Utilidad clínica de la agregometría plaquetaria / Clinical utility of platelet aggregometry

Resumen: La acción de las plaquetas en la hemostasia primaria comprende la adhesión a losvasos sanguíneos afectados, la activación, la secreción del contenido granular, y posteriormente,la agregación plaquetaria para la formación del tapón hemostático primario. Bajo las condicionesfisiológicas de flujo vascular, estos procesos requieren la acción sinérgica de varias proteínasy receptores plaquetarios, como también de agonistas que inducen la activación plaquetaria.Por ello, las mutaciones de los genes que codifican para moléculas y receptores de superficieimplicados en estos procesos darán origen a desórdenes hemorrágicos como la enfermedad devon Willebrand, la trombastenia de Glanzmann, el síndrome de Bernard Soulier y la deficienciade gránulos plaquetarios, entre otros. El diagnóstico de estas enfermedades se realiza medianteensayos de función plaquetaria que simulan los procesos fisiológicos de activación, adhesión,liberación del contenido granular y agregación. Una de las pruebas de función plaquetaria másutilizada es la agregometría. En este artículo de revisión se describe la utilidad de esta prueba parael diagnóstico de desórdenes hemorrágicos hereditarios y del síndrome de la plaqueta pegajosa,un desorden trombótico hereditario caracterizado por hiperagregabilidad. Adicionalmente, se revisa el fundamento de esta prueba, las condiciones preanalíticas, analíticas y posaanaliticas, analiticas y poanaliticas las indicaciones las contraindicaciones y la interpetación de los resultados.

Abstract: The role of platelets in primary hemostasis involves their adherence to sites of vessel injury, activation, secretion of platelet granule content, and finally, aggregation to form the primaryhemostatic plug. Under physiologic conditions of vascular flow, these processes require thesynergistic action of several proteins and platelet receptors, and also the action of physiologicalagonists that stimulate the activation of the platelets. As a result, hereditary mutations of genescodifying for molecules and surface receptors implied in primary hemostasis will be expressedas hemorrhagic disorders, including von Willebrand disease, Glanzmann thrombasthenia,Bernard Soulier syndrome, storage pool diseases, among others. The diagnosis of these diseases is possible through platelet function assays that resemble the physiological processesof activation, adhesion, release of granule content, and aggregation. Platelet aggregometry isone of the most frequently used tests. This review article intends to describe the utility of plateletaggregometry for the diagnosis of hereditary hemostatic disorders and sticky platelet syndrome, a hereditary thrombotic disorder characterized by increased platelet aggregability. In addition, the fundamentals of the test, the pre-analytical, analytical and post-analytical conditions, the test indications, contraindications and results interpretation are discussed.

Diferencias en la agregación plaquetaria de sangre coronaria y periférica de pacientes con enfermedad coronaria: implicaciones clínicas / Differences in platelet aggregation in coronary and peripheral blood of patients with coronary disease: clinical implications

INTRODUCCIÓN: los fenómenos trombóticos son más frecuentes en las coronarias y, al parecer, los cambios que produce la enfermedad aterosclerótica en la reología y en la superficie endotelial son los responsables de este fenómeno. OBJETIVO: cuantificar la diferencia en la agregación plaquetaria de sangre venosa coronaria y sangre venosa periférica en pacientes con enfermedad coronaria severa. METODOLOGÍA: se seleccionaron pacientes mayores de treinta años, con enfermedad coronaria severa, de quienes se obtuvieron muestras de sangre periférica y del seno coronario, y se realizaron agregaciones plaquetarias por el método de absorbancia con ADP 10 mmol, ácido araquidónico (AA), epinefrina (Epi) 300 mmol y colágeno 10 mg/mL. RESULTADOS: se incluyeron en total 32 pacientes con edad promedio de 65 más o menos 10 años, 22 hombres, 10 (31 porciento) pacientes con enfermedad estable y 22 (69 porciento) con inestable. La agregación plaquetaria en sangre del seno coronario fue mayor con todos los agonistas usados, así: ADP 61,8 porciento vs. 53,4 porciento (p= 0,001), AA 15,1 porciento vs. 13,8 porciento (p= 0,48), colágeno 72,6 porciento vs. 69,2 porciento (p= 0,048) y Epi 58 porciento vs. 51,6 porciento (p= 0,01). Los pacientes con enfermedad inestable muestran una mayor agregación con ADP en el seno coronario: 58,5 porciento vs. 49,2 porciento (p= 0,001) y no hay diferencias en los inestables. La resistencia a la Aspirina fue similar (p= 1), sin embargo la resistencia al clopidogrel fue mayor en el seno coronario: 56 porciento vs. 48 porciento (p= 0,24).

