Serial studies of platelet factor 4 and beta thromboglobulin during exercise in patients with coronary artery disease

In vivo activation of platelets can be accurately measured by radioimmunoassays of platelet factor 4 (PF4) and beta thromboglobulin (beta TG). Studies that attempt to correlate increases in PF4 and beta TG levels with exercise-induced myocardial ischemia have yielded conflicting results. To further examine the natural history of release of PF4 and beta TG we used a method of serial samplings of these proteins during and after exercise in nine normal subjects and 24 patients with coronary artery disease (CAD). Mean values for PF4 and beta TG at rest, during each stage, and immediately after treadmill exercise were the same for normal subjects and for patients with positive and negative responses to exercise-tolerance tests (ETTs). However, nonparametric analysis and regression equations disclosed differences in trends of PF4 level during exercise; PF4 levels increased in normal subjects during exercise, while patients with positive ETTs had no change in PF4 levels and patients with negative ETTs actually showed a decrease in PF4. This investigation confirmed that exercise-induced myocardial ischemia is not associated with platelet aggregation as manifested by the release of the platelet-specific proteins PF4 and beta TG. Statistical analysis suggested that prior reports of elevated levels of PF4 during exercise could have been caused by technical and methodologic difficulties that were associated with the collection and handling of the samples.     

Elevated beta thromboglobulin in peripheral venous blood of patients with acute myocardial ischemia: direct evidence for enhanced platelet reactivity in vivo

Levels of beta thromboglobulin, a platelet-specific protein, in platelet-poor plasma from peripheral venous samples of patients with acute myocardial ischemia were measured in order to obtain direct evidence for enhanced platelet reactivity in vivo in these patients and to determine the value of beta thromboglobulin assay in studying platelet reactivity in patients with ischemic heart disease.The normal beta thromboglobulin concentration in peripheral venous plasma, determined from normal volunteers and patients without known ischemic heart disease or disorders associated with enhanced platelet destruction (control group without platelet destruction), was 30.0 ± 12.6 ng/ml (mean ± standarddeviation) (range 10 to 59). The mean beta thromboglobulin level in hospitalized patients with chest pain judged not to be due to acute myocardial ischemia was 33.7 ± 12.0 (range 11 to 65). Patients with deep venous thrombosis, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura and idiopathic thrombocytopenic purpura provided a control group of patients with enhanced platelet destruction; the beta thromboglobulin level in this group was 131.0 ± 12.6 ng/ml (range 38 to 250).Elevated beta thromboglobulin levels were observed in 4 (16 percent) of 25 patients with stable angina pectoris (mean 45.0 ± 22.6 ng/ml, range 22 to 125), in 23 (59 percent) of 39 patients with unstable angina pectoris (mean 83.2 ± 73.7 ng/ml, range 14 to 910) and in 12 (80 percent) of 15 patients with acute myocardial Infarction (mean 118.5 ± 66.2 ng/ml, range 30 to 420) on one or more occasions during hospitalization. The mean values of patients with platelet destruction in the control group (p <0.001), patients with acute myocardial infarction (p <0.005) and patients with unstable angina pectoris (p <0.025) were significantly elevated with respect to values in patients without platelet destruction in the control group. The beta thromboglobulin levels of patients with acute myocardial infarction generally remained elevated during the first 3 to 4 hospital days.Elevation of beta thromboglobulin levels in patients with acute myocardial ischemia provides direct evidence for enhanced platelet reactivity in these patients. However, the temporal relation of the elevated beta thromboglobulin values with clinical deterioration was imprecise, so that it can not be determined from this study whether the enhanced platelet reactivity was a cause or an effect of the acute myocardial ischemia in these patients. Assay of beta thromboglobulin appears to be suitable as an indicator of enhanced platelet reactivity in patients with ischemic heart disease. Its use obviates many of the difficulties in interpretation of the various in vitro analyses of platelet function and platelet survival studies.     

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.     

Platelet tests and antiplatelet drugs in coronary artery disease

This study was designed to clarify discrepancies in the literature concerning platelet survival time and beta-thromboglobulin (beta TG) levels in patients with coronary artery disease (CAD) and the effect of platelet-suppressant drugs on these tests. Platelet survival time and plasma beta TG levels were determined in 48 patients with angiographically documented CAD. The effect of sulfinpyrazone or aspirin/dipyridamole on these measurements was investigated in a double-blind, crossover trial that included a placebo phase. In patients with CAD, the mean plasma beta TG concentration was significantly elevated, but the mean platelet survival time was not significantly different from that in controls. Treatment with sulfinpyrazone or aspirin/dipyridamole did not produce changes in platelet survival time or plasma beta TG concentration that were significantly different from the values during the placebo phase. This study demonstrates that compared with the spontaneous variation in platelet survival time or beta TG concentration, there was no measureable effect of sulfinpyrazone or aspirin/dipyridamole on the results of the tests.     

