In-vivo Platelet Activation and Anomalous Thrombospondin Levels in Severe Falciparum Malaria

To investigate in vivo platelet function in acute falciparum malaria plasma concentrations of β-thromboglobulin (β-TG), platelet factor 4 (PF4) and thrombospondin (TSP) were determined in 10 severely-ill Thai patients and 11 healthy volunteers. 8 patients recovered. At presentation, the platelet counts of the 10 patients were significantly lower (p < 0.025) than those of the controls, and a slight but significant increase (p < 0.05) in β-TG/PF4 ratios in the patients suggested low-grade platelet activation. Presentation plasma β-TG and PF4 concentrations did not differ from control values, probably due to the opposing effects of decreased circulating platelet mass and increased activation. By contrast, admission concentrations of TSP in the surviving patients were markedly lower (p < 0.001) than those of the controls; β-TG/PF4 ratios, but not TSP levels, returned to normal during treatment. Hepatic dysfunction and oliguric renal failure probably contributed to a sustained increase in plasma β - TG and TSP in the 2 fatally ill patients, but associated elevated PF4 levels indicated concomitant platelet activation. Our results support the suggestion that in vivo platelet activation, which appears to be rapidly controlled by treatment, occurs in patients with severe, non-fatal falciparum malaria. TSP production, apparently from non-platelet sources, was decreased and/or its consumption was increased in these patients, perhaps by factors such as cytoadherence of infected erythrocytes and consequent endothelial damage.     

In-vivo Platelet Activation and Anomalous Thrombospondin Levels in Severe Falciparum Malaria

To investigate in vivo platelet function in acute falciparum malaria plasma concentrations of β-thromboglobulin (β-TG), platelet factor 4 (PF4) and thrombospondin (TSP) were determined in 10 severely-ill Thai patients and 11 healthy volunteers. 8 patients recovered. At presentation, the platelet counts of the 10 patients were significantly lower (p < 0.025) than those of the controls, and a slight but significant increase (p < 0.05) in β-TG/PF4 ratios in the patients suggested low-grade platelet activation. Presentation plasma β-TG and PF4 concentrations did not differ from control values, probably due to the opposing effects of decreased circulating platelet mass and increased activation. By contrast, admission concentrations of TSP in the surviving patients were markedly lower (p < 0.001) than those of the controls; β-TG/PF4 ratios, but not TSP levels, returned to normal during treatment. Hepatic dysfunction and oliguric renal failure probably contributed to a sustained increase in plasma β - TG and TSP in the 2 fatally ill patients, but associated elevated PF4 levels indicated concomitant platelet activation. Our results support the suggestion that in vivo platelet activation, which appears to be rapidly controlled by treatment, occurs in patients with severe, non-fatal falciparum malaria. TSP production, apparently from non-platelet sources, was decreased and/or its consumption was increased in these patients, perhaps by factors such as cytoadherence of infected erythrocytes and consequent endothelial damage.     

Exercise induces in vivo platelet activation in patients with coronary artery disease and in healthy individuals

Recently, conflicting results have been published about a possible relationship between platelet activity and exercise-induced myocardial ischemia. The present study was performed to investigate platelet behavior during a graded symptom-limited bicycle ergometer test both in relation to the intensity of exercise and to exercise-induced myocardial ischemia. Plasma concentrations of platelet factor 4 (PF4) and beta-thromboglobulin (beta-TG) were measured by radioimmunoassays in 53 patients who had had acute myocardial infarction 10 weeks before the study and, for comparison, in 9 healthy individuals. In the whole group of the 53 patients there was no significant alteration in platelet-specific proteins during exercise, whereas physical activity induced a 2- to 3-fold increase in beta-TG and PF4 levels in the controls. However, on differentiation of the patients as to their individual exercise performance, significant exercise-associated platelet activation was demonstrable in those who reached more than 75% of their calculated maximal working capacity, whereas no correlation was found between platelet activity and exercise-induced myocardial ischemia. Thus, the results from this study indicate that in vivo platelet activation is a physiological phenomenon which occurs when a certain degree of physical intensity is exceeded, independent of the precipitation of myocardial ischemia.     

