P2Y12-hämmare är läkemedel som påverkar trombocytfunktionen genom att blockera en receptor på trombocyten. Denna receptor har namnet P2Y12 och är trombocyternas ADP (adenosine 5’-diphosphate)-receptor. Därför kallas läkemedel som blockerar denna receptor för P2Y12-hämmare eller ADP-antagonister.[1]Packham MA and Rand ML. Historical perspective on ADP-induced platelet activation. Purinergic signalling. 2011;7:283-92 [2]Opie LH and Gersh BJ. Drugs for the Heart : Expert Consult – Online and Print. Saint Louis: Elsevier Health Sciences; 2014 [3]Wallentin L. P2Y(12) inhibitors: differences in properties and mechanisms of action and potential consequences for clinical use. European heart journal. 2009;30:1964-77. P2Y12-hämmare används inom kardiologi vid akut koronart syndrom och PCI.

Denna sidan ger en koncis överblick över fyra ADP-hämmare. För mer utförlig information om indikationer läs sidorna om dubbel trombocythämning och antitrombotisk trippelterapi.

P2Y12-hämmare:

Clopidogrel och Prasugrel tillhör samma kemiska grupp (Thienopyridiner), Ticagrelor är en Cyclopentyl-triazolopyrimidine och Cangrelor en adenosin- trifosfat analog. Clopidogrel och Prasugrel är prodrugs som behöver konverteras till en aktiv metabolit [4]Niitsu Y, Jakubowski JA, Sugidachi A, Asai F. Pharmacology of CS-747 (prasugrel, LY640315), a novel, potent antiplatelet agent with in vivo P2Y12 receptor antagonist activity. Semin Thromb Hemost. … Continue reading.

P2Y12-hämmare är läkemedel som påverkar trombocytfunktionen genom att blockera en receptor på trombocyten. Denna receptor har namnet P2Y12 och är trombocyternas ADP (adenosine 5’-diphosphate)-receptor. Därför kallas läkemedel som blockerar denna receptor för P2Y12-hämmare eller ADP-antagonister.[5]Packham MA and Rand ML. Historical perspective on ADP-induced platelet activation. Purinergic signalling. 2011;7:283-92 [6]Opie LH and Gersh BJ. Drugs for the Heart : Expert Consult – Online and Print. Saint Louis: Elsevier Health Sciences; 2014 [7]Wallentin L. P2Y(12) inhibitors: differences in properties and mechanisms of action and potential consequences for clinical use. European heart journal. 2009;30:1964-77. P2Y12-hämmare används inom kardiologi vid akut koronart syndrom och PCI.

Adenosine diphosphate (ADP) är en nukleotid som förvaras i trombocyternas dense granules. Vid aktivering släpps ADP ut från trombocyterna och aktiverar andra trombocyter genom att binda till deras P2y12-receptorer. Aktiverade trombocyter ändrar sedan formen av sina glycoprotein IIb/IIIa (GpIIbIIIa)-receptorer på cellmembranen, GpIIbIIIa-receptorerna blir lätt bindande fibrinogen binding sites. Fibrinogen (som delvis cirkulerar fritt, och delvis blir utsläppt från aktiverade trombocyter) binder till (GpIIbIIIa)-receptorerna på flera trombocyter och håller på så sätt samman flera trombocyter: Trombocytaggregation, som blir en tromb. [8]Ruggeri ZM. Platelets in atherothrombosis. Nat Med. 2002 Nov;8(11):1227-34. doi: 10.1038/nm1102-1227. PMID: 12411949.