Evaluation of factors predisposing to arterial thrombosis in coronary artery disease.

Estimation of antithrombin III, alpha 2 macroglobulin and alpha 1 antitrypsin in patients with stable and unstable angina and acute myocardial infarction (15 cases each) were carried out. Twenty age, sex and weight matched healthy subjects were included as controls. Mean platelet factor 4(PF4) levels measured in 10 cases of each subgroup were significantly elevated in myocardial infarction (MI) (48.4 +/- 15.16 ng/ml) and III unstable angina patients (44.7 +/- 15.9 ng/ml) as compared to controls (25.42 +/- 12.47 ng/ml; P less than 0.01). Mean antithrombin III (AT III) levels were markedly reduced in all patients with MI (39.65 +/- 12.8% of normal pooled plasma) and unstable angina (37.9 +/- 16.6% of normal pooled plasma) and in 9 patients with stable angina. Alpha I antitrypsin and alpha 2 macroglobulin levels in these cases showed no significant difference compared to normals. Reduced AT III in coronary artery disease suggests a prethrombotic tendency in these patients. Raised PF4 levels in acute phase of the disease suggests heightened platelet activation.     

内皮素与血小板活化在急性心肌缺血中的作用

为探讨内皮素（ET）的释放与血小板的活化在急性心肌缺血中的作用，分别对19例急性心肌梗塞（AMI组）、26例不稳定型心绞痛（UA组）、15例稳定型心绞痛（SA组）患者及30例正常人进行观察。结果显示：与正常组比较，AMI组与UA组ET与血小板颗粒膜蛋白（GMP-140）均升高，SA组ET与GMP-140升高不明显。其中，AMI组与UA组ET与GMP-140有相关性分别为r＝0．62，P＜0．025；r＝0．41，P＜0．025，SA组ET与GMP-140无相关性（r＝0．31，P＞0．10）。研究结果提示，冠状动脉粥样硬化时，ET与活化的血小板相互作用，加速冠状动脉内血栓形成与痉挛，导致急性心肌缺血的发作。     

Thrombocyte activity in dilatative cardiomyopathy and latent cardiomyopathy compared to coronary heart disease

In a comparative study on the pathomechanism of myocardial hypoxia we determined a parameter each of platelet activity and thrombin activity in 46 patients with angina pectoris, i.e., 15 patients with dilatative cardiomyopathy (DCM), 15 patients with latent cardiomyopathy (LCM) and 16 patients with coronary heart disease (CHD) compared to 15 normal subjects (N). beta-thromboglobulin (beta TG) and fibrinopeptide A (FPA) were measured both at rest (I) and after symptom-limited maximal exercise (II) in plasma. In N, beta TG was not increased in any case, neither at rest nor on exertion (I: 20.5 +/- 6.1 ng/ml, II: 22.4 +/- 6.7 ng/ml). Patients with LCM did not differ significantly from N (I: 20.9 +/- 6.1 ng/ml, II: 22.7 +/- 7.9 ng/ml). beta TG values of some patients with DCM and CHD were increased at rest and especially under exercise (DCM I: 27.9 +/- 9.6 ng/ml, vs. N p less than 0.025; II: 49.9 +/- 45.5 ng/ml, vs. N p less than 0.01; CHD I: 25.2 +/- 7.7 ng/ml, vs. N p less than 0.05; II: 38.6 +/- 34.3 ng/ml, vs. N p less than 0.01). Patients with DCM developing significant angina under exercise showed a higher beta TG under these exercise conditions than those with mild or no angina (p less than 0.01). In patients with coronary heart disease, this correlation was not to be found. With regard to FPA the four investigated groups differed in an analogous way, as they did with regard to beta TG; but only a weak correlation within both values was shown.(ABSTRACT TRUNCATED AT 250 WORDS)     

Time course of platelet alpha granule release in acute myocardial infarction treated with streptokinase.