Comparison of platelet function during exercise in normal subjects and coronary artery disease patients: Potential role of platelet activation in myocardial ischemia

Platelet function parameters as influenced by exercise stress were evaluated in 22 patients with coronary artery disease (CAD) and in 13 normal subjects. Upon exercise stress, 14 CAD patients exhibited positive tests and eight exhibited negative tests. Platelet counts during exercise increased similarly in normal and CAD patients. Platelet aggregation response to ADP was unaffected by exercise both in normal and CAD patients. Platelets from 7 of the 14 CAD patients with positive stress tests had increased sensitivity to endoperoxide analog (U-46619) defined as less than 200 ng/ml U-46619 required for 50% platelet aggregation. Resting plasma beta-thromboglobulin (B-TG) levels, an index of in vivo platelet activation, were significantly higher in CAD patients compared to normal subjects (74 +/- 7 and 41 +/- 5 ng/ml, respectively; p less than 0.02). During exercise plasma B-TG levels increased in normal subjects to 60 +/- 5 ng/ml. In contrast, B-TG levels increased to 102 +/- 14 ng/ml in CAD patients (p less than 0.01 compared to normal subjects). These increases were transient and B-TG declined to preexercise values soon after exercise. Eleven of the 12 CAD patients with positive exercise stress tests had increases in plasma B-TG levels, whereas only three of the eight CAD patients with negative stress tests had any increase. These observations of increased platelet activation in certain CAD patients during exercise may be related to exercise-induced myocardial ischemia.     

Effect of amlodipine on exercise-induced platelet activation in patients affected by chronic stable angina.

BACKGROUND: Literature concerning exercise-induced platelet activation in chronic stable angina is somewhat confusing. The reason lies in the type of exercise as well as in methodological problems. A powerful, recently introduced procedure to detect platelet activation is flow cytometry. Platelet response to activating factors is mediated by calcium uptake; however, calcium antagonist effect on platelet activity is still unclear. HYPOTHESIS: The study was undertaken to investigate exercise-induced platelet activation before and after treatment with amlodipine in chronic stable angina. METHODS: Twenty patients with chronic stable angina were entered into the study. Each subject underwent a symptom-limited cycloergometer stress test following a washout period of 2 weeks. Blood samples were collected before and immediately after exercise. All subjects were then randomized into two groups of 10 patients each, with Group 1 and Group 2 taking amlodipine 10 mg/day, and placebo for 4 weeks, respectively. They subsequently underwent a second exercise stress test, and blood samples were obtained before and immediately after exercise. Flow-cytometric evaluation of platelet activity was performed in order to recognize GMP-140 expression on platelet membrane. RESULTS: Strenuous exercise induced a significant increase in platelet activation in all subjects prior to therapy. No significant differences were observed in platelet activity at rest between Groups 1 and 2, whereas a significant decrease in exercise-induced platelet activation was demonstrated in Group 1 compared with Group 2. CONCLUSION: Our data provide evidence of the favorable effect of amlodipine on exercise-induced platelet activation in patients affected by chronic stable angina.     

A prospective study of haemostatic parameters in relation to the clinical course of myeloproliferative disorders

Abstract: Platelet function and the clinical course of the disease were prospectively investigated in 29 patients with myeloproliferative disorders. Serial determinations (median: 5 investigations per patient within 17 months) of platelet aggregation, plasma and intraplatelet concentrations of β-thromboglobulin (βTG) and platelet factor 4 (PF4), and of fibrino-peptide A (FPA) plasma levels were carried out. In the chronic phase of polycythaemia vera, patients with thrombohaemorrhagic complications during the study period had higher platelet count, more severe platelet aggregation defects, and increased plasma levels of βTG and FPA compared to patients without complications. However, thrombohaemorrhagic complications were not predicted by changes in these parameters in the individual patient during the chronic disease phase. When patients with chronic myelogenous leukaemia entered blast crisis, bleeding complications were related to thrombocytopenia, impaired platelet function and low intraplatelet concentrations of βTG and PF4. Cytoreduction by chemotherapy in the chronic phase of CML did not alter βTG and PF4 plasma levels, whereas treatment of polycythaemia rubra vera by venesection favourably influenced platelet α-granule secretion and increased intraplatelet concentrations of βTG and PF4.     

