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Al-Mamary, Ahmed Hussien Hussien (2018) On-Treatment Platelet Reactivity in Peripheral and Coronary Arterial Blood in Patients Undergoing Primary PCI for ST-Segment Elevation Myocardial Infarction (STEMI). [Ph.D. thesis]

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Abstract (english)

BACKGROUND
Dual antiplatelet therapy is recommended in patients undergoing primary percutaneous coronary intervention (p-PCI) for ST-segment elevation myocardial infarction (STEMI). In the past few decades, oral antiplatelet agents have proved to significantly reduce the incidence of ischemic events in patients with atherothrombotic diseases. Nevertheless, recurrent ischemic events often occur in patients undergoing stent implantation. High platelets reactivity has been associated with a higher risk for major cardiovascular events in patients with acute coronary syndromes (ACS). Several pre-analytical variables may influence platelet function analysis. The aim of our study was to assess the on-treatment platelet reactivity in peripheral and coronary blood, in a group of patients receiving dual antiplatelet therapy undergoing primary percutaneous coronary intervention (p-PCI) for STEMI.

METHODS
Eligible patients for the study were considered as consecutively admitted patients to the emergency department of University-Hospital of Padua with a diagnosis of ACS with ST-segment elevation scheduled for an urgent procedure of coronary angioplasty. One hundred nine patients who consecutively underwent p-PCI (males: 72%, females: 28%; mean age: 64±13 years) were enrolled. Before the coronary angioplasty intervention, the patients were treated with dual antiplatelet therapy (aspirin 250mg I.V in association with one another oral thienopyridines; Clopidogrel 300/600mg, Prasugrel 60 mg or Ticagrelor 180 mg) and with anticoagulant therapy (unfractionated heparin 70U/Kg I.V). During the coronary angioplasty intervention two different samples were obtained, one from peripheral artery and the other from coronary blood. The platelet aggregation was studied using the impedance aggregometry Multiplate®, according to manufacturer’s indications. For each patient the values of “Area Under the Curve” (AUC) in ADP-test and ASPI-test were considered, both in the peripheral and in coronary blood. “Low responders of antiplatelet therapy” were considered when an AUC value of ASPI-test or ADP-test greater than or equal to a pre-established cut-off.
RESULTS
The Multiplate® analysis of ADP-test revealed that mean values were slightly higher in peripheral blood compared to coronary blood (peripheral blood: 41±28 U; coronary blood: 39±28 U), However these values with no statistically significant difference (p=0.68). Likewise, for the ASPI-test; no statistically significant difference between the mean values in the peripheral blood compared to the coronary blood (peripheral blood: 23±4 U; coronary blood: 17±2 U; p=0.06).
The percentage of low-responders to ADP-receptor inhibitors was significantly greater than the percentage of low-responders to acetylsalicylic acid at time of primary PCI both in the peripheral and in the coronary blood samples (peripheral ADP-test: 38%; peripheral ASPI-test: 14%; p<0.01, Coronary ADP-test: 36%; coronary ASPI-test: 11%; p<0.01). In peripheral blood, the prevalence of “low Clopidogrel responders” was higher (45%) than that observed for Prasugrel (36%) and Ticagrelor (33%). Similar results were observed in coronary blood, the prevalence of “low Clopidogrel responders” was higher (40%) than that observed for Prasugrel (36%) and Ticagrelor (29%) however these results were with no significant statistical difference (p >0.05). Finally, a positive and statistically significant linear correlation was observed for both ASPI-test and ADP-test in peripheral and coronary blood (r2 0.23, p <0.001 and r2 0.12, p <0.001; respectively). That means; those who are resistant to acetylsalicylic acid tend to be resistant to ADP receptor inhibitors, and vice versa; those who are sensitive to acetylsalicylic acid therapy tend to be sensitive to ADP inhibitor therapy also. Our observed data did not show a correlation between platelet function and clinical outcome both for in-hospital and 1-year clinical outcomes.