OBJECTIVE: To determine the time course of platelet alpha granule release in patients with acute myocardial infarction treated with streptokinase. DESIGN: A prospective study. SETTING: Coronary care unit. PATIENTS: Nine with myocardial infarction treated with both streptokinase and aspirin, and nine with acute chest pain but without myocardial infarction, who were treated with aspirin only. METHODS: All patients received 250 mg aspirin on admission and 150 mg once daily thereafter. All patients who fulfilled the indications for streptokinase received 1.5 megaunits, in a single infusion. After the initial medication, serial measurements of plasma beta thromboglobulin and plasma platelet factor 4 were performed at fixed intervals after the onset of chest pain. The primary endpoint sought was the peak value of beta thromboglobulin and platelet factor 4 in each individual. RESULTS: The median peak plasma beta thromboglobulin in the infarction group was substantially higher than in those without infarction, at 37 (range 12 to 210) v 15 (9 to 36) mg/litre, P < 0.01. The corresponding values for plasma platelet factor 4 were 4.6 (2.4 to 60.0) v 2.2 (< 2 to 8.5) mg/litre, P < 0.01. Increased values were seen only within the first 12 h after onset of chest pain, and after 12 h there was no difference between the patients with myocardial infarction and those without. Aspirin treatment did not abolish alpha granule release. CONCLUSIONS: In patients with acute myocardial infarction treated with streptokinase the content of the alpha granules is released within the first 12 h after the onset of chest pain. Aspirin apparently does not abolish this release.     

Increased plasma endothelin-1 in the early hours of acute myocardial infarction

Endothelin is a novel endothelium-derived vasoactive peptide with potent vasoconstrictor action in the coronary bed; however, its possible contribution to myocardial ischemia and infarction is not known. Plasma endothelin-1 concentration was measured with use of a radioimmunoassay in serial venous samples from 22 patients over a 72 h period after acute myocardial infarction (14 patients with uncomplicated infarction [group I] and 8 patients with hemodynamic or ischemic sequelae [group II]). Twenty-two normal subjects and seven patients with stable angina served as the control subjects. Endothelin-1 levels in patients with stable coronary disease were not different from those of normal subjects (0.62 +/- 0.56 and 0.76 +/- 0.38 pg/ml, respectively). In group I, plasma levels of endothelin-1 rose sharply after myocardial infarction, reaching a peak of 4.95 +/- 0.78 pg/ml at 6 h after the onset of chest pain (p less than 0.05 compared with values in control subjects) and returning rapidly toward the normal range by 24 h. Patients with complicated infarction (group II) demonstrated a similar rapid increase in plasma endothelin-1 to a peak value of 8.29 +/- 1.95 pg/ml; however, plasma endothelin-1 remained elevated in these patients, becoming significantly different from values in group I at 48 and 72 h. There was no correlation between peak increases in creatine kinase and peak endothelin-1 in either group, suggesting that the stimulus for elevation of endothelin-1 was not myocardial necrosis itself. Furthermore, left ventricular ejection fraction did not correlate with the increase in endothelin-1 in group I patients, whereas there was a significant inverse relation between ventricular function and plasma endothelin-1 in group II.(ABSTRACT TRUNCATED AT 250 WORDS)     

Fibrinopeptide A and beta thromboglobulin in patients with angina pectoris and acute myocardial infarction

The purpose of this study was to investigate the degree of platelet activation and thrombin generation in 40 patients with stable angina pectoris and in 20 patients with acute myocardial infarction (AMI) by determining the plasma beta thromboglobulin (BTG) and fibrinopeptide A (FPA) concentrations. In patients with angina pectoris increased platelet activation correlated with extensive coronary pathology; the activation, however, was not influenced by a previous myocardial infarction, use of oral anticoagulants, beta-blocking agents, or hyperlipidemia. The plasma beta thromboglobulin concentration predicted more accurately the extent of the coronary artery disease than the functional angina pectoris classification. Thrombin generation was within the normal range. In patients with acute myocardial infarction increased platelet activation and enhanced thrombin generation were found, which were not related to the infarct localization, infarct size, or the presence of complications. Consequently, in these patients determination of plasma beta thromboglobulin and fibrinopeptide A concentrations is useless for the diagnosis of venous thromboembolism.     

