Libby P. Circulation 2001;104:365-372.

Adapted from Braunwald E.et al. www.incirculation.net

Gpllb/llla +Gla/lla +Glb/IX TA2 Adapted from Schafer AI. Antiplatelet therapy. Am J Med. 1996;101:199-209.

Adapted from Blatt D.L., Topol E.J. Nature Reviews Drug Discovery 2003;2:15-28

Antman EM. In: Califf RM, ed. Atlas of Heart Diseases, VIII. Philadelphia, PA: Current Medicine, 1996.

Braunwald E. et al. Available at www.acc.org

-NSTE-Q- Q- -STE( - ) Braunwald E. et al. Available at www.acc.org

Adapted from Braunwald E. Circulation 1989; 79: 441-444.

Jarvis B et al. Drugs 2000;60:347377.

Antithrombotic Trialists Collaboration. BMJ 2002; 324: 71-86* RRR - (, , ) Antithrombotic Trialists Collaboration (2002)

Antithrombotic Trialists Collaboration. BMJ 2002; 324: 71-86* RRR - (CCC, , ) Antithrombotic Trialists Collaboration (2002)

Herbert J.M. et al Thrombosis and Hemostasis 1998;80:512518

The CURE Investigators. NEJM 2001;345:494502. RRR 20% p

+ (n = 6303) + (n = 6259) 2.7% 3.7% 0.001 1.8% 2.2% NS* 0.9% 1.5% 0.002 2.4% 5.1% < 0.001P CURE (1999-2001)The CURE Investigators. NEJM 2001;345:494502. * NS (not statistically significant)

Peters RJG et al. Circulation 2003; 108: 16821687. CURE (1999-2001)

* - : - (TIMI 0/1), Sabatine M.S., Cannon C.P., Gibson C.M. et al. NEJM 2005;352:11791189. CLARITY TIMI 28 (2003-2004) + (n=1739) + (n=1752)21.715.05%10%15%20%25% * (%)RRR 36%p

* : , , , . 30 * (%)0%5%10%15%051015202530RRR 20%p=0.03 + 11.6% + 14.1% CLARITY TIMI 28 (2003-2004)Sabatine M.S., Cannon C.P., Gibson C.M. et al. NEJM 2005;352:11791189.

+ + (%)(n=1733) (n=1719) p

( ) 1.31.1NS 1.00.5NS 0.50.7NS

30 1.91.7NS 1.60.9NS 3.42.7NSNS (not statistically significant) CLARITY TIMI 28 (2003-2004)Sabatine M.S., Cannon C.P., Gibson C.M. et al. NEJM 2005;352:11791189.

Chen Z.M. et al. Presentation, ACC 2005. Available at http://www.commit-ccs2.org.* - : , , COMMIT/CCS-2 (1999-2005)

+ + (%) (n=22958) (n=22891)

0.17 0.17 NS 0.07 0.07 NS 0.16 0.16 NS 0.20 0.16 NS 0.58 0.54 NS COMMIT/CCS-2 (1999-2005)Chen Z.M. et al. Presentation, ACC 2005. Available at http://www.commit-ccs2.org.NS (not statistically significant)

+ + (n=22958) (n=22891)

() 069.3%10.9% 7129.7%10.7% 13248.8%8.7% 8.8%9.9% 9.7% 10.3% 9.3%10.1%+ + RR & 95% CI * COMMIT/CCS-2 (1999-2005)Chen Z.M. et al. Presentation, ACC 2005. Available at http://www.commit-ccs2.org.* (, , )

Bhatt D.L., Fox K.A., Hacke W. et al. NEJM 2006;354:1706-1717 CHARISMA (2002-2005)RRR 7.1% =0.22 + 75-162 7.3% 75 + 75-162 6.8% 0%2%4%6%8%0612182430 * (%)* - : , ,

CHARISMA (2002-2005)Bhatt D.L., Fox K.A., Hacke W. et al. NEJM 2006;354:1706-1717 NS (not statistically significant) 0.22 (NS) (n=15603)0.20 (NS) (n=3284) 0.046 - (n=12153) 7.1%-20%12.5%, , (n=9478) 7.9%6.9%RRR6.6%5.5%7.3%6.8%0.0117.1%8.8%7.3%

+ + (%) (n=7802) (n=7801) RR p

1.7 1.3 1.25 0.09 2.1 1.3 1.62

ESC 2007 -NSTEESC 2007 Guidelines for the Diagnosis and Treatment of non-ST-segment elevation Acute coronary syndromes. EHJ 2007;28;1598-1660.