Myocardial infarct of effort with normal coronaries. Study of in vivo platelet activation

Platelet activation may play a part in causing myocardium infarction with angiographically normal coronary arteries. We investigated this possibility by performing ergometric stress testing in a series of 9 patients (Group A) who had suffered myocardial infarction after a violent effort with angiographically documented coronary insufficiency responsible for a stable effort angina (Group B) and 11 healthy subjects (Group C). Blood samples were taken separately before exercise, at the peak of exercise, and during the recovery period. Platelet morphology, a sensitive indication of the degree of platelet activation, was studied by phase contrast microscopy after immediate fixation of the blood. The percentage of non-discoidal platelets presenting with one or several spicules was measured. At the same time, the plasma concentrations of platelet factor 4 (PF4) and beta-thromboglobulin (beta-TG) were measured. At rest, there was no difference in platelet morphology or specific platelet proteins between the 3 groups. At the peak effort, there was a significant increase of the number of morphologically modified platelets in Groups A and B but not in healthy subjects. This platelet activation could not be linked to the presence of myocardial ischaemia because it was found both in patients with a negative maximal exercise stress test (Group A). Finally, no increase of the plasma concentrations of the platelet protein was observed in any of the groups.     

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.     

Effects of a selective thromboxane synthetase inhibitor (OKY-046) in patients with coronary artery disease during exercise

We studied the levels of thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), platelet aggregability, beta-thromboglobulin and platelet factor 4 in 30 coronary artery disease (CAD) patients and 21 normal subjects during exercise. During treadmill exercise, 13 of 30 CAD patients reported chest pain. We administered a selective thromboxane synthetase inhibitor (OKY-046) for 2 weeks to 10 CAD patients with exercise-induced chest pain and studied its effects. At rest, the plasma TXB2 levels and platelet aggregation were significantly lower in normal subjects than in CAD patients, and there was no difference between CAD patients with and without exercise-induced chest pain. On treadmill testing, plasma TXB2 levels and platelet aggregation increased significantly only in the CAD patients with exercise-induced chest pain. Plasma 6-keto-PGF1 alpha levels in normal subjects were significantly higher than those in CAD patients both at rest and during exercise. After administration of OKY-046, mean exercise time increased significantly from 7.5 to 8.6 min (p less than 0.001). Plasma TXB2 level and platelet aggregation decreased significantly after OKY-046 administration both at rest and during exercise. These results suggest that a marked increase in TXA2, with only a minimal change in PGI2, during exercise may contribute to exercise-induced myocardial ischemia, and that OKY-046 is useful in the treatment of CAD patients.     

Heparin-releasable platelet factor 4 in patients with coronary artery disease.

Recently, platelet factor 4 (PF4) release by heparin (heparin-releasable PF4) has been examined as a useful marker of the interaction between the substances liberated from circulating platelets and the vascular endothelium. We compared the plasma levels of PF4 and beta-thromboglobulin (beta-TG) after intravenous heparin injection in patients with coronary artery disease (CAD) and normal control subjects. We also studied the effects of low-dose aspirin (81 mg/day) on the plasma level of heparin-releasable PF4 in the CAD patients. Blood samples were obtained before and 5 min after the intravenous injection of heparin (1,000 IU) from 23 patients with CAD and 15 normal control subjects. Although the plasma beta-TG level remained unchanged after heparin injection, the plasma PF4 level markedly increased in both groups. There was a significant difference in plasma PF4 levels at 5 min after heparin injection between the CAD group (100.1 +/- 38.1) and the control group (61.0 +/- 24.0) (p less than 0.01). The PF4/beta-TG ratio after heparin injection was also higher in the CAD group than in the control group (p less than 0.01). There was a correlation between the PF4/beta-TG ratio after heparin and the Gensini CAD score, which defines the severity of coronary atherosclerosis (r = 0.489, n = 23, p less than 0.01). Low-dose aspirin was administered to 11 CAD patients for 246.0 +/- 28.8 days. Blood samples for the assay of PF4 and beta-TG were obtained as stated above, and platelet aggregation, thromboxane B2 (TxB2), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) levels were also measured before and during aspirin administration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reproducibility and treatment of exercise-induced ventricular tachycardia

Fourteen patients with exercise-induced ventricular tachycardia (VT) underwent serial treadmill testing, and those with reproducible arrhythmia were treated with a β-adrenergic blocking agent. In 11 patients (79%), VT of similar rate, morphologic characteristics and duration was reproduced on 2 consecutive treadmill tests performed 1 to 14 days apart. Beta blockade prevented recurrent VT during acute testing in 10 of 11 patients and during chronic therapy in 9. Eight patients had a consistent relation between a critical sinus rate and the onset of VT. In these patients, successful therapy correlated with preventing achievement of the critical sinus rate during maximal exercise. Thus, serial exercise testing is an appropriate means of assessing efficacy of therapy in patients with exercise-induced VT, provided that reproducibility is established on 2 control tests before beginning treatment. Therapy with β-blocking agents is effective, especially when guided by the presence of a critical sinus rate-VT relation.     

