出血、轻微出血及小出血发生率比较差异均无统计学意义(P>0.05),研究组总出血事件发生率低于对照组(6.67%与24.44%,P<0.05);两组术后1年内心功能恶化、非致死性AMI等主要心血管事件发生率比较差异无统计学意义(P>0.05),研究组术后1年内复发心绞痛、支架内再狭窄发生率(6.67%,4.44%)均低于对照组(20.00%,17.78%,P<0.05)。结论西洛他唑联合替格瑞洛有助于改善AMI病人支架植入术后血小板功能,降低出血事件发生率,且有助于降低复发心绞痛及支架内再狭窄风险。     

Plasma Levels of Platelet Factor 4 in Patients Admitted to a Coronary Care Unit

Blood was obtained from 63 consecutive patients within a 24 h period after the admission to a coronary care unit for the determination of plasma platelet factor 4 (PF-4) concentration. 28 of the subjects proved to have an acute myocardial infarction (MI), 24 had evidence of ischaemic heart disease (IHD) but no MI, and the remaining 11 patients had no signs of IHD. 40 healthy subjects served as controls. The mean PF-4 value in the MI group was 10.5 ±0.8 ng/ml. The corresponding values for patients with and without IHD were 8.7 ±0.6 and 8.3 ±0.6 ng/ml, respectively. The control mean (5.4 ±0.3 ng/ml) was significantly lower (P < 0.001) than the means for all 3 groups of patients studied. The difference between the group of MI patients and patients with IHD as well as patients without IHD was only of borderline significance (0.10 > P > 0.05).     

急性心肌梗死患者血清胎盘生长因子的动态变化

目的:观察急性心肌梗死(AMI)患者血清胎盘生长因子(PIGF)及超敏C-反应蛋白的动态变化及意义.方法:测定60例AMI患者(AMI组)发病第12小时、第3天、第7天血清中PIGF及超敏C-反应蛋白水平,并于第14天行超声心动图检测.另选40例健康体检者为正常对照组.PIGF采用酶联免疫吸附双抗体夹心法原理定量测定.结果:AMI组发病第12小时、第3天PIGF均显著高于正常对照组,差异有统计学意义(P＜0.05),第7天与正常对照组相比差异无统计学意义(P＞0.05);第12小时、第3天、第7天超敏C-反应蛋白均显著高于正常对照组,差异有统计学意义(P＜0.05);血清PIGF与左心室射血分数呈显著负相关(r=-0.654;P＜0.01),与左心室舒张末期容积和左心室舒张末期内径均呈显著正相关(r=0.845,0.684;P＜0.01).结论:AMI时患者血清PIGF水平显著增高,AMI后第3天达到相对高值,第7天降至正常人群水平.P1GF水平可能影响左心室重构.     

经皮冠状动脉介入治疗相关心肌梗死的危险因素和预测模型的建立

目的:筛选经皮冠状动脉介入治疗(PCI)相关心肌梗死(PMI)的危险因素,建立PMI发生风险的危险模型。方法:回顾性分析了北京大学人民医院801例择期PCI患者的临床基线特征、冠状动脉造影检查结果及PCI操作资料,并就此根据临床实际情况分为PMI组(n=113)和无PMI组(n=688)。同时利用多元Logistic回归分析筛选PMI的独立危险因素并建立危险模型。结果:PMI发生率为14.1%(113/801),经过多元Logistic回归分析发现PMI的独立危险因素包括年龄(OR=1.040,95%CI:1.015~1.065,P=0.001),多支病变(OR=1.740,95%CI:1.028~2.945,P=0.039),支架数目(OR=1.787,95%CI:1.404~2.275,P=0.000),旋磨(OR=4.046,95%CI:1.336~12.252,P=0.013),并建立了危险模型。该模型的ROC曲线下面积为0.706(95%CI:0.657~0.754)。结论:年龄、多支病变、支架数目及旋磨均为PMI发生的独立危险因素,由此建立的危险模型能够较好地指导临床工作者评估PMI风险。     