CONCLUSIONS
In this study we observed that the overall platelet reactivity in coronary blood is lower than in peripheral blood, though not statistically significant. This more likely appears to be due to high antiplatelet drugs effect at plaque ulceration/thrombus site, where the hemostatic process is highly active at onset of STEMI. Larger studies are needed for better evaluation of these mechanisms in term of pharmacodynamic, pharmacokinetic and receptor kinetic properties of antiplatelet agents.
The other interesting result emerging from data processing is the high incidence (about 30%) of low response to thienopyridine type antiplatelet drugs at the time of primary angioplasty. This result, moreover known for Clopidogrel in addition our results include patients treated with Prasugrel and Ticagrelor also. An explanation of this phenomenon which also involves potent recent drugs, requires careful analysis and further studies. The significant direct correlation between platelet reactivity in peripheral and in coronary blood is still a matter of debate. Larger studies are needed for in-depth assessment of any correlation between on–treatment platelet reactivity measured in coronary blood and clinical outcome.

Abstract (italian)

INTRODUZIONE
La doppia terapia antiaggregante (DAPT) è raccomandata in pazienti sottoposti ad intervento di angioplastica coronarica primaria (p-PCI) per infarto miocardico acuto con sopraslivellamento del tratto ST (STEMI). Infatti, il trattamento con farmaci antipiastrinici orali ha dimostrato di ridurre significativamente l'incidenza di eventi ischemici nei pazienti con malattie aterotrombotiche sia in fase acuta che in fase cronica. Tuttavia, spesso si verificano eventi ischemici ricorrenti nei pazienti sottoposti ad angioplastica ed impianto di stent. È stato dimostrato che una delle cause di recidiva ischemica sia l’elevata reattività delle piastrine. Pertanto, lo studio della funzione piastrinica diventa un elemento sempre più importante per valutare questo tipo di pazienti. Diverse variabili pre-analitiche possono influenzare l'analisi della funzione piastrinica. Lo scopo del nostro studio è stato quello di valutare la reattività piastrinica del sangue periferico e coronarico in un gruppo di pazienti trattati con DAPT e sottoposti p-PCI per STEMI.

METODI
Abbiamo considerato eleggibili allo studio tutti i pazienti consecutivamente giunti in urgenza al Pronto Soccorso dell’Azienda Ospedaliera di Padova con diagnosi di sindrome coronarica acuta con sopraslivellamento del tratto ST per i quali fosse indicata l’esecuzione in urgenza di una procedura di angioplastica coronarica. Sono stati arruolati 109 pazienti (maschi: 72%, femmine: 28%; età media: 64±13 anni). I pazienti arruolati nello studio sono stati trattati, prima di essere sottoposti alla procedura di angioplastica primaria, con doppia terapia antiaggregante (aspirina 250 mg e.v in associazione con uno dei seguenti tre farmaci: Clopidogrel 300/600 mg per os, Prasugrel 60 mg per os o Ticagrelor 180 mg per os) e con terapia anticoagulante (eparina non frazionata 70 U/Kg e.v). Durante la procedura di angioplastica primaria sono stati eseguiti due tipi di prelievo, uno dal sangue arterioso periferico ed uno dal sangue arterioso coronarico. L’aggregazione piastrinica è stata studiata con l’aggregometro Multiplate® secondo le indicazioni fornite dal costruttore. Per ogni paziente sono stati valutati i valori di “Area Under the Curve” (AUC) nell’ADP-test e nell’ASPI-test, ottenuti sul sangue periferico e sul sangue coronarico. “Low responders alla terapia antiaggregante” sono stati definiti quei pazienti con valori di “Area Under Curve” (AUC) all’ASPI test o all’ADP test sono maggiore o uguale a un range prestabilito.

