The Quantitation of Platelet Aggregation Induced by Four Compounds: A Study in Relation to Myocardial Infarction

1966 ◽  
Vol 16 (03/04) ◽  
pp. 752-767 ◽  
Author(s):  
J. R O’Brien ◽  
F. C Path ◽  
Joan B. Heywood ◽  
J. A Heady
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Myocardial Infarct ◽  
Control Groups ◽  
The Mean ◽  
Platelet Shape

SummaryMethods for measuring and comparing day to day differences in the response of platelet aggregation in platelet-rich plasma to added ADP, 5-H.T., adrenaline and collagen are reported. Platelet aggregation induced by ADP, 5-H.T. and adrenaline was studied in patients with acute myocardial infarction and in others 3 months to 5 years after an infarct; some were receiving anti-coagulants and others not: these three groups were compared with three control groups. The mean platelet shape was rounder and the response to ADP and to 5-H.T. and one parameter of the response to adrenaline was significantly greater in all groups of patients with myocardial infarct taken together than in the controls. The platelet-rich plasma from patients with recent infarction were most responsive to ADP and 5-H.T. immediately after the infarct. Anti-coagulants had no effect on these tests. However, there was wide variation within the individuals and much overlap between groups, and these tests can only reliably distinguish between groups and not between individuals. The significance of these findings is discussed.

scholarly journals Platelet aggregation, mean platelet volume and plasma fibrinogen as risk factors for acute myocardial infarction

2018 ◽  
Vol 6 (11) ◽  
pp. 3552 ◽  
Author(s):  
Geeta Yadav ◽  
Rashmi Kushwaha ◽  
Wahid Ali ◽  
Uma S. Singh ◽  
Ashutosh Kumar ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Aggregation ◽  
Mean Platelet Volume ◽  
Screening Tools ◽  
Plasma Fibrinogen ◽  
Healthy Controls ◽  
Platelet Volume ◽  
Increased Risk ◽  
The Mean

Background: The Aim of this study was to assess the role of platelet aggregation, mean platelet volume (MPV) and plasma fibrinogen levels in the pathogenesis of acute myocardial infarction (AMI).Methods: A prospective case control study was conducted on 30 cases of AMI and 30 normal healthy age and sex matched controls. The cases and controls were investigated for platelet aggregation studies (done in platelet rich plasma (PRP) using light transmission chrono-log optical aggregometer), MPV (measured by automated cell counter) and plasma fibrinogen levels (estimated by Clauss method).Results: The mean platelet aggregation (%) in cases AMI was 57.61±11.91 which was significantly higher compared with 35.00±10.40 for healthy controls (p<0.001). Using Receiver Operating Characteristic (ROC) analysis, most patients of AMI had a platelet aggregability of ≥49% on optical aggregometry (sensitivity = 83.3 % and specificity = 93.7%). The MPV (fL) in cases of AMI was 8.04±0.39 which was significantly larger when compared with 7.67±0.43 for controls (p= 0.001). The mean plasma fibrinogen concentration in cases of AMI was 383.1±48.3mg/dl which was significantly higher when compared with 271.33±57.7mg/dl for healthy controls (p<0.001).Conclusions: Platelet hyperaggregability, elevated MPV and plasma fibrinogen levels are found in patients with AMI and contribute significantly to risk of developing coronary thrombosis. These variables should be considered as additional screening tools to identify individuals at increased risk of developing AMI.

scholarly journals Serum Magnesium in Acute Myocardial Infarction: Observation from Bangladeshi Patients

2020 ◽  
Vol 14 (2) ◽  
pp. 71-73
Author(s):  
Mohammad Rezaul Quader ◽  
Sharmin Rahman ◽  
Nasima Sultana ◽  
Suranjit Kumar Saha
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Serum Magnesium ◽  
Serum Magnesium Level ◽  
Control Groups ◽  
Mean Values ◽  
Medical College ◽  
Important Trace Element ◽  
The Mean ◽  
And Control