Platelet secretory activities in acute malaria (Plasmodium falciparum) infection

During acute Plasmodium falciparum infection in man, plasma concentrations of platelet-specific proteins, beta-thromboglobulin (beta TG) and platelet factor 4 (PF4) were significantly elevated. For beta TG, the mean concentration was 136.24 +/- 71.58 ng/ml in patients, and 50.53 +/- 25.42 ng/ml in control subjects (t = 5.3794; p = 0.0001), while for PF4 mean values were, respectively, 75.35 +/- 23.09 and 18.64 +/- 13.42 ng/ml (t = -6.0897; p less than 0.0001). Platelet LDH loss in vitro in response to stimulation with 0.5 U of thrombin was 57.0 +/- 29.5% in patient samples and 24.8 +/- 16.9% (control); the values being significantly different from each other (t = 2.888; p less than 0.025). With serotonin (5HT) uptake and release however, the values were essentially normal, in spite of marginal difference observed in the uptake value of patients compared to control. The data indicate that there was in vivo platelet activation during the infection, with the haemostatic balance titled towards hypercoagulability. There was also associated easy platelet lysis with stimulation. It is also suggested that the latter finding may be one of the mechanisms of reduced circulating platelet numbers observed in patients in the acute disease.     

The worse hospital outcome of diabetic patients is not explained by the severity of underlying coronary artery disease.

INTRODUCTION: Diabetes mellitus has a high prevalence in developed countries and is associated with high cardiovascular morbidity and mortality rates. In this study we evaluated in-hospital evolution of diabetic patients admitted to a cardiac care unit with acute coronary syndrome without ST segment elevation. METHODS: We analyzed a population of 176 consecutive patients, 36 (21%) with diabetes, admitted with chest pain at rest, elevated biological markers for myocardial necrosis and/or ST segment/T wave changes suggestive of myocardial ischemia. RESULTS: The groups were similar in terms of age, sex, presence of other risk factors for coronary artery disease (CAD), past history of CAD or myocardial revascularization. There were no differences between the groups with respect to extent of CAD, left ventricular function or blood levels of biological markers. The comparison between the two groups did not show any statistical difference concerning the following in-hospital events: non-Q wave MI, Q-wave MI, PTCA and death. On the other hand, the diabetic patients had a worse outcome in term of congestive heart failure (25% and 11%, p = 0.04), CABG (25% and 10%, p = 0.02) and combination of death, congestive heart failure and Q-wave MI (42% and 23%, p = 0.02). CONCLUSION: In spite of similar extent of CAD and similar left ventricular function, diabetes mellitus in patients with acute coronary syndrome without ST segment elevation identifies a higher-risk population with more complicated in-hospital outcome.     

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).     

Plasma interleukin-18 concentration: a novel marker of myocardial ischemia rather than necrosis in humans

OBJECTIVE: Myocardial ischemia contributes to cytokine expression in the myocardium in animals; therefore, plasma interleukin-18 concentration may be a good marker of myocardial ischemia/injury in patients with possible acute coronary syndrome. We sought to determine whether increases in plasma interleukin-18 concentrations might be indicative of myocardial ischemia in patients with acute coronary syndrome. METHODS: Plasma interleukin-18 concentrations were assessed in 27 acute coronary syndrome patients in whom creatine kinase activity was within normal range on admission, in addition to 10 controls. Myocardial infarction was retrospectively evidenced in 15 of the 27 patients. All patients with acute coronary syndrome were treated by emergent coronary interventions just after admission. Blood sampling was done immediately after admission to determine plasma IL-18 concentration and biochemical markers of myocardial infarction. RESULTS: An increase in plasma interleukin-18 concentration was observed in acute coronary syndrome patients on admission, regardless of the retrospective evidence of myocardial necrosis. Plasma interleukin-18 elevation preceded creatine kinase-MB elevation in myocardial infarction patients. Plasma interleukin-18 concentrations on admission did not correlate with peak creatine kinase-MB (r=0.38, P=n.s.) or with left ventricular ejection fraction (r=-0.14, P=n.s.). CONCLUSIONS: Plasma interleukin-18 concentration elevates quickly after severe myocardial ischemic event regardless of evolving myocardial necrosis. Thus, plasma interleukin-18 concentration may be a good and early marker to identify whether the symptom is due to myocardial ischemia, and therefore, may be used in deciding the therapeutic strategy in individual patients with possible acute coronary syndrome.     

