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).

• 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

• MeSH
• Platelet Aggregation physiology   drug effects   MeSH
• Purinergic P2Y Receptor Antagonists pharmacology   therapeutic use   MeSH
• Diabetes Mellitus, Type 2 drug therapy   physiopathology   MeSH
• Platelet Aggregation Inhibitors administration & dosage   pharmacology   MeSH
• Clopidogrel * administration & dosage   pharmacology   MeSH
• Drug Resistance MeSH
• Humans MeSH
• Prasugrel Hydrochloride pharmacology   therapeutic use   MeSH
• Platelet Function Tests methods   instrumentation   MeSH
• Dose-Response Relationship, Drug MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

Kyselina acetylsalicylová (aspirin, ASA) v sekundární prevenci kardiovaskulárních příhod u pacientů s aterosklerotickým postižením koronárních i periferních tepen snižuje výskyt úmrtí a závažných ischemických cévních příhod o 22 %. Pokud je však laboratorně měřena účinnost antiagregační terapie aspirinem, neodpovídá kolem jedné třetiny pacientů adekvátním způsobem. Pro tento fenomén se vžil název aspirinová rezistence. Většina studií a metaanalýzy, které se zabývaly aspirinovou rezistencí, potvrdily korelaci různými metodami zjištěné aspirinové rezistence s horšími klinickými výsledky. V metaanalýze dvaceti studií s témě? 3?000 pacienty ?inil pom?r ?anc? (pooled odds ratio) pro kardiovaskul?rn? p??hodu u?pacient? rezistentn?ch na terapii ASA 3,8. Frekvence v?skytu aspirinov? rezistence se v?jednotliv?ch studi?ch ?asto dramaticky li?? od?t?m?? nulov?ch hodnot po?hodnoty p?es 70?%. K?t?mto markantn?m rozd?l?m doch?z? p?edev??m v?z?vislosti na?pou?it? laboratorn? metod?, klinick? situaci (stabiln?, nebo akutn? onemocn?n?, p??padn? zdrav? dobrovoln?ci) a?dal??ch aspektech, jako jsou l?kov? interakce atd. V?n?sleduj?c?m textu se pokus?me nazna?it, jak? klinick? a?laboratorn? aspekty ovliv?uj? v?skyt aspirinov? rezistence a?jak?m zp?sobem naopak aspirinov? rezistence ovliv?uje progn?zu pacienta. V?sou?asn? dob? nen? dostupn? p?esv?d?iv? d?kaz o?efektivit? ?pravy medikace na?z?klad? laboratorn? zji?t?n? aspirinov? rezistence, uv?d?me v?ak postupy, kter? byly pou?ity v?klinick?ch studi?ch za???elem zv??en? laboratorn? odpov?di na?antiagrega?n? terapii. ř 3 000 pacienty činil poměr šancí (pooled odds ratio) pro kardiovaskulární příhodu u pacientů rezistentních na terapii ASA 3,8. Frekvence výskytu aspirinové rezistence se v jednotlivých studiích často dramaticky liší od téměř nulových hodnot po hodnoty přes 70 %. K těmto markantním rozdílům dochází především v závislosti na použité laboratorní metodě, klinické situaci (stabilní, nebo akutní onemocnění, případně zdraví dobrovolníci) a dalších aspektech, jako jsou lékové interakce atd. V následujícím textu se pokusíme naznačit, jaké klinické a laboratorní aspekty ovlivňují výskyt aspirinové rezistence a jakým způsobem naopak aspirinová rezistence ovlivňuje prognózu pacienta. V současné době není dostupný přesvědčivý důkaz o efektivitě úpravy medikace na základě laboratorně zjištěné aspirinové rezistence, uvádíme však postupy, které byly použity v klinických studiích za účelem zvýšení laboratorní odpovědi na antiagregační terapii.