Läs alltid även på FASS.se. Källor [9]Collet JP, Thiele H, Barbato E, et al. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation [published online ahead of … Continue reading [10]Valgimigli M, Bueno H, Byrne RA, et al. 2017 ESC focused update on dual antiplatelet therapy in coronary artery disease developed in collaboration with EACTS: The Task Force for dual antiplatelet … Continue reading

Clopidogrel (patentfri, förut Plavix)

  • Indikation:
    • Tillsammans med ASA som DAPT vid AKS: Vid AKS är DAPT med ASA + Ticagrelor eller Prasugrel förstahandsval. Clopigrel används vid AKS om Ticagrelor eller Prasugrel är kontraindicerade, vid hög blödningsrisk, eller om patienten planeras för oral antikoagulation.
    • Tillsammans med ASA som DAPT vid CCS (stabil angina): Efter PCI för stabil angina/CCS är Clopidogrel den enda P2Y12 antagonist som används.
  • Kontraindikation: Hög blödningsrisk.
  • Dosering:
    • Laddningsdos 600 mg (8 tabletter à 75 mg) om effekt önskas så snabbt som möjligt (laddning på PCI-lab, eller om laddning ska ges ett fåtal timmar innan planerad PCI). Annars 300 mg laddningsdos (t.ex laddning dagen innan planerad PCI)
    • Underhållsdos 75 mg 1×1
  • Behandlingstid: Vid DAPT: Se DAPT
  • Kommentar:
    • Enda P2Y12-antagonist som används vid PCI för stabil angina och vid PCI på patienter med indikation för oral antikoagulation.
    • Ingen dosjustering vid kronisk njursvikt, dock ingen data för GFR<15 eller dialys.
    • Läkemedelseffekt 2-6 timmar efter laddningsdos.

Ticagrelor (Brilique)

  • Indikation: Tillsammans med ASA som DAPT.
    Se även EMA-produktresumé Tiagrelor/Brilique (svenska)
  • Kontraindikation: Hög blödningsrisk, pågående blödning. Ges ej samtidigt som oral antikoagulation.
  • Dosering:
    • Laddningdos 180 mg (2 tabletter à 90 mg)
    • Underhållsdos 90 mg 1×2 (60 mg 1×2 är undantagsfall vid långtidsbehandling, se läkemedelsbehandling CCS)
  • Behandlingstid: Vid DAPT: Se DAPT
  • Biverkning: Dyspné
  • Kommentar:
    • Ingen dosjustering vid kronisk njursvikt, dock ingen data för GFR<15 eller dialys.
    • Läkemedelseffekt 0,5-2 timmar efter laddningsdos.
    • En antidot är under utveckling [11]Buchanan A, Newton P, Pehrsson S, Inghardt T, Antonsson T, Svensson P, Sjögren T, Öster L, Janefeldt A, Sandinge AS, Keyes F, Austin M, Spooner J, Gennemark P, Penney M, Howells G, Vaughan T, … Continue reading [12]Pehrsson S, Johansson KJ, Janefeldt A, Sandinge AS, Maqbool S, Goodman J, Sanchez J, Almquist J, Gennemark P, Nylander S. Hemostatic effects of the ticagrelor antidote MEDI2452 in pigs treated with … Continue reading.

Prasugrel (Efient)

  • Indikation: Tillsammans med ASA som DAPT.
  • Kontraindikation: Hög blödningrisk, pågående blödning. Kontraindicerat vid tidigare stroke/TIA/intrakraniell blödning. Ges ej samtidigt som oral antikoagulation.
    • Laddningdos 60 mg p.o.
    • Underhållsdos 10 mg 1×1 (vikt <60 kg eller ålder ≥75 år ges 5 mg 1×1) [13]Collet JP, Thiele H, Barbato E, et al. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation [published online ahead of … Continue reading [14]Wiviott SD, Braunwald E, McCabe CH, Montalescot G, Ruzyllo W, Gottlieb S, Neumann FJ, Ardissino D, De Servi S, Murphy SA, Riesmeyer J, Weerakkody G, Gibson CM, Antman EM; TRITON-TIMI 38 … Continue reading
  • Behandlingstid: Vid DAPT: Se DAPT
  • Kommentar:
    • Ingen dosjustering vid kronisk njursvikt, dock ingen data för GFR<15 eller dialys.
    • Läkemedelseffekt 0,5-4 timmar efter laddningsdos.
    • Prasugrel testades mot Clopidogrel i TRITON-TIMI 38.
    • Prasugrel testades som förbehandling (mot icke-förbehandling) på NSTE-ACS-patienter i ACCOAST-studien, studien avslutades i förtid pga skadlig effekt av förbehandling. [15]Montalescot G, Bolognese L, Dudek D, Goldstein P, Hamm C, Tanguay JF, ten Berg JM, Miller DL, Costigan TM, Goedicke J, Silvain J, Angioli P, Legutko J, Niethammer M, Motovska Z, Jakubowski JA, Cayla … Continue reading
    • Prasugrel är en prodrug som behöver konverteras till en aktiv metabolit [16]Niitsu Y, Jakubowski JA, Sugidachi A, Asai F. Pharmacology of CS-747 (prasugrel, LY640315), a novel, potent antiplatelet agent with in vivo P2Y12 receptor antagonist activity. Semin Thromb Hemost. … Continue reading.