Platelet hyperactivity in acute myocardial infarction in man--effects of prostacyclin

There is increasing evidence that platelets play an important role in the pathogenesis of acute ischemic heart disease. Therefore, an understanding of factors which impact on platelet performance is important. The present study was undertaken 1. to characterize during evolving myocardial infarction (MI) platelet activity in the peripheral circulation and across the ischemic/infarcting myocardial compartment, the locus of presumed platelet hyperactivity, and 2. to evaluate the effects of prostacyclin (PGI2), a most potent antiplatelet agent and vasodilator. A total of 59 patients with evolving MI were studied. 22 patients were instrumented with arterial and coronary sinus catheters and received intravenous infusion of PGI2, 13 +/- 4.5 ng/kg/min (mean +/- SD), for 90 minutes. In 15 of these patients, who had an anterior MI, transcardiac platelet function and response to PGI2 were studied. The results are as follows: Plasma levels of beta-thromboglobulin (beta-TG) and of thromboxane B2 (TxB2), in vivo measures of platelet activity, are elevated three and ten fold. 6-keto-prostaglandin F1 alpha, the stable end product of PGI2, is less than 10 pg/ml, reflecting a leftward shift of the TxB2/PGI2 ratio. Platelets, circulating during evolving MI ("ischemic platelets") are hyperaggregable in response to adenosine diphosphate and relatively resistent to PGI2, both in vivo and in vitro. Concentrations of platelet cyclic adenosine monophosphate and the cAMP response to PGI2 are diminished. The platelet hyper-reactivity is most intense early during infarct evolution and decreases with time. Transcardiac measurements indicate that thromboxane is produced across the ischemic/infarcting compartment in ten of 15 patients with anterior MI. The antiplatelet effect of PGI2 is greatly diminished. In summary, the data define an abnormal pattern of platelet behavior during evolving MI characterized by a pro-aggregatory environment, heightened platelet re-activity, both in the peripheral and coronary circulation, and relative resistance to PGI2. The clinical consequence of the data are that the infarct patient in the acute phase may benefit from platelet function suppression and requires significantly greater doses of prostacyclin than normal subjects. The data also suggest future directions for therapeutic manipulation of platelet hyper-reactivity in the setting of acute myocardial ischemia.     

Platelet function and conjugated diene concentrations in diabetic and non-diabetic survivors of acute myocardial infarction.

STUDY OBJECTIVE--The aim was to compare platelet function in diabetic and non-diabetic survivors of acute myocardial infarction and to relate it to an index of free radical activity in these patients. DESIGN--In vivo and in vitro indices of platelet function and diene conjugate molar ratios were measured in diabetic and non-diabetic infarct survivors on admission to hospital and sequentially for 72 h. PATIENTS--The patients were 17 diabetics (age 61.9 years, range 32-74) and 12 non-diabetics (60.8 years, range 39-75) admitted to hospital with acute myocardial infarction confirmed according to WHO criteria. MEASUREMENTS AND MAIN RESULTS--Agonist induced platelet aggregation, beta thromboglobulin levels, and linoleic acid 18:2(9,11)/18:2(9,12) molar ratios did not differ between diabetic and non-diabetic patients on admission. Concentrations of adrenaline producing 50% maximum platelet aggregation (EC50) in whole blood on admission were lower than non-infarct controls in both patient groups. The EC50 values in platelet rich plasma in both groups fell during the 72 h following admission (increases in platelet sensitivity). beta Thromboglobulin concentrations fell following admission in the diabetic group. Diene conjugate molar ratios were higher at 12 h and 24 h compared to admission in diabetic patients. Increases in diene conjugate ratios between admission and 24 h correlated with peak aspartate transaminase levels in both patient groups. No correlations were observed between platelet aggregation, beta thromboglobulin levels, or diene conjugate molar ratios. CONCLUSIONS--During 72 h following myocardial infarction there is a reduction in platelet activation in vivo and an increase in platelet sensitivity to exogenous agonists in vitro. Free radical generated isomers of linoleic acid increase in relation to infarct size, but are unrelated to platelet function. There were no differences in platelet function between diabetic and non-diabetic subjects.     

Effect of pacing-induced myocardial ischemia on platelet activation and fibrin formation in the coronary circulation

The effect of pacing-induced myocardial ischemia on platelet activation and fibrin formation was investigated in seven patients with severe proximal lesions of the left anterior descending coronary artery to determine if acute ischemia activates the coagulation system. Fibrin formation was assessed from plasma levels of fibrinopeptide A. Platelet activation was assessed by levels of platelet factor 4, beta-thromboglobulin and thromboxane B2. Plasma levels were measured before, during and after acute myocardial ischemia induced by rapid atrial pacing. Blood samples were collected from the ascending aorta and from the great cardiac vein through heparin-bonded catheters. The occurrence of anterior myocardial ischemia was established by electrocardiography and by myocardial lactate extraction. No significant transmyocardial gradients in the levels of fibrinopeptide A, platelet factor 4, beta-thromboglobulin or thromboxane B2 were found at rest, during ischemia or in the recovery period, and levels in the great cardiac vein did not change in response to ischemia. These data indicate that pacing-induced myocardial ischemia does not result in release of fibrinopeptide A, platelet factor 4, beta-thromboglobulin or thromboxane B2 into the coronary circulation, and imply that acute ischemia does not induce platelet activation or fibrin formation in the coronary circulation.     