Acetylsalicylic acid (aspirin, ASA) reduces mortality and major adverse cardiovascular events by 22% when used in coronary and peripheral artery disease secondary prevention. Laboratory assessed aspirin antiplatelet therapy effectiveness showed an inadequate response to the ASA treatment in about one third of patients. This phenomenon is often called “aspirin resistance”. Most of the studies and metaanalyses regarding the aspirin resistance proved a certain correlation between the ASA resistance assessed by various laboratory methods and the worst clinical outcomes. In the metaanalysis with nearly 3,000 patients the pooled odds ratio of cardiovascular events in ASA resistant patients was 3.8. The ASA resistance frequency shown in various clinical studies varies from almost zero values to as much as 70% of resistant patients. The distinct differences in the ASA resistance frequency are caused by variability in used laboratory methods, different clinical situations in particular studies (stable or acute cardiovascular disease or healthy volunteers) and other aspects as drug interactions etc. In the text as follows, we describe the clinical and laboratory aspects influencing the ASA resistance incidence and the influence of the ASA resistance on patient prognosis. Nowadays, there is no solid proof available which would confirm the fact that the ASA resistance guided treatment modification is associated with better clinical outcomes. Nevertheless, herein we describe various methods of therapy modification used in clinical studies for improving the laboratory ASA treatment response.

• Keywords
• aspirinová rezistence, agregometrie,
• MeSH
• Anti-Inflammatory Agents, Non-Steroidal MeSH
• Aspirin * pharmacology   therapeutic use   MeSH
• Cyclooxygenase 1 metabolism   MeSH
• Cyclooxygenase 2 metabolism   MeSH
• Platelet Aggregation Inhibitors pharmacology   MeSH
• Proton Pump Inhibitors MeSH
• Cardiovascular Diseases prevention & control   MeSH
• Drug Resistance * MeSH
• Drug Interactions * MeSH
• Humans MeSH
• Drug Monitoring MeSH
• Thromboxane B2 metabolism   MeSH
• Platelet Function Tests methods   MeSH
• Check Tag
• Humans MeSH

Metóda rotačnej tromboelastometrie (ROTEM) je v súčasnosti čoraz viac a s obľubou používaná v manažmente perioperačného krvácania. Ako ,,bed-side“ test v určitom zmysle nahrádza bežné koagulačné testy v tejto situácii a tým, že umožňuje poskytovať cielenú liečbu koagulopatie, vedie k zníženiu podávania transfúznych prípravkov a zníženiu krvácania. V tomto článku popisujeme jednoduchým spôsobom princíp metódy, vyšetrované parametre, používane špecifické testy, problematiku nastavenia teploty prístroja, limity metódy a poskytujeme prehľad rozmedzí normálnych hodnôt parametrov pre jednotlivé vekové skupiny a tehotné ženy a vysvetľujeme postup a schému manažmentu krvácania. V závere popisujeme prípad traumatického krvácania manažovaného pomocou ROTEM, kde poukazujeme, že podávanie čerstvej mrazenej plazmy k terapii ťažkej traumatickej koagulopatie nevedie k dostatočnej korekcii tejto koagulopatie a je nutné terapiu zintenzívniť podávaním ďalších zrážacích faktorov, ako je fibrinogen či faktory protrombinového komplexu.

Rotational thromboelastometry (ROTEM) is currently increasingly used in the management of perioperative bleeding. As a bed-side test it replaces conventional coagulation tests in this situation and allows to provide targeted treatment of the coagulopathy, leading to reduced bleeding and reduced administration of transfusion products. This article describes in a simple way the principle of the method, the investigated parameters, specific tests, the issue of the temperature setting and the limitations of the method. It provides an overview of the normal ranges of parameters for different age groups and for pregnant women, and explains the steps and scheme of the management of acute bleeding. In conclusion, we describe a case of traumatic bleeding managed by ROTEM, where we point out that the administration of fresh frozen plasma for the treatment of severe traumatic coagulopathy did not lead to satisfactory correction of coagulopathy and had to be accompanied by administration of other clotting factors such as fibrinogen and prothrombin complex factors.