Ticlopidine (Tiklid)

  • Ticlopidine (Tiklid)
    • den första P2Y12-hämmaren, ej längre i bruk.
    • samma effekt och samma blödningsrisk som efterträdaren Clopidogrel, men andra allvarliga biverkningar dessutom.

Cangrelor (Kengrexal)

  • Indikation: Intravenös P2Y12-hämmare. Ges när P2Y12-blockad behövs direkt eller orala P2Y12 antagonister inte kan ges (t.ex intuberad patient utan V-sond)[17]Kordis P, Bozic Mijovski M, Berden J, Steblovnik K, Blinc A, Noc M. Cangrelor for comatose survivors of out-of-hospital cardiac arrest undergoing percutaneous coronary intervention: the … Continue reading eller om snabb offset-effekt önskas (t.ex. nyligen stentad patient som har en akut operationsindikation). [18]Capodanno D, Milluzzo RP, Angiolillo DJ. Intravenous antiplatelet therapies (glycoprotein IIb/IIIa receptor inhibitors and cangrelor) in percutaneous coronary intervention: from pharmacology to … Continue reading[19]Qamar A, Bhatt DL. Current status of data on cangrelor. Pharmacol Ther. 2016 Mar;159:102-9. doi: 10.1016/j.pharmthera.2016.01.004. Epub 2016 Jan 21. PMID: 26802900.
    Se assessment report, European Medicines Agency och EMA-produktresumé Cangrelor (svenska)
  • Dosering:
    • En flaska Cangrelor innehåller 50 mg pulver, som ska spädas.
    • PCI-dosering (patienter som inte är förbehandlade med en oral P2Y12-hämmare): Bolus 30 μg/kg i.v. (bolus ges innan PCI börjas, kan ges under <1 minut) följt av 4 μg/kg/min infusion under minst 2 timmar, upp till 4 timmar (oral P2Y12-hämmare behöver ges innan/kort efter avslutad infusion, se nedan).
    • Bridging-dosering (patienter som står på oral P2Y12-hämmare som behöver sättas ut inför operation): 0.75 μg/kg/min startas utan bolusdos när den orala P2Y12 hämmaren pausas. Infusionen avslutas senast 1 timme innan operationen. Denna dosen är testad i upp till 7 dygn.[20]Angiolillo DJ, Firstenberg MS, Price MJ, Tummala PE, Hutyra M, Welsby IJ, Voeltz MD, Chandna H, Ramaiah C, Brtko M, Cannon L, Dyke C, Liu T, Montalescot G, Manoukian SV, Prats J, Topol EJ; BRIDGE … Continue reading[21]assessment report, European Medicines Agency.
    • Se även FASS.se/Cangrelor
  • Byta till oral P2Y12-hämmare:
    • Byte till Ticagrelor eller Prasugrel: Ge ladningsdos Ticagrelor 180 mg eller Prasugrel 60 mg 30 minuter innan Cangrelorinfusionen avslutas.
    • Byte till Clopidogrel: På grund av en interaktion har Clopidogrel laddningdosen inte full effekt om den ges under pågående Cangrelorinfusion. Bolusdos Clopidogrel ska därför ges direkt (ett par minut) efter avslutad Cangrelorinfusion.
  • Kommentar:

Antidoter

Än så länge finns det ingen antidot mot trombocythämmare (men det är under utveckling för Ticagrelor, detaljer se Ticagrelor).

