In Vivo Platelet Activation Following Myocardial Infarction and Acute Coronary Ischaemia

1982 ◽  
Vol 48 (02) ◽  
pp. 133-135 ◽  
Author(s):  
A Hughes ◽  
S Daunt ◽  
G Vass ◽  
J Wickes
Keyword(s):  
Myocardial Infarction ◽  
Chest Pain ◽  
Acute Chest Pain ◽  
Normal Subjects ◽  
Specific Protein ◽  
Control Group ◽  
Platelet Activity ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates

SummaryForty-seven patients presenting with acute chest pain had in vivo platelet activity assessed by measuring plasma levels of the platelet-specific protein beta thromboglobulin (BTG), and by screening for the presence of circulating platelet aggregates. Nineteen patients with transmural myocardial infarction (MI), 21 patients with acute coronary ischaemia (CI), and 7 patients with non-cardiac chest pain (NCCP) were investigated in a serial study and compared with a normal control group. The means of all BTG determinations in the MI (34, ± SD = 21-57) and CI (33, ± SD = 19-57) groups were significantly higher than those in the NCCP group (24, ± SD = 17-34; p Ã0.01) and normal subjects (22,5, ± SD = 14-37; p Ã0.001). There was no difference in BTG between those with MI or CI, nor between the NCCP group and normal subjects. Raised numbers of circulating platelet aggregates could not be detected in either MI or CI. The mean BTG levels in both MI and CI patients were significantly raised, compared to normal subjects, on the first day of admission to hospital and remained so on each of the subsequent nine days. Neither heparin plus warfarin nor sulphinpyrazone had any significant effect in lowering BTG levels. 15/40 patients (37.5%) following MI and CI had repeatedly raised BTG levels throughout the study period, and it is suggested that these patients represent an “at risk” group that may benefit from anti-platelet therapy in secondary prevention studies.

scholarly journals Do patients with thromboembolic disease have circulating platelet aggregates?

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 205-209 ◽  
Author(s):  
FH Kohanna ◽  
MH Smith ◽  
EW Salzman
Keyword(s):  
Platelet Rich Plasma ◽  
Venous Blood ◽  
Adenosine Diphosphate ◽  
Normal Subjects ◽  
Thromboembolic Disease ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Lower Ratio

Reports of circulating platelet aggregates (ie, microemboli) in thromboembolism and other vascular disorders are based on a method (Wu and Hoak , 1974) in which venous blood is collected via scalp vein needle and tubing into either formaldehyde, which fixes aggregates, or EDTA, which disperses them. The ratio of platelet counts in platelet- rich plasma (PRP) from the two blood samples after centrifugation is interpreted as a measure of platelet aggregates in the circulation in vivo. We compared this standard Wu and Hoak technique with a modified one, in which blood was drawn directly into a syringe, and with a third method that avoided centrifugation by counting single platelets in whole blood. Both modified techniques could detect aggregates generated in vitro with adenosine diphosphate (ADP). In 12 normal subjects, the three methods were equivalent, but in 37 patients with thromboembolic disorders, the standard Wu and Hoak method gave a lower ratio than the other methods. Similar results were found in a subset of eight patients with myocardial infarction. Heparin treatment of patients did not influence the results. The data suggest that formation of platelet aggregates occurred during venipuncture. Platelets may be hyperactive in patients with thromboembolic disease and may form aggregates in vitro during collection, but the concept of chronic microembolism in such patients should be reassessed.

Detection of Circulating Platelet Aggregates in Thrombo-Embolic Disease

1979 ◽  
Author(s):  
Marie Scrobohaci ◽  
Teodora Petrilă ◽  
M. Constantinescu ◽  
Magdolnra Stadler ◽  
Doina Mihšilă ◽  
...  
Keyword(s):  
Body Weight ◽  
Normal Subjects ◽  
Experimental Conditions ◽  
Aggregation Index ◽  
Leriche Syndrome ◽  
Circulating Platelet Aggregates ◽  
Valvular Diseases ◽  
Platelet Aggregates ◽  
Iliac Occlusion

SummaryThe method of Wu and Hoak in determining circulating platelet aggregates in vivo was used.In different cardiac and vascular states, a low aggregation index is found: aorto-iliac occlusion(Leriche syndrome)- 38 cases(index X ± SD 0.52 ±0.05 in comparison with normal subjects 0.91± 0.05):valvular diseases - 24 cases (0.40±0.006); during extracorporeeal circulation- 14 cases(0. 5±0.021) ; thrombophlebitis-25 cases(0.84±0.065).After an antiaggregation treatment(Dipiridamol) in 12 cases of aorto - iliac ocdusion the value of the aggregation index normalised(0.84±0.065) Experimentally, lo rabbits were perfused with thrombin so ution(2 u./body weight k.);the lower values of the aggregation index(0.91±0.085 before and 0.43±0.035 after the thrombin perfusion) prove the fidelity of the method.The simplicity of the technique, the reproductibility in experimental conditions and the normalisation of the values after treatment prove the practical value in determining the circulating platelet aggregates.