• MeSH
• Adult MeSH
• Fibrinogen therapeutic use   MeSH
• Blood Coagulation Disorders * diagnosis   etiology   therapy   MeSH
• Blood Transfusion MeSH
• Blood Loss, Surgical * MeSH
• Hemorrhage diagnosis   etiology   therapy   MeSH
• Humans MeSH
• Multiple Trauma MeSH
• Abdominal Injuries complications   MeSH
• Thrombelastography * methods   instrumentation   utilization   MeSH
• Blood Viscosity physiology   MeSH
• Platelet Function Tests methods   MeSH
• Blood Coagulation Tests methods   MeSH
• Check Tag
• Adult MeSH
• Humans MeSH
• Female MeSH
• Publication type
• Case Reports MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH

In cardiology, functional platelet activity is not routinely monitored. Platelet function assays should be able to identify patients with high residual platelet reactivity (HPR). High on-treatment platelet reactivity is apparent risk factor for atherothrombosis, however not the only one. Since there are many contributing factors (platelet activation, endothelial dysfunction, and plaque rupture) influencing atherothrombosis. Antiplatelet treatment is targeted to diminish platelet activation. The unique pharmacodynamics, pharmacokinetics of each agent and the pharmacogenetic profile of the recipient need to be taken into consideration. The aim of this review article is to summarize current knowledge of platelet function monitoring and its usefulness in clinical cardiology.

• Keywords
• aspirinová/clopidogrelová rezistence, vysoká reziduální reaktivita,
• MeSH
• Platelet Activation genetics   immunology   drug effects   MeSH
• Aspirin administration & dosage   adverse effects   therapeutic use   MeSH
• Plaque, Atherosclerotic diagnosis   etiology   complications   MeSH
• Cyclooxygenase 1 MeSH
• Platelet Aggregation Inhibitors * administration & dosage   adverse effects   therapeutic use   MeSH
• Cyclooxygenase Inhibitors MeSH
• Drug Resistance genetics   immunology   drug effects   MeSH
• Humans MeSH
• Meta-Analysis as Topic MeSH
• Risk Factors MeSH
• Statistics as Topic MeSH
• Cytochrome P-450 Enzyme System MeSH
• Ticlopidine analogs & derivatives   administration & dosage   adverse effects   MeSH
• Thrombosis diagnosis   etiology   complications   MeSH
• Platelet Function Tests methods   utilization   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

BACKGROUND: The antiplatelet effect of acetylsalicylic acid (ASA) varies among individual patients. We assessed the short-term reproducibility (STR) and long-term reproducibility (LTR) of light transmission aggregometry (LTA). METHODS: Residual platelet reactivity was measured twice using LTA in a group of 207 consecutive patients (56 females, mean age 67 ± 9 years) on ASA therapy in 10 ± 6 months interval. The STR was assessed in 15 patients (6 females, mean age 61 ± 7 years) with 10 measurements on 2 consecutive days. RESULTS: There was no correlation between both measurements in the long-term part of the study, and also Bland-Altman plot showed a diverging pattern. However, LTA STR was good with a correlation coefficient of .800 (P < .05) confirmed by Bland-Altman plot. CONCLUSIONS: Although short-term intraindividual reproducibility of LTA assessment of platelet reactivity is very good, in the long-term perspective the antiplatelet ASA effectivity may be influenced by additional variables and repeated measurements are warranted.

• MeSH
• Platelet Aggregation drug effects   MeSH
• Aspirin pharmacology   MeSH
• Time Factors MeSH
• Electric Impedance MeSH
• Hirudins pharmacology   MeSH
• Platelet Aggregation Inhibitors pharmacology   MeSH
• Cardiovascular Diseases blood   MeSH
• Smoking blood   MeSH
• Drug Interactions MeSH
• Middle Aged MeSH
• Humans MeSH
• Follow-Up Studies MeSH
• Nephelometry and Turbidimetry methods   MeSH
• Kidney Diseases blood   MeSH
• Obesity blood   MeSH
• Area Under Curve MeSH
• Prospective Studies MeSH
• Reproducibility of Results MeSH
• Aged MeSH
• Platelet Function Tests methods   MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Comparative Study MeSH
• Validation Study MeSH