Switching mellan olika P2Y12-antagonister:

Se avnitt om switching på DAPT-sidan här

Preoperativ utsättning av P2Y12-antagonister:

Se avnitt om DAPT vid (icke-hjärt) kirurgi här

Historisk utveckling av P2Y12-receptorantagonister

(originalpublikationen- en disputation från 2019 – är på engelska):

The first P2Y12 –receptor antagonist was coincidentally developed in the 1970s, and although the prothrombotic effect of ADP has by this time already been known for some years, it took 30 more years until the P2Y12 receptor was isolated as the target of this drug.  

In 1960, A.J. Hellem observed at Rikshospitalet in Oslo that a small molecule originating from red blood cells caused platelets to adhere to glass.[23]Packham MA and Rand ML. Historical perspective on ADP-induced platelet activation. Purinergic signalling. 2011;7:283-92 The next year, researchers in Oslo identified this small molecule as the purine adenosine diphosphate (ADP), proved that it converts non-adhesive platelets into adhesive platelets and thus causes platelet aggregation, and assumed that ADP release based on cellular damage might play an important role in thrombosis.[24]Gaarder A, Jonsen J, Laland S, Hellem A and Owren PA. Adenosine diphosphate in red cells as a factor in the adhesiveness of human blood platelets. Nature. 1961;192:531-2. ADP does not normally circulate in the bloodstream, but is stored in large quantities in platelets’ dense granules, which can release ADP when they are stimulated by other substances, like collagen or thrombin. [25]Packham MA and Rand ML. Historical perspective on ADP-induced platelet activation. Purinergic signalling. 2011;7:283-92. [26]Gachet C, Cattaneo M, Ohlmann P, Hechler B, Lecchi A, Chevalier J, Cassel D, Mannucci PM and Cazenave JP. Purinoceptors on blood platelets: further pharmacological and clinical evidence to suggest … Continue reading [27]Storey RF. The P2Y12 receptor as a therapeutic target in cardiovascular disease. Platelets. 2001;12:197-209 [28]Dorsam RT and Kunapuli SP. Central role of the P2Y12 receptor in platelet activation. The Journal of clinical investigation. 2004;113:340-5 ADP causes platelets to change shape from disc-shaped to a spherical structure with pseudopods with a substantial increase in surface area [29]Packham MA and Rand ML. Historical perspective on ADP-induced platelet activation. Purinergic signalling. 2011;7:283-92 to increase cytosolic free calcium, to express a fibrinogen binding site (GP IIb/IIIa receptor), [30]Gachet C, Cattaneo M, Ohlmann P, Hechler B, Lecchi A, Chevalier J, Cassel D, Mannucci PM and Cazenave JP. Purinoceptors on blood platelets: further pharmacological and clinical evidence to suggest … Continue reading and finally to aggregate to a white thrombus by adhering to each other with the help of fibrin links. [31]Born GV, Honour AJ and Mitchell JR. INHIBITION BY ADENOSINE AND BY 2-CHLOROADENOSINE OF THE FORMATION AND EMBOLIZATION OF PLATELET THROMBI. Nature. 1964;202:761-5 In 1964, it was determined that other purines, adenosine and adenosine triphosphate, [32]Abbracchio MP, Burnstock G, Boeynaems JM, Barnard EA, Boyer JL, Kennedy C, Knight GE, Fumagalli M, Gachet C, Jacobson KA and Weisman GA. International Union of Pharmacology LVIII: update on the P2Y G … Continue reading are inhibitors of ADP-induced platelet aggregation.  [33]Packham MA and Rand ML. Historical perspective on ADP-induced platelet activation. Purinergic signalling. 2011;7:283-92 [34]Born GV, Honour AJ and Mitchell JR. INHIBITION BY ADENOSINE AND BY 2-CHLOROADENOSINE OF THE FORMATION AND EMBOLIZATION OF PLATELET THROMBI. Nature. 1964;202:761-5 [35]Husted S and van Giezen JJ. Ticagrelor: the first reversibly binding oral P2Y12 receptor antagonist. Cardiovascular therapeutics. 2009;27:259-74.