Dyslipidemia is an established risk factor of acute myocardial infarction (AMI), but measurement of macro metals like magnesium can be helpful in the prevention and better management of AMI. The aim of this study was to estimate serum magnesium in AMI. This is a case control type of study carried out in the Department of Biochemistry, Dhaka Medical College, Dhaka during the period of January 2015 to December 2015 with a total number of 100 study subjects. Acute myocardial infarction patients were selected as case (50) from coronary care unit (CCU), Department of Cardiology, Dhaka Medical College Hospital. Normal healthy individuals were selected as control (50) from the attendants of patients, relatives and doctors. Serum level of magnesium were assessed for both case and control groups. The mean values of the variable were compared between them by statistical analysis using SPSS version 16. For all the statistical analysis P<0.05 was considered as significant. The mean values of serum magnesium were 1.63±0.27mg/dl in cases. The mean values of serum magnesium were 2.35±0.28 mg/dl in control group. Significant differences were found in mean values between case and control groups and differences were highly significant (p<0.001). In AMI, serum magnesium level was found to be lower in this study. Serum magnesium is an important trace element that act as cofactor in many biochemical reactions. Decrease level of this important trace element may contribute to pathogenesis of AMI. So with other biochemical risk parameters, routine assessment of serum magnesium level is advocated, which might be helpful for prevention and better management of AMI. Faridpur Med. Coll. J. Jul 2019;14(2): 71-73

An Abnormal Pattern of Adenosine Diphosphate-Induced Platelet Aggregation in Acute Myocardial Infarction

1969 ◽  
Vol 21 (01) ◽  
pp. 076-088 ◽  
Author(s):  
J Zahavi ◽  
F Dreyfuss
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Coarse Aggregates ◽  
Initial Rise ◽  
Abnormal Pattern ◽  
Male Patients ◽  
Definition Of

SummaryPlatelet aggregation as induced by A.D.P. has been studied using the fragiligraph. With this instrument continuous registration for 60 min of the aggregation - disag gregation - behaviour of platelet rich plasma (P.R.P.) has become practicable and a number of parameters of the curves could then be defined and analysed. Specimens from 24 male patients with acute myocardial infarction and 14 normal controls were compared. P.R.P. of the controls exhibited a short phase of an initial rise in optical density (O.D.) lasting 10-20 sec, a phase of decreasing O.D. (5 min), pointing to platelet aggregation and a phase of disaggregation afterwards. The samples of the myocardial patients differed clearly in several aspects : in most of them (18) the initial rise in O.D. was absent and aggregation started immediately; it was though slower but reached a greater extent. The time of maximum aggregation was significantly greater in the patients and there was no overlap with the controls. Coarse aggregates were clearly visible. Final disaggregation was either minimal or absent. At a concen tration of A.D.P. 0.59 γ/ml, the aggregation curve was biphasic in most patients, whereas it was monophasic in the controls. The curves obtained were mathematically analysed including the definition of a parameter called “aggregation time”, τ, and an attempt was made to clarify several of the properties of the curves in terms of platelet behaviour.

The Clinical Usefulness of the Platelet Aggregation Test for the Diagnosis of Heparin-Induced Thrombocytopenia

1993 ◽  
Vol 69 (04) ◽  
pp. 344-350 ◽  
Author(s):  
B H Chong ◽  
J Burgess ◽  
F Ismail
Keyword(s):  
Platelet Aggregation ◽  
Heparin Therapy ◽  
Serotonin Release ◽  
Point System ◽  
Control Groups ◽  
Heparin Induced Thrombocytopenia ◽  
Heparin Concentration ◽  
Release Test ◽  
The Mean ◽  
Normal Controls

SummaryThe platelet aggregation test is widely used for the diagnosis of heparin-induced thrombocytopenia (HIT), a potentially serious complication of heparin therapy. We have evaluated its sensitivity and specificity in comparison with those of the 14C-serotonin release test. The sensitivity of the platelet aggregation test was found to vary with the heparin concentration and the donor of the platelets used in the test. The optimal heparin concentrations were between 0.1 and 1.0 U/ml. Using these heparin concentrations, the mean sensitivity varied from 39% (with the least reactive platelets) to 81% (with the most reactive platelets). In comparison, the sensitivity of the release test ranged from 65% to 94%. The specificities of the platelet aggregation test were 82%, 90% and 100% for the following control groups: (1) non-thrombocytopenic patients given heparin, (2) patients with thrombocytopenia due to other causes, and (3) normal controls not given heparin, respectively. The corresponding specificities for the release test was 94%, 90% and 100%. The specificities can be further increased to 100% for all controls with the adoption of a two-point system which defines a positive result as one in which platelet aggregation occurs with a low heparin concentration (0.5 U/ml) but not with 100 U heparin/ml. For optimal results, a two-point platelet aggregation test should be performed with heparin concentrations of 0.5 and 100 U/ml and using platelets of more reactive donors.