Cieľ práce:Liečba kyselinou acetylsalicylovou (ASA) a klopidogrelom (KLP) je spojená s vysokým stupňom variability v liečebnej odpovedi a niektorí pacienti sú na liečbu rezistentní. Cieľom našej štúdie bolo posúdenie individuálnej odpovede na protidoštičkovú liečbu u pacientov s vysokým rizikom kardiovaskulárnych príhod liečených ASA (n = 131), KLP (n = 51) alebo ASA + KLP (n = 34). Materiál a metódy: Vyšetrenia sa u nich uskutočnili svetelnou transmisnou agregometriou a u vybraných pacientov pri liečbe KLP aj VASP fosforyláciou. Výsledky: Dobrú odpoveď na liečbu ASA s inhibíciou agregácie krvných doštičiek po indukcii kyselinou arachidonovou < 20 % dosia­hlo 75 % pacientov, parciálnu odpoveď s 20–40% inhibíciou 12,9 % pacientov a nedostatočnú odpoveď s > 40% inhibíciou 12,1 % pacientov. Dobrú odpoveď na liečbu KLP s inhibíciou agregácie krvných doštičiek po indukcii 20 μmol/l ADP < 60 % dosiahlo 66,1 % pacientov, parciálnu odpoveď s 60–70% inhibíciou 13,9 % pacientov a nedostatočnú odpoveď > 70 % malo 20 % pacientov. U pacientov liečených KLP + ADP indukovaná agregácia krvných doštičiek korelovala s VASP fosforyláciou. Zistilo sa, že 50 % pacientov pri liečbe KLP a 44,4 % pri liečbe ASA dosiahlo primeranú odpoveď na liečbu až zlepšením kompliancie. U 80 % pacientov, ktorí opakovane neodpovedali na liečbu KLP v dávke 75 mg denne, došlo po zvýšení dávky na 150 mg denne k dosiahnutiu požadovanej odpovede na liečbu. Zvýšenie dávky ASA nad 100 mg denne neviedlo u našich pacientov k zlepšeniu odpovede na liečbu. U tých pacientov, ktorí nevykazovali dostatočnú odpoveď na liečbu nízkou dávkou ASA (< 100 mg denne), však zvýšenie dávky na 100 mg denne viedlo k efektívnemu ovplyvneniu agregačnej odpovede. Záver: Laboratórne monitorovanie individuálnej odpovede umožňuje optimalizovať protidoštičkovú liečbu. Možno pritom selektovať pacientov, ktorí by mohli profitovať z iného typu protidoštičkovej liečby, akými sú napr. prasugrel a tikagrelor. Kľúčové slová: kyselina acetylsalicylová – klopidogrel – protidoštičková liečba – svetelná transmisná agregometria (LTA)

Objective: Acetylsalicylic acid (ASA) and clopidogrel (KLP) therapy is associated with the high degree of variability in response to the drug and some patients are drug-resistant. The aim of our study was to evaluate the individual response to antiplatelet therapy in patients at high risk of cardiovascular events treated with ASA (n = 131), KLP (n = 51) or ASA + KLP (n = 34). Subjects and methods: Investigations were performed in them by light transmission aggregometry and in selected patients by VASP fosforylation. Results: Good response to ASA treatment with arachidonic acid-induced platelet aggregation inhibition < 20% reached 75.0% of patients, partial response with 20–40% inhibition 12.9% of patients and poor response with > 40 % inhibition 12.1 % of patients. Good response to KLP treatment with 20 ?mol/l ADP-induced platelet aggregation inhibition < 60% reached 66.1% of patients, partial response with 60–70% inhibition 13.9% of patients and poor response > 70% in 20% of patients. In patients treated by KLP + ADP induced platelet aggregation correlated with VASP fosforylation. We found, that 50% of KLP-treated and 44.4% of ASA-treated patients obtained the adequate response to therapy by compliance improvement. In 80% of patients, which did not respond to KLP therapy in daily dose of 75 mg, the adequate response after the increase to daily dose of 150 mg was observed. The increase of ASA daily dose above 100 mg did not improve in our patients their response to therapy. However, in those patients without a good response to low-dose ASA (< 100 mg daily) the increase to daily dose of 100 mg effectively influenced the aggregatory response. Conclusion: Laboratory monitoring of individual response allows the optimalization of the antiplatelet therapy. The patients who could profit from other type of antiplatelet therapy, such as prasugrel and ticagrelor, can be selected by this method. Key words: acetylsalicylic acid – clopidogrel – antiplatelet therapy – light transmission aggregometry (LTA)