Ticlopidine and clopidogrel were developed when the exact site of action of these thienopyridines was still unknown and the first antagonist of the P2Y12 receptor was created by chance [36]Packham MA and Rand ML. Historical perspective on ADP-induced platelet activation. Purinergic signalling. 2011;7:283-92 [37]Gachet C, Cattaneo M, Ohlmann P, Hechler B, Lecchi A, Chevalier J, Cassel D, Mannucci PM and Cazenave JP. Purinoceptors on blood platelets: further pharmacological and clinical evidence to suggest … Continue reading: In 1972, French scientists were searching for new anti-inflammatory drugs related to Tinoridine, a drug from the chemical class thienopyridine with anti-inflammatory properties that was published in 1970, and started synthesizing derivates and testing them on rats. [38]Maffrand J-P. The story of clopidogrel and its predecessor, ticlopidine: Could these major antiplatelet and antithrombotic drugs be discovered and developed today? Comptes Rendus Chimie. … Continue reading They did not succeed in finding anti-inflammatory agents, but some of the compounds showed unanticipated antiplatelet activity and the most active was selected for further development and named ticlopidine.[39]Maffrand J-P. The story of clopidogrel and its predecessor, ticlopidine: Could these major antiplatelet and antithrombotic drugs be discovered and developed today? Comptes Rendus Chimie. … Continue reading In 1978, the thienopyridine ticlopidine hit the market in France under the name Ticlid, was tested in clinical trials (initially in stroke patients), [40]Hass WK, Easton JD, Adams HP, Jr., Pryse-Phillips W, Molony BA, Anderson S and Kamm B. A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk … Continue reading and reached the U.S. market in 1991. Soon after marketing, the drug showed severe side effects in some patients: agranulocytosis and pancytopenia. So, in France, the search for ticlopidine analogs with an improved benefit/risk ratio continued, and after testing thousands of analogs, clopidogrel was found. The preclinical development started in 1987 and led to the worldwidelaunch of clopidogrel in 1998, which became the second-bestselling drug in the first decade of the 21stcentury. [41]Maffrand J-P. The story of clopidogrel and its predecessor, ticlopidine: Could these major antiplatelet and antithrombotic drugs be discovered and developed today? Comptes Rendus Chimie. … Continue reading

Today, we know that there are different types of purinergic receptors (P-receptors) on platelets (as on other cell surfaces). [42]Burnstock G. Purinergic signaling and vascular cell proliferation and death. Arteriosclerosis, thrombosis, and vascular biology. 2002;22:364-73 In 1995, a French-Italian team was able to show that there are at least two different P2-receptors for ADP on platelets, one inducing shape change and another coupled to the inhibition of adenylyl cyclase and causing platelet aggregation, with the latter being receptive to thienopyridines. [43]Gachet C, Cattaneo M, Ohlmann P, Hechler B, Lecchi A, Chevalier J, Cassel D, Mannucci PM and Cazenave JP. Purinoceptors on blood platelets: further pharmacological and clinical evidence to suggest … Continue reading This receptor then had several names (P2T for thrombocyte, P2YAC for adenylyl cyclase, P2YADP) and was finally called the P2Y12 receptor when it was cloned and analyzed in San Francisco in 2001 [44]Gachet C, Cattaneo M, Ohlmann P, Hechler B, Lecchi A, Chevalier J, Cassel D, Mannucci PM and Cazenave JP. Purinoceptors on blood platelets: further pharmacological and clinical evidence to suggest … Continue reading [45]Hollopeter G, Jantzen HM, Vincent D, Li G, England L, Ramakrishnan V, Yang RB, Nurden P, Nurden A, Julius D and Conley PB. Identification of the platelet ADP receptor targeted by antithrombotic … Continue reading and identified as the clopidogrel-receptor. [46]Savi P, Labouret C, Delesque N, Guette F, Lupker J and Herbert JM. P2y(12), a new platelet ADP receptor, target of clopidogrel. Biochemical and biophysical research communications. … Continue reading

