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The effect of warfarin administration on platelet aggregation
M. Chylova, Z. Motovska, A. Fialova, I. Stetkarova, T. Peisker, P. Kalvach
Language English Country Slovakia
Document type Clinical Study, Research Support, Non-U.S. Gov't
- MeSH
- Platelet Aggregation * drug effects MeSH
- International Normalized Ratio MeSH
- Myocardial Ischemia drug therapy MeSH
- Humans MeSH
- Regression Analysis MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Statistics as Topic MeSH
- Platelet Function Tests methods instrumentation statistics & numerical data MeSH
- Warfarin * pharmacology therapeutic use MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Clinical Study MeSH
- Research Support, Non-U.S. Gov't MeSH
BACKGROUND: The aim of this study was to assess the effect of anticoagulation treatment on platelet aggregation. METHODS: The study group consisted of 24 patients on long-term warfarin therapy without any antiaggregation therapy. Platelet aggregation was measured using VerifyNow with arachidonic acid (AA) as an inducer in 23 patients and with light transmission aggregometry (LTA) in 19 patients using four different agonists. All patients had their international normalized ratio (INR) checked regularly. RESULTS: The mean INR value was 2.07 (SD 0.6). The average aggregation measured by VerifyNow was found to be 637.5 (SD 36.6) aspirin reaction units. The values of average aggregability in LTA were 73.3 % (SD 4.5 %), 73.2 % (SD 6 %) and 72.1 % (SD 4.8 %) in case of aggregation induced by AA, ADP, and collagen, respectively. Epinephrine-induced aggregability was 65.3 % (SD 14.7 %). Regression analysis between INR and values of collagen- or epinephrine-induced aggregability (r = 0.654 and 0.575) was found statistically signifi cant (p = 0.004 and 0.016); every increase in INR by 0,1 brings about an increase in collagen- and epinephrine-induced aggregation values by 1.5 and 4, respectively. CONCLUSION: Administration of warfarin does not produce a signifi cant reduction in platelet aggregation. On the contrary, prolonged INR evokes a mild increase in aggregation induced by collagen or epinephrine (Tab. 2, Fig. 3, Ref. 32).
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Literatura
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- $a Chýlová, Miroslava $7 xx0256464 $u Department of Neurology, Third Faculty of Medicine, Charles University and University Hospital Královské Vinohrady, Prague, Czech Republic
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- $a BACKGROUND: The aim of this study was to assess the effect of anticoagulation treatment on platelet aggregation. METHODS: The study group consisted of 24 patients on long-term warfarin therapy without any antiaggregation therapy. Platelet aggregation was measured using VerifyNow with arachidonic acid (AA) as an inducer in 23 patients and with light transmission aggregometry (LTA) in 19 patients using four different agonists. All patients had their international normalized ratio (INR) checked regularly. RESULTS: The mean INR value was 2.07 (SD 0.6). The average aggregation measured by VerifyNow was found to be 637.5 (SD 36.6) aspirin reaction units. The values of average aggregability in LTA were 73.3 % (SD 4.5 %), 73.2 % (SD 6 %) and 72.1 % (SD 4.8 %) in case of aggregation induced by AA, ADP, and collagen, respectively. Epinephrine-induced aggregability was 65.3 % (SD 14.7 %). Regression analysis between INR and values of collagen- or epinephrine-induced aggregability (r = 0.654 and 0.575) was found statistically signifi cant (p = 0.004 and 0.016); every increase in INR by 0,1 brings about an increase in collagen- and epinephrine-induced aggregation values by 1.5 and 4, respectively. CONCLUSION: Administration of warfarin does not produce a signifi cant reduction in platelet aggregation. On the contrary, prolonged INR evokes a mild increase in aggregation induced by collagen or epinephrine (Tab. 2, Fig. 3, Ref. 32).
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