Beta Thromboglobulin and Myocardial Infarction

1979 ◽  
Author(s):  
A. Hughes ◽  
S. Daunt ◽  
G. Vass ◽  
J. Wickes
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Chest Pain ◽  
Myocardial Ischaemia ◽  
Normal Population ◽  
Acute Chest Pain ◽  
Specific Protein ◽  
Normal Individuals ◽  
Significant Difference ◽  
Secondary Phenomenon

Beta thromboglobulin. a platelet specific protein liberated during the release reaction, has been measured in normal individuals (n=285),and in patients presenting with acute chest pain. The latter group consisted of those with acute myocardial infarction (n=19),those with acute myocardial ischaemia (n=21),and those with chest pain of non cardiac origin (n-7). In the patient groups beta thromboglobulin was measured on admission to hospital, and thereafter daily until the patient was discharged. There was no significant difference between the normal population (mean 22.5 ng/ml),and the patients with with non cardiac chest pain (mean .24 ng/ml). There was a significant difference between the normal population and the patients with acute myocardial infarction (mean 34 ng/ml),and acute myocardial ischaemia (mean 33 ng/ml), p<0.001. There was also a significant difference between these two groups and the patients with non cardiac chest pain, p<0.01.We would conclude that platelet activation occurs in acute myocardial infarction and ischaemia, but it is not clear if this is a primary or a secondary phenomenon.

scholarly journals Lipid Profile of Patients with Acute Myocardial Infarction and its Correlation with Systemic Inflammation

2013 ◽  
Vol 8 ◽  
pp. BMI.S11015 ◽  
Author(s):  
Haseeb A. Khan ◽  
Abdullah S. Alhomida ◽  
Samia H. Sobki
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Chest Pain ◽  
Lipid Profile ◽  
Systemic Inflammation ◽  
Density Lipoprotein ◽  
Normal Subjects ◽  
Lipoprotein Cholesterol ◽  
Control Group ◽  
Hs Crp

The biomarker potential of using various lipids fractions for predicting risk of acute myocardial infarction (AMI) is controversial. We therefore compared the lipid profiles, including serum total cholesterol (TC), low-density lipoprotein cholesterol (LDL), high-density lipoprotein cholesterol (HDL) and triglycerides (TG), in 67 AMI patients. Patients included 28 STEMI (ST-elevated myocardial infarction) patients, 39 NSTEMI (non-ST-elevated myocardial infarction) patients and 25 patients with chest pain. Control group included 54 age- and gender-matched normal subjects. We also studied the correlation between lipid profile and systemic inflammation in these subjects. There were significant decreases in TC, LDL and HDL levels in both STEMI and NSTEMI patients as compared to normal subjects; however, patients with chest pain did not show any significant change in these lipids. Serum TG levels did not differ significantly among the study groups. There were significant increases in serum high-sensitive C-reactive protein (hs-CRP) levels in STEMI and NSTEMI patients, as compared to control group. Serum hs-CRP showed significant inverse correlation with HDL; however, hs-CRP was not correlated with TC, LDL, and TG. In conclusion, our findings suggest that reduction in serum TC does not prevent the risk of AMI, whereas a decrease in serum HDL and increase in hs-CRP strongly predisposes the risky individuals to an AMI event. We emphasize the importance of HDL and CRP measurements for the assessment of a combined lipid-inflammation risk factor that could be a useful predictor of high risk individuals, as well as a prognostic marker in AMI patients.

scholarly journals Do patients with thromboembolic disease have circulating platelet aggregates?