The scientists who developed the new antiplatelet drugs knew that clopidogrel, like ticlopidine, was a prodrug that had to be ingested orally to be processed in the liver by cytochrome P450 pathways to an active metabolite, but it was not until 2001, 30 years after the discovery of ticlopidine, that some of them succeeded in isolating the active metabolite.[47]Maffrand J-P. The story of clopidogrel and its predecessor, ticlopidine: Could these major antiplatelet and antithrombotic drugs be discovered and developed today? Comptes Rendus Chimie. … Continue reading Interestingly, the detection of ticlopidine as an active antiplatelet drug would not have been possible if  the initial tests had not been performed on rats but instead on, e.g., guinea pigs, which lack the enzyme to produce the active metabolite. [48]Maffrand J-P. The story of clopidogrel and its predecessor, ticlopidine: Could these major antiplatelet and antithrombotic drugs be discovered and developed today? Comptes Rendus Chimie. … Continue reading

It has been argued that clopidogrel’s main drawbacks are based on its status as a prodrug: Because of the mandatory cytochrome P450-dependent metabolism in the liver, the pharmacodynamic effect is delayed and varies substantially between individuals (15–40% of patients are poor responders). [49]Wallentin L. P2Y(12) inhibitors: differences in properties and mechanisms of action and potential consequences for clinical use. European heart journal. 2009;30:1964-77[50]Cattaneo M. New P2Y(12) inhibitors. Circulation. 2010;121:171-9. In addition, clopidogrel binds (like all thienopyridines45) irreversibly to the P2Y12 receptor so that the effect lasts until new thrombocytes are ready to replace them. Because of these downsides of clopidogrel, the search for an ideal antiplatelet drug continued and led to the last-generation P2Y12antagonists prasugrel and ticagrelor. 

Prasugrel, a third-generation thienopyridine, is a prodrug like the second-generation thienopyridineclopidogrel, but is less dependent on hepatic cytochrome P450 activity and therefore faster acting (maximal effect after approximately 30 minutes instead of 3–5 hours for clopidogrel) and shows less variation in the effect size. [51]Wallentin L. P2Y(12) inhibitors: differences in properties and mechanisms of action and potential consequences for clinical use. European heart journal. 2009;30:1964-77. [52]Cattaneo M. New P2Y(12) inhibitors. Circulation. 2010;121:171-9 [53]Wiviott SD, Antman EM and Braunwald E. Prasugrel. Circulation. 2010;122:394-403. The differences are in the pharmacokinetics; The active metabolites of clopidogrel and prasugrel are chemically similar and have the same potency.[54]Valgimigli M, Bueno H, Byrne RA, Collet JP, Costa F, Jeppsson A, Juni P, Kastrati A, Kolh P, Mauri L, Montalescot G, Neumann FJ, Petricevic M, Roffi M, Steg PG, Windecker S, Zamorano JL and Levine … Continue reading [55]Cattaneo M. New P2Y(12) inhibitors. Circulation. 2010;121:171-9. Prasugrel was tested in the TRITON TIMI-38 trial(2007) [56]Wiviott SD, Braunwald E, McCabe CH, Montalescot G, Ruzyllo W, Gottlieb S, Neumann FJ, Ardissino D, De Servi S, Murphy SA, Riesmeyer J, Weerakkody G, Gibson CM and Antman EM. Prasugrel versus … Continue reading against clopidogrel in invasively treated ACS patients following coronary angiography and the trial found higher efficiency but lower safety for prasugrel. The FDA later criticized the trial for shortcomings in design and disadvantages for patients treated with clopidogrel. [57]Serebruany VL. Timing of thienopyridine loading and outcomes in the TRITON trial: the FDA Prasugrel Action Package outlook. Cardiovasc Revasc Med. 2011;12:94-8