ACC/AHA 2007 Guidelines for the Management of Patients with Unstable Angina / Non ST-Elevation Myocardial Infarction. Circulation 2007;116;803-877. -NSTE 75-162 .

-NSTE 75 1 .

-NSTE 162-325 : 1 ; 3 - ; 6 - ;

75-162 .

-NSTE , , 75 1 .

/ 2007 -NSTE

2007 Focuced Update of the ACC/AHA 2004 for the Management of Patients with ST-Elevation Myocardial Infarction. Circulation 2008;117;296-329 -STE 75 1 , .

-STE 14 .

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(- , , ) .*

.*

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*****Platelet Plug FormationPlatelets play a central role in the development of thrombi and subsequent ischemic events. The process of platelet-mediated thrombus formation involves adhesion, activation, and aggregation.Within seconds of injury, platelets adhere to collagen fibrils through glycoprotein Ia/Iia GPIa/IIa) receptor. An adhesive glycoprotein, von Willebrand factor (vWF), allows platelets to stay attached to the subendothelial vessel wall (via GPIb) despite high shear forces. Following adhesion, platelets are activated to secrete a variety of agonists including thrombin, serotonin, adenosine diphosphate (ADP), and thromboxane A2 (TXA2). These agonists, which further augment the platelet activation process, bind to specific receptor sites on the platelets to activate the GPIIb/IIIa receptor complex, the final common pathway to platelet aggregation. Once activated, the GPIIb/IIIa receptor undergoes a conformational change that enables it to bind with fibrinogen. Fibrinogen links platelets together to form a platelet plug.[1,2]

1.Handin RI. Bleeding and thrombosis. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrisons Principles of Internal Medicine. Vol 1. 14th ed. New York, NY: McGraw-Hill; 1998:339345. 2.Schafer AI. Antiplatelet therapy. Am J Med. 1996;101:199209. *Platelet Plug FormationPlatelets play a central role in the development of thrombi and subsequent ischemic events. The process of platelet-mediated thrombus formation involves adhesion, activation, and aggregation.Within seconds of injury, platelets adhere to collagen fibrils through glycoprotein Ia/Iia GPIa/IIa) receptor. An adhesive glycoprotein, von Willebrand factor (vWF), allows platelets to stay attached to the subendothelial vessel wall (via GPIb) despite high shear forces. Following adhesion, platelets are activated to secrete a variety of agonists including thrombin, serotonin, adenosine diphosphate (ADP), and thromboxane A2 (TXA2). These agonists, which further augment the platelet activation process, bind to specific receptor sites on the platelets to activate the GPIIb/IIIa receptor complex, the final common pathway to platelet aggregation. Once activated, the GPIIb/IIIa receptor undergoes a conformational change that enables it to bind with fibrinogen. Fibrinogen links platelets together to form a platelet plug.[1,2]

1.Handin RI. Bleeding and thrombosis. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrisons Principles of Internal Medicine. Vol 1. 14th ed. New York, NY: McGraw-Hill; 1998:339345. 2.Schafer AI. Antiplatelet therapy. Am J Med. 1996;101:199209. *Reference

Herbert JM, Dol F, Bernat A et al. Thromb Haemost 1998;80:512518.

****Platelet Plug FormationPlatelets play a central role in the development of thrombi and subsequent ischemic events. The process of platelet-mediated thrombus formation involves adhesion, activation, and aggregation.Within seconds of injury, platelets adhere to collagen fibrils through glycoprotein Ia/Iia GPIa/IIa) receptor. An adhesive glycoprotein, von Willebrand factor (vWF), allows platelets to stay attached to the subendothelial vessel wall (via GPIb) despite high shear forces. Following adhesion, platelets are activated to secrete a variety of agonists including thrombin, serotonin, adenosine diphosphate (ADP), and thromboxane A2 (TXA2). These agonists, which further augment the platelet activation process, bind to specific receptor sites on the platelets to activate the GPIIb/IIIa receptor complex, the final common pathway to platelet aggregation. Once activated, the GPIIb/IIIa receptor undergoes a conformational change that enables it to bind with fibrinogen. Fibrinogen links platelets together to form a platelet plug.[1,2]

1.Handin RI. Bleeding and thrombosis. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrisons Principles of Internal Medicine. Vol 1. 14th ed. New York, NY: McGraw-Hill; 1998:339345. 2.Schafer AI. Antiplatelet therapy. Am J Med. 1996;101:199209. ****Reference

Herbert JM, Dol F, Bernat A et al. Thromb Haemost 1998;80:512518.

**NEJM****************