Platelet aggregation ratio in myocardial infarction

1978 ◽  
Vol 37 (1) ◽  
pp. 52-52 ◽  
Author(s):  
T. F. Rohrer
Keyword(s):  
Myocardial Infarction ◽  
Platelet Aggregation ◽  
Aggregation Ratio ◽  
Platelet Aggregation Ratio

Platelet Function Tests in Relation to Retinopathy and Neuropathy in Well Controlled Diabetic Patients

1979 ◽  
Author(s):  
M.A.G. Pannebakker ◽  
J.J.C. Jonker ◽  
A.C. de Boer ◽  
G.J.H. den Ottolander
Keyword(s):  
Platelet Aggregation ◽  
Threshold Concentration ◽  
Proliferative Retinopathy ◽  
Diabetic Patients ◽  
Conduction Time ◽  
Abnormal Laboratory ◽  
Normal Volunteers ◽  
The Mean ◽  
Aggregation Ratio ◽  
Platelet Aggregation Ratio

The following tests were done in 61 well controlled diabetic patients: Platelet survival time (PST), platelet aggregation ratio acc. to Wu and Hoak (PAR), platelet aggregation test 1 acc. to Breddin (PAT 1), ADP-threshold concentration and filtragometer aggregation time acc. to Hornstra (Ta). The mean PST in 20 healthy volunteers was 99 hours ± 13,4 hrs.: in 12 pat. wihtout retinopathy 88,6 ± 12,8 hrs.; in 28 pat. with non-proliferative retinopathy 103,9 ± 18,2 hrs. and in 1 par. with proliferative retinopathy 105,8 ± 7,5 hrs. In 16 pat. with a disturbed nerve conduction time the mean PST was 102,2 ± 21,5 hrs. and 96,0 ± 21,9 hrs, in 28 pat. with a normal time. The PST was shortened (mean-1 ED) in 12 pat. out of 44 pat. The mean PAR was 0,37 ± 0,11 in 27 normal volunteers and 0,78 ± 0,12 in 61 diabetics. The PAR was < 0,71 in 16 out of 61 pat. The mean PAT 1 was 1,7 in 27 normal volunteers and 1,5 in 61 diabetics; the test was abnormal in 6 out of 61 pat. The ADP-threshold concentration was < 0,75 mumol ADP/L in only 4 out of 61 pat. The mean Ta was 242 ± 50,5 sec. in 16 normal volunteers and 167 ± 83 sec. in 44 pat.; the Ta was < 150 sec. in 23 out of 44 pat. There was no correlation between the severity of retino- and/or neuropathy with the PST, PAR, PAT 1, ADP-threshold or Ta or between the laboratory values. There was no abnormal laboratory test in 2 3 pat., one in 19, two in 16 and three in 3 pat. There was no relationship between the severity of retino- and/or neuropathy and number of abnormal laboratory tests.

scholarly journals Impedance Aggregometry Reveals Increased Platelet Aggregation during Liver Transplantation

2019 ◽  
Vol 8 (11) ◽  
pp. 1803 ◽  
Author(s):  
Mohamed Soliman ◽  
Matthias Hartmann
Keyword(s):  
Liver Transplantation ◽  
Arachidonic Acid ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Fold Increase ◽  
Surgical Patients ◽  
Platelet Activity ◽  
Impedance Aggregometry ◽  
Aggregation Ratio ◽  
Platelet Aggregation Ratio

In patients presenting for liver transplantation, increased platelet aggregation as well as thrombocytopenia have been demonstrated, but bedside assays have not been investigated. We compared platelet aggregation in liver transplantation patients and control surgical patients using impedance aggregometry. We hypothesized that platelet activity is not altered during liver transplantation. After the allowance of the ethics committee, platelet aggregation was determined using impedance aggregometry with the activators ristocetin, adenosine diphosphate (ADP), arachidonic acid, collagen, and thrombin receptor-activating peptide (TRAP) in liver transplantation patients at four time points (start of surgery, anhepatic phase, reperfusion, end of surgery) and in control surgical patients. Moreover, platelet count was determined using a Coulter counter. To compensate for the thrombocytopenia often present in patients presenting for liver transplantation, the ratio between impedance aggregometry finding and platelet count was used. For statistical evaluation, the t-test or the Mann–Whitney U-test were used, as appropriate. Platelet aggregation ratio showed a 3.1-fold increase in liver transplantation patients (n = 37) in comparison to control surgical patients (n = 10) when ristocetin was used as the activator (p = 0.001). Moreover, an approximately twofold increase of ADP-, arachidonic acid-, collagen-, and TRAP-induced platelet aggregation ratio was determined. Platelet aggregation normalized at the end of the transplantation procedure. Impedance aggregometry revealed a markedly increased platelet aggregation in some liver transplantation patients and might be suitable to guide platelet transfusion and antiplatelet therapy.