Ticagrelor is the first oral non-thienopyridine P2Y12 antagonist, an ATP analog that belongs to the new chemical class of cyclopentyl-triazolopyrimidines. [58]Cattaneo M. New P2Y(12) inhibitors. Circulation. 2010;121:171-9 [59]Husted S and van Giezen JJ. Ticagrelor: the first reversibly binding oral P2Y12 receptor antagonist. Cardiovascular therapeutics. 2009;27:259-74 It is a direct-acting drug (i.e., not a prodrug that requires conversion to an active metabolite) and a reversible P2Y12 antagonist [60]Cattaneo M. New P2Y(12) inhibitors. Circulation. 2010;121:171-9. that binds to a P2Y12 binding site that differs from the adenosine binding site. [61]Husted S and van Giezen JJ. Ticagrelor: the first reversibly binding oral P2Y12 receptor antagonist. Cardiovascular therapeutics. 2009;27:259-74. The PLATO trial, published in 2009, [62]Wallentin L, Becker RC, Budaj A, Cannon CP, Emanuelsson H, Held C, Horrow J, Husted S, James S, Katus H, Mahaffey KW, Scirica BM, Skene A, Steg PG, Storey RF, Harrington RA, Freij A and Thorsen M. … Continue reading compared the use of ticagrelor and clopidogrel in ACS patients and reported better prevention of the composite endpoint death, MI, or stroke without differences in overall bleeding (but an increase in non-CABG bleeding).

Litteratur

ESC 2017 update DAPT

ESC Guideline NSTE-ACS 2020

Intravenous antiplatelet therapies (glycoprotein IIb/IIIa receptor inhibitors and cangrelor) in percutaneous coronary intervention: from pharmacology to indications for clinical use. (Capodanno 2019) [63]Capodanno D, Milluzzo RP, Angiolillo DJ. Intravenous antiplatelet therapies (glycoprotein IIb/IIIa receptor inhibitors and cangrelor) in percutaneous coronary intervention: from pharmacology to … Continue reading

Current status of data on cangrelor (2016) [64]Qamar A, Bhatt DL. Current status of data on cangrelor. Pharmacol Ther. 2016 Mar;159:102-9. doi: 10.1016/j.pharmthera.2016.01.004. Epub 2016 Jan 21. PMID: 26802900.

EMA-produktresumé Cangrelor (svenska)

Platelets in atherothrombosis [65]Ruggeri ZM. Platelets in atherothrombosis. Nat Med. 2002 Nov;8(11):1227-34. doi: 10.1038/nm1102-1227. PMID: 12411949.

Antiplatelet agents for the treatment and prevention of atherothrombosis [66]Patrono C, Andreotti F, Arnesen H, Badimon L, Baigent C, Collet JP, De Caterina R, Gulba D, Huber K, Husted S, Kristensen SD, Morais J, Neumann FJ, Rasmussen LH, Siegbahn A, Steg PG, Storey RF, Van … Continue reading

Relaterade sidor

ASA/Trombyl
Dubbel trombocythämning (DAPT) vid PCI och AKS
Antitrombotisk trippelbehandling efter PCI (DAPT+OAK)
GPIIb/IIIa antagonister: Integrilin, Aggrastat
DAPT-History

Last Updated on December 30, 2022 by Christian Dworeck

Christian Dworeck
Latest posts by Christian Dworeck (see all)

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