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 205-209 ◽  
Author(s):  
FH Kohanna ◽  
MH Smith ◽  
EW Salzman
Keyword(s):  
Platelet Rich Plasma ◽  
Venous Blood ◽  
Adenosine Diphosphate ◽  
Normal Subjects ◽  
Thromboembolic Disease ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Lower Ratio

Abstract Reports of circulating platelet aggregates (ie, microemboli) in thromboembolism and other vascular disorders are based on a method (Wu and Hoak , 1974) in which venous blood is collected via scalp vein needle and tubing into either formaldehyde, which fixes aggregates, or EDTA, which disperses them. The ratio of platelet counts in platelet- rich plasma (PRP) from the two blood samples after centrifugation is interpreted as a measure of platelet aggregates in the circulation in vivo. We compared this standard Wu and Hoak technique with a modified one, in which blood was drawn directly into a syringe, and with a third method that avoided centrifugation by counting single platelets in whole blood. Both modified techniques could detect aggregates generated in vitro with adenosine diphosphate (ADP). In 12 normal subjects, the three methods were equivalent, but in 37 patients with thromboembolic disorders, the standard Wu and Hoak method gave a lower ratio than the other methods. Similar results were found in a subset of eight patients with myocardial infarction. Heparin treatment of patients did not influence the results. The data suggest that formation of platelet aggregates occurred during venipuncture. Platelets may be hyperactive in patients with thromboembolic disease and may form aggregates in vitro during collection, but the concept of chronic microembolism in such patients should be reassessed.

scholarly journals Experimental Study of a platelet Antiaggregating Agent - Application to Ticlopidine

1977 ◽  
Author(s):  
J.F. Stoltz ◽  
M. Verry ◽  
B. Farge
Keyword(s):  
Arterial Disease ◽  
Biochemical Properties ◽  
Control Group ◽  
Group Index ◽  
Aggregation Index ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Definition Of ◽  
Induced Aggregation

The authors consider the various methods suitable for in vivo study of the anti-aggregating properties of a new drug - Ticlopidine :- study of photometric ADP-induced aggregation and screen filtration pressure in vivo in the rabbit treated per os for 5 days with doses of 25 and 50 mg/kg/d. This gave average inhibitions of 30% and 45% respectively.- study of circulating platelet aggregates using the method of Wu and Hoak after continuous infusion of ADP or of thrombin. The principle of the method involves definition of an aggregation index : the ratio between the platelet counts in the two specimens (EDTA + formol 1 % + EDTA alone).The average results showed : control group index 0.9 -after infusion of ADP 0.57- after infusion of ADP under the influence of Ticlopidine (50 and 100 mg/kg/d) 0.66 to 0.78.- the mechanism of action of the drug was studied using crossed aggregation experiments and by the study of interference with ionised or ionisable groups of the platelet membrane (isotope method, electrophoresis in liquid phase).In parallel with these experiments, studies in vivo in the rabbit and in patients (obliterative arterial disease, Raynaud’s syndrome) are in progress : interference with membrane groups, rheological properties (viscosity, rouleau formation, erythrocyte deformability) and biochemical properties (erythrocyte glycolysis enzymes).

Detection of Circulating Platelet Aggregates in Thromboembolic Disease

1979 ◽  
Author(s):  
Lorène Scrobohaci Marie ◽  
Teodora Petrilǎ ◽  
M. Constantinescu ◽  
Magdolna Stadler ◽  
Doina Mihǎilǎ ◽  
...  
Keyword(s):  
Normal Subjects ◽  
Thromboembolic Disease ◽  
Experimental Conditions ◽  
Aggregation Index ◽  
Leriche Syndrome ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Aortoiliac Occlusion ◽  
Iliac Occlusion

Summary: The method of Wu and Hoak in det rmining circulating platelet aggregates in vivo was used.In different cardiac and vascular states, a low aggregation index is found: aorto-iliac occlusion (Leriche syndrome)- 38 csses(index X ± SD 0.52 ± 0.05 in comparison with normal subjects 0.91 ± 0.05); valvular diseasses (0.40±0.006); during extracorporeeal circulation - 14 cases (0.5±0.02l); thrombophlebitia-25 casea(0.84±0.065).After an antiaggaagation treatment (Dipiridamol) in 12 cases of aortoiliac occlusion the value of the aggregation index normalised(0.84±0.065) Experimenntlllly, 10 rabbits were perfused wi th thrombin soution (2 u./body woight k.); the lower values of the aggreeation index (0.91±0.085 brfore Emd 0.43±0.035 after the thromhin perfuaion) prove the fidelity of the method.The simplicity of the technique, the reproducti bili ty in experimental conditions and the normalisation of the valuwa after treatment prove the practical value in determining the circulating platelet aggregates.