• Keywords
• světelná transmisní agregometrie (LTA), VASP fosforylace,
• MeSH
• Platelet Aggregation drug effects   MeSH
• Aspirin * administration & dosage   therapeutic use   MeSH
• Adult MeSH
• Cholesterol, HDL blood   MeSH
• Hematologic Tests methods   MeSH
• Body Mass Index MeSH
• Platelet Aggregation Inhibitors administration & dosage   therapeutic use   MeSH
• Drug Therapy, Combination methods   MeSH
• Cholesterol, LDL blood   MeSH
• Drug Resistance drug effects   MeSH
• Middle Aged MeSH
• Humans MeSH
• Reproducibility of Results MeSH
• Aged MeSH
• Statistics as Topic MeSH
• Case-Control Studies MeSH
• Ticlopidine * analogs & derivatives   administration & dosage   therapeutic use   MeSH
• Triglycerides blood   MeSH
• Platelet Function Tests * methods   statistics & numerical data   MeSH
• Dose-Response Relationship, Drug MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Female MeSH

Relativně známým fenoménem v kardiologii je nedostatečná inhibice destičkové aktivity při standardní protidestičkové léčbě. Problémem je správná definice (nejčastěji volíme termín selhání léčby či vysoká reziduální destičková reaktivita). Existuje řada příčin nedostatečné suprese destičkové aktivity při terapii a k dispozici je řada testů k monitorování destičkových funkcí. Otázkou je role zánětu a dědičných vlivů ve vztahu k destičkové aktivitě. Problematika selhání protidestičkové léčby je tématem řady odborných prací. Hlavní otázkou nadále zůstává klinický význam laboratorně zjištěných výsledků a možnost použití monitorování destičkových funkcí v rutinní praxi s cílem optimalizace terapie u pacientů s ischemickou chorobou srdeční.

Inadequate platelet suppression by acetylosalicylic acid is a relatively well known phenomenon in cardiology. How to define it properly ? Persistent high residual platelet reactivity or treatment failure seems to be the best term. There are several reasons for an inadequate platelet suppression and several techniques may be used to assess platelet function and the effectiveness of antiplatelet therapy. The role of inflammation and genetic polymorphisms in high residual platelet activity and atherothrombosis was studied with inconsistent results. There are still no clinical data to support change in antiplatelet therapy in the correlation with the laboratory results in patients with coronary artery disease.

• Keywords
• kardiovaskulární riziko, antiagregační léčba, destičková reaktivita,
• MeSH
• Platelet Aggregation physiology   drug effects   MeSH
• Platelet Activation physiology   drug effects   MeSH
• Aspirin administration & dosage   pharmacology   therapeutic use   MeSH
• Financing, Organized MeSH
• Platelet Aggregation Inhibitors pharmacology   therapeutic use   MeSH
• Myocardial Ischemia drug therapy   prevention & control   MeSH
• Cardiovascular Diseases drug therapy   prevention & control   MeSH
• Drug Resistance MeSH
• Humans MeSH
• Platelet Count MeSH
• Blood Platelets physiology   MeSH
• Platelet Function Tests methods   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