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.

The C50T polymorphism of the cyclooxygenase-1 gene and the risk of thrombotic events during low-dose therapy with acetyl salicylic acid

2008 ◽  
Vol 100 (07) ◽  
pp. 70-75 ◽  
Author(s):  
Martijn G. H. van Oijen ◽  
Santosh Sundaresan ◽  
Marc A. Brouwer ◽  
Rene H. M. te Morsche ◽  
Wessel Keuper ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Platelet Aggregation ◽  
Primary Endpoint ◽  
Low Dose ◽  
Cardiovascular Death ◽  
Hazard Ratio ◽  
Cyclooxygenase 1 ◽  
Thromboxane Production ◽  
The Common ◽  
Cox 1

SummaryAspirin prevents thrombotic events by inhibiting platelet cyclooxygenase-1 (COX-1), thus reducing thromboxane A2 formation and platelet aggregation. The C50T polymorphism of COX-1 is associated with an impaired inhibition of both thromboxane production and in-vitro platelet aggregation by aspirin. We studied whether this polymorphism is also associated with the risk of clinical thrombotic events in patients using aspirin. We included 496 patients admitted to our Coronary Care Unit for various indications treated with aspirin 80 mg daily. Genotyping for the C50T polymorphism demonstrated that 86.7% of the patients had the common genotype, and 13.3% had the variant (12.5% heterozygous, 0.8% homozygous). Baseline variables were well balanced, except that patients with the common genotype more frequently used aspirin prior to admission compared to those patients with the variant genotype. The composite primary endpoint of myocardial infarction, stroke, and/or cardiovascular death occurred in 98 patients (19.8%). Myocardial infarction occurred in 9.6% of patients, stroke in 1.6%, and cardiovascular death in 12.1%.The unadjusted hazard ratio (95% CI) for the primary endpoint for patients with the variant versus the common genotype was 1.07 (0.62–1.85), p=0.8.The adjusted hazard ratio was 0.86 (0.49–1.50), p=0.6. In prior laboratory studies the COX-1 C50T polymorphism was associated with an impaired inhibitory effect of aspirin on thromboxane production and platelet function. However, in this cohort of patients using low-dose aspirin for secondary prevention the polymorphism was not associated with a higher risk of atherothrombotic events.

Abstract 177: Ticagrelor, but not Clopidogrel, Protects the Heart Against Reperfusion Injury and Improves Remodeling After Myocardial Infarction

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Yumei Ye ◽  
Jose R Perez-Polo ◽  
Manjyot K Nanhwan ◽  
Sven Nylander ◽  
Yochai Birnbaum
Keyword(s):  
Myocardial Infarction ◽  
Platelet Aggregation ◽  
Reperfusion Injury ◽  
Heart Function ◽  
Oral Treatment ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Coronary Artery Ligation ◽  
Ventricular Ejection Fraction