Platelet functions in patients with acute myocardial infarction

The changes of platelet functions including platelet membrane microviscosity (PMMV), plasma 5-HT, plasma TXB2 and 6-K-PGF1a were studied in 30 cases of AMI and 13 cases of unstable angina (UA), 20 normal subjects as control. After onset of AMI, PMMV, plasma 5-HT, 6-k-PGF1a all increased quickly, especially on the 1st day (P less than 0.001-0.01). During 3 weeks observation, only 6-K-PGF1a decreased to the normal level on 14th day. There were no obvious decrease of plasma TXB2, 5-HT and PMMV. It showed that in acute phase of AMI without intervention of any antiplatelet drugs the platelets were activated continuously. Plasma 5-HT was the most sensitive predictor for the severity of AMI as observed by the comparison between the cases with complications and serum peak CK greater than 1000 U/L, and those without complications and peak CK less than 1000 U/L (P less than 0.001-0.05). The great change of PMMV was a bad prognosis. In patients with UA, during acute myocardial ischemia, the platelets were also activated significantly, but the extent was not as high as that in AMI.     

Plasma concentrations of myeloperoxidase predict mortality after myocardial infarction.

OBJECTIVES: This study investigated relationships between plasma myeloperoxidase (MPO), protein oxidation markers, and clinical outcome retrospectively in patients after acute myocardial infarction (MI). BACKGROUND: Reactive oxidants are implicated in cardiovascular disease, and elevated plasma MPO is reported to predict adverse outcome in acute coronary syndromes. METHODS: Detailed demographic information, radionuclide ventriculography, neurohormone measurements, and clinical history were obtained for 512 acute MI patients at hospital admission. Plasma levels of MPO and protein carbonyls were measured in patients and 156 heart-healthy control subjects. 3-chlorotyrosine was measured in selected patients. Patient mortality was followed for 5 years. RESULTS: Plasma MPO and protein carbonyl concentrations were higher in MI patients 24 h to 96 h after admission than in control subjects (medians: MPO 55 ng/ml vs. 39 ng/ml, and protein carbonyls 48 pmol/mg vs. 17 pmol/mg protein, p < 0.001 for each). Both markers were significantly correlated with each other and with cardiovascular hormone levels. Chlorotyrosine was not elevated in patients with high MPO or carbonyl levels. Above-median levels of MPO but not protein carbonyls were independently predictive of mortality (odds ratio 1.8, 95% confidence interval 1.0 to 3.0, p = 0.034). Patients with above-median MPO levels in combination with above-median plasma amino-terminal pro-brain natriuretic peptide (NT-proBNP) or below-median left ventricular ejection fraction (LVEF) had significantly greater mortality compared with other patients. CONCLUSIONS: Myeloperoxidase and protein carbonyl levels are elevated in plasma after acute MI, apparently via independent mechanisms. High MPO is a risk factor for long-term mortality and adds prognostic value to LVEF and plasma NT-proBNP measurements.     

Raised concentrations of glucose and adrenaline and increased in vivo platelet activation after myocardial infarction

Plasma concentration of beta thromboglobulin was used as an index of in vivo platelet activation in 36 patients after acute myocardial infarction. Twelve patients had diabetes, seven had pulmonary oedema or cardiogenic shock (pump failure) or both, and 17 had uncomplicated infarcts. On the first day of admission, concentrations of beta thromboglobulin were higher in the patients with diabetes and those with pump failure than in those with uncomplicated infarcts. Concentrations of beta thromboglobulin in the non-diabetic patients were studied by multiple regression analysis and were significantly associated with plasma concentrations of adrenaline, pump failure, and glucose but not with noradrenaline or infarct size. When all subjects were considered together, glucose, adrenaline, and pump failure were associated with the beta thromboglobulin concentration but diabetes was without significant effect. Hyperglycaemia and raised plasma adrenaline concentration after myocardial infarction may activate platelets, and this could contribute to poor outcome in such patients.