Relationship of Platelet Specific Proteins and Other Factors to Atherosclerosis in Various Stages of Hypertension

There is considerable evidence from previous studies that platelets play an important role in the development and progression of atherosclerosis in hypertension, more so in relation to the stage of hypertension. Seventy one hypertensive patients (WHO stage I: 39, stage II: 23, stage III: 9) aged 19–84 (mean age: 56, normal controls in this study 59 and 62 respectively for each stage) and 37 aged 22-72 with a mean age of 52) were involved Hematocrit, beta-thromboglobulin (β-TG), platelet factor 4 (PF4), β-TG/PF4 ratio, total cholesterol (TC), low density lipoprotein-C, and triglycerides were higher in the hypertensive group while platelet count, circulating platelet aggregates, and high density lipoprotein-C were higher in the normotensive group. Among the hypertensives, stage I11 patients showed the highest β-TG, PF4, β-TG/PF4 ratio, triglycerides, and stage I with the least elevation. There were no significant differences noted in the ADP or epinephrine-induced platelet aggregation in both the normal and hypertensive patients. Other parameters such as heart rate, serum sodium, potassium, renal and liver function tests, plasma renin activity, aldosterone, fibrinogen thromboxane B and 6-Keto-PGF1jI showed no significant differences in both groups. This study clearly showed that β-TG/PF4 ratio and triglycerides are closely related to the stage of hypertension and are good indicators of in vivo platelet activation in hypertensives which may account for the acceleration of hypertensive vascular complications secondary to atherogenesis.     

Measurement of soluble C-type lectin-like receptor 2 in human plasma

Detection of platelet activation in vivo is useful to identify patients at risk of thrombotic diseases. Platelet factor 4 (PF4) and β-thromboglobulin (β-TG) are used for this purpose; however, they are easily released upon the minimal platelet activation that occurs during sampling. Soluble forms of several platelet membrane proteins are released upon platelet activation; however, the soluble form of C-type lectin-like receptor 2 (sCLEC-2) has not yet been fully investigated. Western blotting with an anti-CLEC-2 antibody showed that sCLEC-2 was released from washed human platelets stimulated with collagen mimetics. To detect sCLEC-2 in plasma, we established a sandwich enzyme-linked immunosorbent assay (ELISA) using F(ab′)2 anti-CLEC-2 monoclonal antibodies. Although plasma mixed with citrate, adenosine, theophylline and adenosine (CTAD) is needed for the PF4 and β-TG assays, effects of anti-coagulants (EDTA, citrate and CTAD) on the sCLEC-2 ELISA were negligible. Moreover, while special techniques are required for blood sampling and sample preparation for PF4 and β-TG assay, the standard blood collections procedures used in daily clinical laboratory tests have shown to suffice for sCLEC-2 analysis. In this study, we found that two forms of sCLEC-2 are released after platelet activation: a shed fragment and a microparticle-bound full-length protein, both of which are detected by the sCLEC-2 ELISA. The average concentration of sCLEC-2 in the plasma of 10 healthy individuals was 97?±?55?pg/ml, whereas that in the plasma of 25 patients with diabetes mellitus (DM) was 149?±?260?pg/ml. A trend towards an increase in sCLEC-2 concentration in the DM patients may reflect in vivo platelet activation in the patients, suggesting that sCLEC-2 may have clinical significance as a biomarker of in vivo platelet activation.     

Platelet Activation in Response to Phlebotomy

ABSTRACT. Plasma concentrations of β-thromboglobulin (BTG) and platelet factor 4 (PF4) were measured in three consecutive blood samples from 29 healthy male blood donors. The first sample was collected after 15 min of rest, the second immediately after a phlebotomy of 450 ml blood and the third after a further 15 min of rest. The mean baseline plasma BTG and PF4 values were 68 × 5 and 13.8 ± 0.7 ng/ml, respectively. The second sample's mean plasma values of these two platelet-specific proteins were significantly higher (88 ± 9 and 24.1 ± 4.1 ng/ml, respectively). The plasma concentrations of BTG and PF4 in the last sample, however, had returned to baseline levels. It is concluded that significant but short-lasting platelet activation and secretion take place in healthy subjects in response to an acute but comparatively mild blood loss even though the platelets do not participate in the process of hemostasia.     