Background: Clopidogrel (C) and Ticagrelor (T) are P2Y12 ADP receptor antagonists. In addition, ticagrelor inhibits adenosine cell uptake. In PLATO trial T reduced the incidence of the primary composite endpoint myocardial infarction, stroke or cardiovascular death over C in patients with acute coronary syndromes. Previous data show that 7d pretreatment with T limits infarct size (IS) in rats. We compared the effects of C and T, administered just before reperfusion on IS. We also assessed the effect of T and C, administered just before reperfusion and/or 6w oral treatment on cardiac remodeling. Methods: Rats underwent 30min coronary artery ligation. 1) At 25min of ischemia rats received intraperitoneal (IP) vehicle, T (10 or 30mg/kg), or C (12.5mg/kg). Area at risk (AR) was assessed by blue dye and IS by TTC staining 24h after reperfusion. 2) Rats received vehicle without (sham) or with (control) coronary ischemia, T (30mg/kg) IP (TIP), T (300mg/kg/d) oral for 6w, started a day after reperfusion (TPO), TIP+PO (TIPPO), or C (12.5mg/kg IP +62.5mg/kg/d PO for 6w). LV dimensions and function was assessed by echo at 6w. Results: 1) AR was comparable among groups. IS was 45.3±1.7% of the AR in the control group. T10 (31.5±1.8%; p=0.001) and T30 (21.4±2.6% p<0.001) significantly reduced IS, whereas C (42.4±2.6%) had no effect. Platelet aggregation in the controls was 64.7±1.3% and was comparable in T30 (24.9±1.8%) and C (23.2±1.8%) at 2h post reperfusion. T30 increased Akt, eNOS and ER1/2 phosphorylation 4h after reperfusion, whereas C had no effect. 2) Platelet aggregation at 1w oral treatment was 59.7±3.2% in the control group and was comparable in TIPPO (18.1±1.3%) and C (17.4±0.7%). Left ventricular ejection fraction was 77.6±0.9%*, 44.8±3.5%, 69.5±1.6%*, 69.2±1.0%*, 76.3±1.2%*, and 37.4±3.7% in the sham, vehicle, TIP, TPO, TIPPO and C treated group, respectively (*p<0.001 vs. vehicle). Left ventricular diameters at diastole and systole showed the same pattern. Conclusions: T, but not C, administered just before reperfusion protects against reperfusion injury. Oral T (in combination or not with acute treatment just before reperfusion) treatment for 6w improves heart function. C, despite achieving similar degree of platelet inhibition had no effect on remodeling.

scholarly journals Gene mutations of platelet glycoproteins and response to tirofiban in acute coronary syndrome

2016 ◽  
Vol 134 (3) ◽  
pp. 199-204
Author(s):  
Antonio de Padua Mansur ◽  
Alessandra Roggerio ◽  
Júlio Yoshio Takada ◽  
Pérola Michelle Vasconcelos Caribé ◽  
Solange Desirée Avakian ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Platelet Aggregation ◽  
Unstable Angina ◽  
Gene Mutations ◽  
Coronary Intervention ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment ◽  
Percutaneous Coronary ◽  
Glycoprotein Iiia

CONTEXT AND OBJECTIVES: Glycoprotein inhibitors (abciximab, eptifibatide and tirofiban) are used in patients with unstable angina and non-ST-segment elevation myocardial infarction before percutaneous coronary intervention. Of these, tirofiban is the least effective. We hypothesized that the response to tirofiban might be associated with glycoprotein gene mutations. DESIGN AND SETTING: Prospective study at Emergency Unit, Heart Institute (InCor), University of São Paulo. METHOD: Intrahospital evolution and platelet aggregation in response to tirofiban were analyzed in relation to four glycoprotein mutations in 50 patients indicated for percutaneous coronary intervention: 17 (34%) with unstable angina and 33 (66%) with non-ST-segment elevation myocardial infarction. Platelet aggregation was analyzed using the Born method. Blood samples were obtained before and one hour after tirofiban infusion. Glycoproteins Ia (807C/T ), Ib (Thr/Met) , IIb (Ile/Ser ) and IIIa (PIA ) were the mutations selected. RESULTS: Hypertension, dyslipidemia, diabetes, smoking, previous coronary artery disease and stroke were similar between the groups. Mutant glycoprotein IIIa genotypes had lower platelet aggregation before tirofiban administration than that of the wild genotype (41.0% ± 22.1% versus 55.9% ± 20.8%; P = 0.035). Mutant glycoprotein IIIa genotypes correlated moderately with lower platelet inhibition (r = -0.31; P = 0.030). After tirofiban administration, platelet glycoprotein Ia, Ib, IIb and IIIa mutations did not influence the degree of inhibition of platelet aggregation or intrahospital mortality. CONCLUSIONS: Mutations of glycoproteins Ia, Ib, IIb and IIIa did not influence platelet aggregation in response to tirofiban in patients with unstable angina and non-ST-segment elevation myocardial infarction.

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