INTRODUCTION: thrombotic events are more frequent in the coronary arteries and apparently the changes in rheology and endothelial surface produced by atheroesclerotic disease are responsible for this phenomenon. OBJETIVE: quantify the difference in platelet aggregation of coronary venous blood and peripheral venous blood in patients with severe coronary disease. METHODOLOGY: we selected patients older than 30 years with severe coronary disease and obtained samples of peripheral and coronary sinus blood. Platelet aggregation was realized by the absorbance method with ADP 10 mmol, arachidonic acid (AA), epinephrine (Epi) 300 mmol and collagen 10 ug/mL. RESULTS: we included a total of 32 patients with mean age 65 more or less 10 years. 22 were men; 10 patients (31 percentage) had stable disease and 22 (69 percentage) unstable disease. Platelet aggregation in coronary sinus blood was higher with all agonists used as follows: ADP 61.8 percentage vs. 53.4 percentage (p = 0.001), AA 15.1 percentage vs.13.8 percentage (p = 0.48), collagen 72.6 percentage vs. 69.2 percentage (p = 0.048) and Epi 58 precentage vs. 51.6 percentage (p = 0.01). Patients with unstable disease show increased aggregation with ADP in the coronary sinus 58.5 percentage vs. 49.2 percentage (p = 0.001) and there are no differences in the unstable. Aspirin resistance was similar (p = 1); however, clopidogrel resistance was higher in the coronary sinus 56 percentage vs. 48 percentage (p = 0.24). CONCLUSION: we describe the presence of higher platelet aggregation in the coronary sinus of patients with atheroesclerotic disease that is significant for ADP, collagen and epinephrine, and suggest the appearance of local factors associated with the coronary disease that increase platelet aggregation. Peripheral platelet aggregation doesn't reflect the local behavior in patients with coronary atheroesclerosis.

Inibição e reversão da agregação plaquetária de eqüinos in vitro com o uso de ketoprofeno, fenilbutazona e flunixim meglumine / In vitro inibition and reversion of equine platelet aggregation using ketoprophen, phenylbutazone and flunixin meglumin

Como são várias as enfermidades e os distúrbios que induzem à hipercoagulabilidade e à pré-ativação de plaquetas em eqüinos. A atividade de medicamentos utilizados para controle dessas enfermidades sobre a agregação de plaquetas pode, não apenas servir para avaliar sua evolução, como também a resposta terapêutica. Com o objetivo de avaliar a prevenção e a reversão da agregação plaquetária de eqüinos in vitro foram utilizados os antiinflamatórios não esteroidais (AINES): ketoprofeno, fenilbutazona e flunixim meglumine. A comparação demonstrou que a fenilbutazona e o ketoprofeno previnem a agregação de plaquetas de eqüinos induzida pelo ADP, de forma mais eficaz do que o flunixim-meglumine e, superior ao fragmento monoclonal de anticorpo Reopro, sendo semelhante a dos bloqueadores de receptores de membrana Ro-438857 e RGDS. Quanto a reverão da agregação plaquetária tanto a fenilbutazona quanto o ketoprofeno demonstraram efeitos dose-dependente.

Several diseases may lead to platelet pre-activation and hypercoagulability states in horses. The activity of many drugs against platelet aggregation may, not only contribute to the evaluation of a disease but also its response to the therapy. With the aim to study in vitro prevention and reversion of platelet aggregation, the non steroidal anti-inflammatory drug (NSAID): ketoprophen, phenylbutazone and flunixin-meglumin were evaluated. The comparison demonstrated that phenylbutazone and ketoprophen prevented platelet aggregation induced by ADP better than flunixin-meglumin, in a superior manner to the monoclonal antibody Reopro, and in a better way than the membrane receptor blockers Ro-438857 and RGDS. The reversion of platelet aggregation demonstrated that even phenylbutazone or ketoprophen have a dose-dependent effect.