Influence of Acute Myocardial Infarction and rt-PA Therapy on Circulating Fibrinogen

1993 ◽  
Vol 69 (04) ◽  
pp. 321-327 ◽  
Author(s):  
E Seifried ◽  
M Oethinger ◽  
P Tanswell ◽  
E Hoegee-de Nobel ◽  
W Nieuwenhuizen
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Thrombolytic Agent ◽  
Degradation Products ◽  
Maximum Plasma ◽  
Normal Range ◽  
Fibrinogen Degradation Products ◽  
Fibrin Degradation Products ◽  
Rebound Phenomenon ◽  
The Mean

SummaryIn 12 patients treated with 100 mg rt-PA/3 h for acute myocardial infarction (AMI), serial fibrinogen levels were measured with the Clauss clotting rate assay (“functional fibrinogen”) and with a new enzyme immunoassay for immunologically intact fibrinogen (“intact fibrinogen”). Levels of functional and “intact fibrinogen” were strikingly different: functional levels were higher at baseline; showed a more pronounced breakdown during rt-PA therapy; and a rebound phenomenon which was not seen for “intact fibrinogen”. The ratio of functional to “intact fibrinogen” was calculated for each individual patient and each time point. The mean ratio (n = 12) was 1.6 at baseline, 1.0 at 90 min, and increased markedly between 8 and 24 h to a maximum of 2.1 (p <0.01), indicating that functionality of circulating fibrinogen changes during AMI and subsequent thrombolytic therapy. The increased ratio of functional to “intact fibrinogen” seems to reflect a more functional fibrinogen at baseline and following rt-PA infusion. This is in keeping with data that the relative amount of fast clotting “intact HMW fibrinogen” of total fibrinogen is increased in initial phase of AMI. The data suggest that about 20% of HMW fibrinogen are converted to partly degraded fibrinogen during rt-PA infusion. The rebound phenomenon exhibited by functional fibrinogen may result from newly synthesized fibrinogen with a high proportion of HMW fibrinogen with its known higher degree of phosphorylation. Fibrinogen- and fibrin degradation products were within normal range at baseline. Upon infusion of the thrombolytic agent, maximum median levels of 5.88 μg/ml and 5.28 μg/ml, respectively, were measured at 90 min. Maximum plasma fibrinogen degradation products represented only 4% of lost “intact fibrinogen”, but they correlatedstrongly and linearly with the extent of “intact fibrinogen” degradation (r = 0.82, p <0.01). In contrast, no correlation was seen between breakdown of “intact fibrinogen” and corresponding levels of fibrin degradation products. We conclude from our data that the ratio of functional to immunologically “intact fibrinogen” may serve as an important index for functionality of fibrinogen and select patients at high risk for early reocclusion. Only a small proportion of degraded functional and “intact fibrinogen”, respectively, is recovered as fibrinogen degradation products. There seems to be a strong correlation between the degree of elevation of fibrinogen degradation products and the intensity of the systemic lytic state, i.e. fibrinogen degradation.

Product licences and devious promotion

1990 ◽  
Vol 28 (5) ◽  
pp. 20-20
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Aggregation ◽  
Unstable Angina ◽  
Platelet Aggregation Inhibitor ◽  
Aggregation Inhibitor

Platet 300 Cleartab (Nicholas) is an effervescent buffered aspirin formulation which the maker has described as “a new cardiovascular-specific presentation of aspirin “and” the only platelet aggregation inhibitor to be licensed for use following acute myocardial infarction, or in patients with unstable angina, to reduce the risk of infarction”.

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