RISULTATI
Non abbiamo osservato differenza statisticamente significativa tra i valori medi di ADP-test calcolati su sangue periferico e su sangue coronarico. I valori medi delle AUC sono risultati lievemente superiori nel sangue periferico che nel sangue coronarico (sangue periferico: 41±28 U; sangue coronarico: 39±28 U; p=0.68). Allo steso modo, non è stata riscontrata differenza statisticamente significativa tra i valori medi di ASPI-test calcolati su sangue periferico e su sangue coronarico. Anche in questo caso abbiamo osservato valori medi di AUC lievemente superiori nel sangue periferico che nel sangue coronarico (sangue periferico: 23±4 U; sangue coronarico: 17±2 U; p=0.06). Sia nel sangue periferico che nel sangue coronarico la percentuale di pazienti “low responders” al trattamento con inibitori del recettore per l’ADP è risultata essere statisticamente superiore alla percentuale di pazienti “low responders” alla terapia con acido acetilsalicilico al momento dell’angioplastica primaria (ADP-test periferico: 38%; ASPI-test periferico: 14%; p<0.01. ADP-test coronarico: 38%; ASPI-test coronarico: 11%; p<0.01). Nel sangue periferico la prevalenza di "low responders” al Clopidogrel era superiore (45%) a quella osservata rispettivamente per Prasugrel (36%) e Ticagrelor (33%). Risultati simili sono stati osservati nel sangue coronarico. In particolare, la prevalenza di "low responders” al Clopidogrel è stata superiore (40%) rispetto a quella osservata per Prasugrel (36%) e Ticagrelor (29%). Non è stata osservata alcuna differenza significativa (p> 0,05) nella prevalenza dei pazienti con valori di ADP-test superiori al cut-off prestabilito, considerando separatamente le tre diverse tienopiridine. Infine è stata individuata una correlazione lineare statisticamente significativa tra “low responders” all’acido acetilsalicilico e “low responders” agli inibitori del recettore dell’ADP. Questa osservazione indica come i pazienti resistenti al trattamento con acido acetilsalicilico tendono ad essere resistenti anche al trattamento con inibitori del recettore per l’ADP e, viceversa, pazienti “sensibili” alla terapia con acido acetilsalicilico tendono ad essere “sensibili” anche al trattamento con inibitori del recettore per l’ADP. Questi resultati sono stati osservati sia su sangue periferico (r2 0.23, p<0.001) che su sangue coronarico (r2 0.12, p<0.001). I dati che abbiamo osservato non mostrano un’associazione tra funzione piastrinica e outcome clinico nè per quanto riguarda gli “in-hospital outcome” né per quanto riguarda gli outcome a distanza di 1 anno.

CONCLUSIONI
I dati analizzati ci hanno permesso di dimostrare che la reattività piastrinica nel sangue coronarico era inferiore rispetto a quella osservata nel sangue periferico. Sembrerebbe quindi che, la risposta alla terapia farmacologica con doppia antiaggregante prima della procedura sia maggiore proprio laddove il processo emostatico è più attivo, ossia a livello della placca aterosclerotica sede della formazione del trombo responsabile dell’insorgenza della STEMI. Questo meccanismo necessità di conferma in termini di farmacodinamica, farmacocinetica e di cinetica recettoriale. L’altro dato estremamente interessante emerso dall’elaborazione dei dati è l’elevata incidenza (circa 30%) dei pazienti “low responders” al trattamento con farmaci antiaggreganti di tipo tienopiridinico al momento della angioplastica primaria. Questo risultato, peraltro noto per il Clopidogrel, comprende anche pazienti trattati con Prasugrel e Ticagrelor. Una possibile spiegazione di questo fenomeno, che coinvolge anche i farmaci di “seconda generazione”, necessita di un’attenta analisi. Abbiamo infine osservato una significativa correlazione tra reattività piastrinica nel sangue periferico e nel coronario. I nostri risultati, che alla luce dei limiti del nostro lavoro devono considerarsi come preliminari, necessitano di essere confermati su casistiche più numerose soprattutto per quanto riguarda la correlazione tra “on-treatment platelet reactivity” misurata nel sangue coronarico e outcomes clinici.

Statistiche Download
EPrint type:Ph.D. thesis
Tutor:Iliceto, Sabino
Supervisor:Iliceto, Sabino
Ph.D. course:Ciclo 29 > Corsi 29 > SCIENZE MEDICHE, CLINICHE E SPERIMENTALI
Data di deposito della tesi:07 June 2018
Anno di Pubblicazione:04 January 2018
Key Words:primary PCI, antiplatlet, Aspi test, ADP test
Settori scientifico-disciplinari MIUR:Area 06 - Scienze mediche > MED/11 Malattie dell'apparato cardiovascolare
Struttura di riferimento:Dipartimenti > Dipartimento di Scienze Cardiologiche, Toraciche e Vascolari
Istituti > Istituto di Anatomia Patologica
Codice ID:11246
Depositato il:08 Nov 2018 09:47
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