Platelet activation and hypercoagulability following treatment with porcine factor VIII (HYATE:C)

Activation of platelets and coagulation in vivo was studied in nine patients with hemophilia A and inhibitors to human Factor VIII, prior to and following treatment with porcine Factor VIII (PFVIII; HYATE:C). In addition, six hemophiliac patients were similarly studied after treatment with recombinant Factor VIII (rFVIII). Platelet activation was also examined in vitro using porcine von Willebrand factor (PvWF)-enriched and PvWF-depleted fractions obtained by fractionation of PFVIII. Coagulation was assessed by measuring the concentrations of plasma prothrombin fragment 1+2 concentrations (prothrombinase generation) and Factor Xa-ATIII. Patients treated with PFVIII had significantly increased numbers of circulating platelets expressing CD62 and CD63 (markers of platelet activation) and annexin V (marker of platelet procoagulant activity) compared to patients treated with rFVIII; the former patients also demonstrated an increase in plasma coagulability after therapy. In in vitro experiments it was observed that the platelet-activating and procoagulant capacity of PFVIII resided in the PvWF-enriched fraction, and the same was true for the plasma hypercoagulability following exposure of platelets to PFVIII. These results support the hypothesis that PFVIII-induced platelet activation provides a mechanism for enhancing hemostasis, separate from, and additional to, that due to increased circulating Factor VIII, and it is due to residual PvWF in the PFVIII preparation.     

The Assessment of the Platelet Function During the Acute Phase of ST-segment Elevation Myocardial Infarction in Essential Thrombocythemia

We encountered a case of ST-segment elevation myocardial infarction (STEMI) as the first clinical manifestation of essential thrombocythemia (ET). Platelet function tests revealed high thrombogenicity during primary percutaneous coronary intervention compared with general cardiovascular patients, whereas the platelet function two weeks after admission was effectively suppressed by dual antiplatelet therapy. The patient, who lacked cytoreduction, suffered from recurrent STEMI because of poor compliance with antiplatelet drugs. The risk of acute coronary occlusion may be high during the acute phase of STEMI in ET patients because of high thrombogenicity. Insufficient antiplatelet therapy and no cytoreduction are also risk factors for recurrent coronary events.     

Incidence of Factor V Leiden in Patients with Acute Myocardial Infarction

The genetic defect of coagulation factor V known as factor V Leiden produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thromboembolism. The data on arterial thrombosis associated with APC resistance are still not clearly defined. We conducted a study in patients presenting with acute myocardial infarction (MI) to assess whether factor V Leiden increases the risk of arterial thrombosis. We studied 109 patients who had a diagnosis of acute MI (69 males and 40 females, aged 25–91 years), and 112 controls. The study population was identified by characteristic ECG changes and elevation of serum CK-MB, whereas the control subjects were anonymous healthy blood donors with no known history of coronary artery disease. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. Heterozygous factor V Leiden mutation was found in 9 of 109 (8%) MI patients and 5 of 112 (4%) control subjects (P = .42). In conclusion, this study shows no evidence of an association between factor V Leiden and acute MI.     

Classification of Myocardial Infarction: Frequency and Features of Type 2 Myocardial Infarction

Background

The classification of myocardial infarction into 5 types was introduced in 2007 as an important component of the universal definition. In contrast to the plaque rupture–related type 1 myocardial infarction, type 2 myocardial infarction is considered to be caused by an imbalance between demand and supply of oxygen in the myocardium. However, no specific criteria for type 2 myocardial infarction have been established.

Methods

We prospectively studied unselected hospital patients who had cardiac troponin I measured on clinical indication. The diagnosis and classification of myocardial infarction were established, and the frequency and features of type 2 myocardial infarction were investigated by use of novel developed criteria.

Results

From January 2010 to January 2011, a total of 7230 consecutive patients who had cardiac troponin I measured were evaluated, and 4499 patients qualified for inclusion. The diagnosis of myocardial infarction was established in 553 patients, of whom 386 (72%) had a type 1 myocardial infarction and 144 (26%) had a type 2 myocardial infarction. Patients in the group with type 2 myocardial infarction were older and more likely to be female, and had more comorbidities. The proportion of patients without significant coronary artery disease was higher in those with type 2 myocardial infarction (45%) than in those with type 1 myocardial infarction (12%) (P < .001). Tachyarrhythmias, anemia, and respiratory failure were the most prevalent mechanisms causing type 2 myocardial infarction.