冠心病患者纤溶活性、血小板功能及内皮素在运动前后的变化及其临床意义

目的研究冠心病患者在运动前后纤溶活性、血小板活化状态及血管内皮功能的变化。方法根据冠状动脉造影结果，选择冠心病患者（ＣＨＤ组）３７例，分为单支及多支病变组；另选健康人２７例为对照组（Ｃ组）。采用次极量运动试验观察上述部分指标在运动前后的变化。结果（１）运动前，组织型纤溶酶原激活剂（ｔＰＡ）、纤溶酶原激活剂抑制因子１（ＰＡＩ１）活性、血浆５羟色胺（５ＨＴ）水平及血小板５ＨＴ２Ａ受体密度，ＣＨＤ组均高于Ｃ组（Ｐ＜０．０５）；血浆内皮素（ＥＴ）１浓度两组差异无显著性（Ｐ＞０．０５）。（２）运动后，ＣＨＤ组ｔＰＡ活性下降（Ｐ＜０．０５），ＰＡＩ１活性上升（Ｐ＜０．０２５）；血浆５ＨＴ水平及血小板５ＨＴ２Ａ受体密度增加（Ｐ＜０．０５）；血浆ＥＴ１浓度上升，与Ｃ组比较差异有显著性（Ｐ＜０．０５）。上述各指标的增高，多支病变组较单支病变组明显（Ｐ＜０．０１～０．００５）。（３）运动前仅ＰＡＩ１活性与心肌缺血面积呈正相关（ｒ＝０．４５２，Ｐ＜０．００５）。结论冠心病患者纤溶活性下降，血小板激活，血管内皮受损，使冠心病患者易发生冠状动脉痉挛及血栓形成。次极量运动使之进一步加重而易诱发冠心病事件。     

Platelet activation indices and apolipoproteins in hypertensive patients

We have studied the platelet activation indices beta-thromboglobulin (beta-TG and platelet factor 4(PF4), triglycerides (TG), total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL) and apolipoprotein (A1, A2, B, C2, C3, E) profiles of 22 untreated essential hypertensive subjects (WHO stages 1 and 2) and 22 controls, to see if there might be some causal relationship between lipoprotein abnormalities and greater platelet activation. The results showed the patients had both greater platelet activation than the controls, as demonstrated by higher plasma beta-TG levels (P less than 0.01) and lower apolipoprotein A2 levels (P less than 0.05). However there were no significant correlations between the platelet activation indices and the plasma levels of apolipoproteins, lipoproteins or lipids in either group.     

Exercise-induced myocardial ischemia in patients with coronary artery disease: lack of evidence for platelet activation or fibrin formation in peripheral venous blood

The hypothesis that exercise-induced myocardial ischemia is associated with abnormal platelet activation and fibrin formation or dissolution was tested in patients with coronary artery disease undergoing upright bicycle stress testing. In vivo platelet activation was assessed by radioimmunoassay of platelet factor 4, beta-thrombo-globulin and thromboxane B2. In vivo fibrin formation was assessed by radioimmunoassay of fibrinopeptide A, and fibrinolysis was assessed by radioimmunoassay of thrombin-increasable fibrinopeptide B which reflects plasmin cleavage of fibrin I. Peripheral venous concentrations of these substances were measured in 10 normal subjects and 13 patients with coronary artery disease at rest and during symptom-limited peak exercise. Platelet factor 4, beta-thromboglobulin and thromboxane B2 concentrations were correlated with rest and exercise catecholamine concentrations to determine if exercise-induced elevation of norepinephrine and epinephrine enhances platelet activation. Left ventricular end-diastolic and end-systolic volumes, ejection fraction and segmental wall motion were measured at rest and during peak exercise by first pass radionuclide angiography. All patients with coronary artery disease had documented exercise-induced myocardial ischemia manifested by angina pectoris, ischemic electrocardiographic changes, left ventricular segmental dyssynergy and a reduction in ejection fraction. Rest and peak exercise plasma concentrations were not significantly different for platelet factor 4, beta-thromboglobulin, thromboxane B2, fibrinopeptide A and thrombin-increasable fibrinopeptide B. Peripheral venous concentrations of norepinephrine and epinephrine increased significantly (p less than 0.001) in both groups of patients. The elevated catecholamine levels did not lead to detectable platelet activation. This study demonstrates that enhanced platelet activation, thromboxane release and fibrin formation or dissolution are not detectable in peripheral venous blood of patients with coronary disease during exercise-induced myocardial ischemia.     