Low Affinity Platelet Factor 4/β-Thromboglobulin (LA-PF4/βTG) Antigen And Circulating Platelet Aggregates During Prostacyclin (PGI2) Therapy

1981 ◽  
Author(s):  
J Musiat ◽  
A Szczeklik ◽  
R Nizankowski
Keyword(s):  
Protein A ◽  
Serum Levels ◽  
Specific Protein ◽  
Intraarterial Infusion ◽  
Platelet Factor ◽  
Arteriosclerosis Obliterans ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Ischemic Ulcers

We have found that continuous intraarterial infusion of PGI2 alleviates rest pain and promotes healing of ischemic ulcers in patients with advanced arteriosclerosis obliterans. Since these effects could be related to the anti-platelet actions of prostacyclin, we studied serum levels of the platelet specific protein, a possible marker of platelet activation in vivo, named LA-PF4/βTG, and compared it with those of serum circulating platelet aggregates. The former was assessed by radioimmunoassay, the latter by method of Wu and Hoak. Determinations were carried out in 16 patients with arteriosclerosis obliterans, initially and during the second day of intraarterial infusion of PGI2 in a mean dose of 6 n9/kg/min. This therapy led to an almost uniform fall in circulating platelet aggregates. In contrast, levels of LA-PF4/β-TG antigen at the beginning of second day or the infusion /mean = 19.19 ng/ml, ± S.D. a 8.97/ did not differ significantly from the initial values /mean = 23.59 ng/ml, ± S.D. = 13.12/.In conclusion: 1/ In our patients vascular disease did not produce any apparent increase in serum LA-PF4/β-TG antigen levels; 2/ Infusions of PGI2 did not affect basal levels of this platelet specific protein, while it markedly depressed the percent of circulating platelet aggregates.

Plasma Fibrinopeptide A and Beta-Thromboglobulin in Patients with Chest Pain

1983 ◽  
Vol 50 (02) ◽  
pp. 541-542 ◽  
Author(s):  
J T Douglas ◽  
G D O Lowe ◽  
C D Forbes ◽  
C R M Prentice
Keyword(s):  
Myocardial Infarction ◽  
Chest Pain ◽  
Unstable Angina ◽  
Plasma Levels ◽  
Thrombin Generation ◽  
Acute Chest Pain ◽  
Fibrinopeptide A ◽  
Control Hospital ◽  
Hospital Patients ◽  
Platelet Release

SummaryPlasma levels of β-thromboglobulin (BTG) and fibrinopeptide A (FPA), markers of platelet release and thrombin generation respectively, were measured in 48 patients within 3 days of admission to hospital for acute chest pain. Twenty-one patients had a confirmed myocardial infarction (MI); 15 had unstable angina without infarction; and 12 had chest pain due to noncardiac causes. FPA and BTG were also measured in 23 control hospital patients of similar age. Mean plasma BTG levels were not significantly different in the 4 groups. Mean plasma FPA levels were significantly higher in all 3 groups with acute chest pain when compared to the control subjects (p < 0.01), but there were no significant differences between the 3 groups. Increased FPA levels in patients with acute chest pain are not specific for myocardial infarction, nor for ischaemic chest pain.

Heparin Neutralizing Activity in the Diagnosis of Acute Myocardial Infarction

1975 ◽  
Author(s):  
J. R. O’Brien ◽  
M. D. Etherington ◽  
S. Jamieson ◽  
J. Sussex
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Chest Pain ◽  
Acute Chest Pain ◽  
Platelet Factor 4 ◽  
Clotting Time ◽  
Platelet Factor ◽  
Neutralizing Activity ◽  
Platelet Poor Plasma ◽  
Activated Platelets

We have previously demonstrated that, relative to controls, patients long after myocardial infarction and patients with atherosclerosis have highly significantly shorter heparin thrombin clotting times (HTCT) using platelet poor plasma; but there was considerable overlap between the two groups.We have now studied 89 patients admitted with acute chest pain. In 54 of these a firm diagnosis of acute myocardial infarction (ac-MI) was made and the HTCT was very short (mean 12.8 sees) and in 48 it was less than 16 sees. In 34 patients, ac-MI was excluded and the diagnosis was usually “angina”; the HTCT was much longer (mean 25.1 sees) and in 32 it was over 16 sees. Thus there was almost no overlap between these two groups. It is suggested that this test should be adopted as a quick and reliable further test to establish a diagnosis of ac-MI (providing other reasons for very short HTCTs can be excluded, e.g. D. I. C., and provinding the patient’s thrombin clotting time is normal).This HTCT measures non-specific heparin neutralizing activity; nevertheless the evidence suggests that it is measuring platelet factor 4 liberated from damaged or “activated” platelets into the plasma. These findings underline the probable important contribution of platelets in ac-MI.

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