Conclusions

In a cohort of patients with myocardial infarction who were admitted consecutively through 1 year, the category of type 2 myocardial infarction comprised one fourth when diagnosed by the use of newly developed criteria. Approximately half of patients with type 2 myocardial infarction had no significant coronary artery disease.     

Reduced High Density Lipoproteins as a Risk Factor after Acute Myocardial Infarction

ABSTRACT. FranzÉn J, Johansson BW, Gustafson A (Department of Internal Medicine, University Hospital, Lund and Section of Cardiology, Department of Internal Medicine, MalmÖ General Hospital, MalmÖ, Sweden). Reduced high density lipoproteins as a risk factor after acute myocardial infarction. In a group of normocholesterolemic, non-diabetic middle-aged males surviving an acute myocardial infarction for 4±2 years (mean ± SD), we have previously described a low apolipoprotein A-1 and a deficient fibrinolytic activity as two major characteristics. In the present study we have followed morbidity and mortality risk factors for five years in these males. Mortality was 40% in a hypertensive group and 16% in a normotensive group. In the normotensive group mortality was related to reinfarction. Furthermore, patients with a poor prognosis in the normotensive group had lower high density lipoprotein (HDL) cholesterol and lower apolipoprotein A-I concentration in plasma than patients with a good prognosis. Unexpectedly, in the hypertensive group death was related to a low (p<0.05) cortisol concentration in urine. It is concluded that a low HDL level may be a bad prognostic sign in males who have sustained an acute myocardial infarction and show no evidence of other risk factors, such as diabetes, hypercholesterolemia or hypertension.     

ST段抬高急性心肌梗死高血糖发生的危险因素分析

目的探讨急性心肌梗死患者（acute myocardial infarction,AMI）早期出现空腹高血糖的相关危险因素,以早期识别高危患者,改善其预后。方法分析阜外医院2005年8月至2007年8月收治的初次发生ST段抬高AMI且在12h内接受急诊经皮冠状动脉介入治疗的连续276例住院患者,以空腹血糖11．1mmol／L（200mg／d1）为标准划分为高血糖组和普通血糖组,分析空腹高血糖发生的危险因素及两组患者住院期间主要不良心脏事件（major adverse cardiac events,MACE）。结果全组共53例发生高血糖（53／276,19．2％）。与普通血糖组相比,高血糖组患者的年龄偏大[（70±14）岁vs（59±11）岁,P=0．039]、女性患者较多（38％vs26％,P=0．001）、糖尿病患者较多（45％vs17％,P〈0．001）、心功能Killip分级≥Ⅱ级者较多（72％vs16％,P〈0．001）、血糖值偏高[（14．3±2．3）mmol／L vs （6．6±1．4）mmol／L,P〈0．001],心力衰竭（5％vs 1％,P=0．008）和MACE发生率增高（26％vs7％,P〈0．01）。多因素logistic回归提示高龄[OR 1．048,95％CI 1．014to1．085,P=0．006],女性[OR 2．528,95％CI 1．036 to 6．159,P=0．042],心功能Killip分级≥Ⅱ[OR 11．412,95％CI 5．144 to 25．338,P〈0．001]合并糖尿病[OR 1．024,95％CI 1．089 to 1．467,P〈0．001]是空腹高血糖发生的危险因素。276例患者中院内总病死率3．6％（10／276）;与普通血糖组相比,空腹高血糖组患者死亡率增高3．5倍（9％vs 2％,P=0．025）,MACE发生率增高2．7倍（26％vs 7％,P〈0．01）。结论高龄、女性、糖尿病史、心功能≥II级（Killip分级）是空腹高血糖发生的危险因素,入院早期高血糖提示AMI患者住院期间预后不良。