Enhanced platelet release reaction in insulin-dependent and insulin-independent diabetic patients

Plasma beta thromboglobulin (BTG) and platelet factor 4 (PF4) levels were measured and correlated with plasma lipid and lipoprotein patterns in 20 insulin-independent diabetics, in 10 insulin-dependent diabetics and in 30 healthy controls matched to patients as to age, sex and weight. Increased plasma BTG and PF4 levels both in insulin-dependent and in insulin-independent diabetics indicate enhanced in vivo platelet activation and release reaction in these patients. No difference in BTG and PF4 values between these two groups of diabetic patients was observed in our study. A marked correlation between plasma PF4 values and plasma glucose levels was shown in insulin-dependent diabetics only whereas a significant positive correlation with plasma triglycerides and plasma triglyceride VLDL and a negative correlation with cholesterol-HDL was shown in insulin-independent diabetics.     

Platelet function during the acute phase of dengue hemorrhagic fever

Platelet aggregation, plasma betathromboglobulin (BTG) and platelet factor 4 (PF4) were studied in 35 children with dengue hemorrhagic fever. The suppression of platelet aggregation was demonstrated during acute phase of DHF in both shock and non-shock patients. Simultaneous with abnormal platelet aggregation, there was increased release of BTG and PF4 from platelets into plasma during the acute phase which lasted only 3-4 days after shock or subsidence of fever. Acute phase plasma during DHF infection was also shown to have a stimulatory effect on the aggregation of autologous platelets. In this study we showed that there was an increase in platelet secretory activity of BTG and PF4 along with an impairment of the platelet aggregation during acute phase of DHF.     

The immediate effect of aerobic exercise on haemostatic parameters in patients with recently diagnosed mild to moderate essential hypertension

Background Exercise is frequently recommended for the treatment of patients with arterial hypertension. Previous studies have shown an enhanced coagulation state after exercise. Our study investigates the alterations observed after a single session of submaximal aerobic exercise concerning coagulation, fibrinolysis, platelet activation as well as endothelial function in patients with recently diagnosed essential hypertension. Methods Twenty non-diabetic patients with recently diagnosed essential hypertension participated in a 45 min submaximal exercise test on a bicycle ergometer. Blood samples were drawn before and after exercise in order to determine parameters of coagulation activation (Prothrombin time [PT], activated Partial Thromboplastin time [aPTT], fibrinogen, D-Dimers, prothrombin fragments 1 + 2 [PF1+2], thrombin-antithrombin III complex [TAT] and factors VII, VIII and XII), platelet activation (Platelet count, Platelet factor 4 [PF4] and β-thromboglobulin [β-TG]), fibrinolysis activation (Plasmin-a₂ antiplasmin complex, PAP) and endothelial function (soluble Thrombomodulin [sTM] and von Willebrand factor [vWf]). Soluble P-selectin served as a marker for endothelial and platelet activation. Results All patients completed the exercise test. aPTT (P < 0.001) and factor VII (P = 0.01) significantly decreased while PT (P = 0.04), fibrinogen (P = 0.008), factor VIII (P < 0.001), platelet count (P = 0.002) and β-TG levels (P = 0.01) significantly increased as a result of exercise. Compared to baseline there was an 11% increase in TAT (P = 0.04) and a 28% increase in PAP (P < 0.001) at peak exercise. One hour post exercise, there was a 43% increase in PAP whereas TAT levels became similar to those at baseline. Additionally vWf (P = 0.01) and sP-selectin (P = 0.02) levels significantly increased throughout the exercise protocol. Conclusions Patients with recently diagnosed and never treated mild to moderate essential hypertension undergoing submaximal aerobic exercise present evidence of enhanced fibrinolysis compared with a mild increase of coagulation indices. However, whether there is a favourable effect of exercise on fibrinolysis over coagulation and/or endothelial involvement during exercise needs to be further investigated.