Průtoková cytometrie hraje významnou roli v charakterizaci krevních destiček a v analýze jejich funkcí ve vztahu k riziku trombózy a krvácení. V klinické praxi se uplatňuje v diagnostice vrozených poruch funkce destiček, imunitních a megakaryocytárních trombocytopenií, v analýze polymorfie systému lidských trombocytárních antigenů (HPA) ve vztahu k aloimunizaci, neonatální trombocytopenii, potransfuzní purpuře nebo refrakternosti na trombocytární přípravky. Klinicky významná je analýza aktivity cirkulujících destiček a stanovení trombocytárních mikročástic u pacientů s tranzitorní ischemickou atakou, akutním koronárním syndromem, kardiopulmonálním bypassem. V posledních letech se průtoková cytometrie uplatňuje úspěšně v měření účinnosti antiagregační léčby inhibitory receptoru P2Y12 a antagonisty komplexu IIb/IIIa. Relativním nedostatkem běžně používaných metod je nedostatečná standardizace a reprodukovatelnost. Cílem této práce je poskytnout přehled současných možností vyšetření krevních destiček a jejich funkcí metodou průtokové cytometrie v kontextu zavedených standardních postupů na našem pracovišti.

Flow cytometry is a significant tool for platelet characterization and functional analysis in relation to the risk of bleeding and thrombosis. In clinical practice it is useful for the diagnosis of inherited platelet disorders, immune and megakaryocytic thrombocytopenias, for platelet HPA-1 polymorphism analysis in association with alloimmunization, neonatal alloimmune thrombocytopenia, post-transfusion purpura or refractoriness to platelet infusion. The analysis of platelet reactivity and platelet microparticles in patients with transitory ischemic attack, acute coronary syndrome or cardiopulmonary bypass is clinically significant. In recent years, flow cytometry plays an increasing role in monitoring of antiplatelet therapy with P2Y12 receptor inhibitors and IIb/IIIa antagonists. Relative limitation of the majority of methods in use is poor standardization and reproducibility. The aim of this work is to review the potential role of flow cytometry analysis of platelets and their function in the context of the standardized techniques adopted in our laboratory.

• MeSH
• Platelet Activation physiology   drug effects   MeSH
• Platelet Membrane Glycoproteins analysis   immunology   MeSH
• Humans MeSH
• Platelet Count methods   MeSH
• Flow Cytometry methods   instrumentation   MeSH
• Reproducibility of Results MeSH
• Thrombasthenia diagnosis   blood   MeSH
• Thrombocytopenia diagnosis   blood   MeSH
• Platelet Glycoprotein GPIIb-IIIa Complex analysis   genetics   MeSH
• Platelet Function Tests methods   MeSH
• Check Tag
• Humans MeSH

Antiagregancia patří mezi skupinu široce používaných léčiv v klinické praxi. V současné době zaznamenáváme velmi rychlý vývoj nových antiagregačních preparátů a jsme také svědky rozsáhlých diskusí o rezistenci na antiagregační léčbu. Cílem tohoto článku je popsat základy farmakologických vlastnosti již déle užívaných i nových antiagregačních léčiv, představit metody umožňující identifikovat pacienty rezistentní na antiagregační léčbu a ukázat na možný přínos těchto metod v běžné klinické praxi.

Antiaggregation treatment is widely used in daily clinical practice. New antiaggregation drugs have been presented and other are under rapid development. Physicians are facing large discussions regarding resistance and responsiveness to antiaggregation treatment. The goal of this review article is to describe pharmacological effect of previously used and new antiaggregant, present methods that can identify patients resistant to treatment and show possible impact of this testing in daily clinical practice.

• Keywords
• laboratorní metody,
• MeSH
• Adenosine Diphosphate antagonists & inhibitors   MeSH
• Platelet Aggregation drug effects   MeSH
• Aspirin pharmacokinetics   therapeutic use   MeSH
• Financing, Organized MeSH
• Drug Evaluation MeSH
• Platelet Aggregation Inhibitors pharmacokinetics   pharmacology   therapeutic use   MeSH
• Ischemia MeSH
• Cardiovascular Diseases drug therapy   prevention & control   MeSH
• Clinical Trials as Topic MeSH
• Drug Resistance MeSH
• Humans MeSH
• Flow Cytometry methods   utilization   MeSH
• Pyridines pharmacokinetics   classification   therapeutic use   MeSH
• Sensitivity and Specificity MeSH
• Platelet Function Tests methods   utilization   MeSH
• Treatment Outcome MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH