Journals / MN Kardiyoloji / 2005 / Cilt: 12 - Sayı: 1

The use of low molecular weight heparin in acute coronary syndromes

Düşük molekül ağırlıklı heparinlerin akut koroner sendromlarda kullanımı

Pages
56–65
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In this article efficacy of low-molecular-weight heparin therapy in acute coronary syndromes is discussed.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:The pathophysiology of acute coronary syndromes consists of platelet aggregation and consequently thrombus formation over an eroded or ruptured atherosclerotic plaque.
📊
Key Findings & Data:As platelets play a pivotal role in the pathogenesis of acute coronary syndromes, antithrombotic therapy with unfractionated heparin and low-molecular-weight heparins became an important part of the therapy.
💡
Conclusion & Impact:In this article efficacy of low-molecular-weight heparin therapy in acute coronary syndromes is discussed.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Koroner hastalık · Heparin · Heparin

Abstract

The pathophysiology of acute coronary syndromes consists of platelet aggregation and consequently thrombus formation over an eroded or ruptured atherosclerotic plaque. As platelets play a pivotal role in the pathogenesis of acute coronary syndromes, antithrombotic therapy with unfractionated heparin and low-molecular-weight heparins became an important part of the therapy. Although the efficacy of unfractioned heparin in non ST segment elevation acute coronary syndromes is proven, its combination with thrombolytic agents in ST segment elevation myocardial infarction is debatable yet. Due to low bioavailability and unpredictable dose response of unfractioned heparin, low-molecular-weight heparins became an alternative therapy. In this article efficacy of low-molecular-weight heparin therapy in acute coronary syndromes is discussed.

Özet

Akut koroner sendromun patofizyolojisi aterosklerotik plağın fissüre veya rüptüre olmasını takiben ortaya çıkan platelet aggregasyonunu ve sonuçta trombüs oluşmasını içermektedir. Trombositlerin akut koroner sendromun patogenezinde önemli rol oynaması nedeniyle antitrombotik ilaçlar olan anfraksiyone heparin ve düşük molekül ağırlıklı heparinlerin bu alanda kullanımları önem kazanmıştır. Anfraksiyone heparinin ST segment elevasyonsuz akut koroner sendromda etkili olduğu gösterilmekle beraber, ST segment elevasyonlu miyokard infarktüsünde trombolitik tedavi ile birlikte kullanımı tartışmalıdır. Anfraksiyone heparinin biyoyararlanımının ve terapötik aralığının değişken olması nedeniyle düşük molekül ağırlıklı heparinler kullanıma girmiş ve bu konuda klinik çalışmalar yapılmıştır. Bu yazıda düşük molekül ağırlıklı heparinlerin etkinliği ve akut koroner sendromlarda kullanımı incelenmiştir.

🔖

Cite This Article

AKAR, N., CANBAY, A., GÜLEN, O., DİKER, E., AYDOĞDU, S. (2005). The use of low molecular weight heparin in acute coronary syndromes. MN Kardiyoloji, Cilt: 12 - Sayı: 1, 56–65. https://ajindex.com/articles/297984

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (12)

  1. Graves EJ. Detailed diagnosis and prosedures: National Hospital Discharge Survey, 1990. National Center for Health Statistics. Vital Health Stat {13}. 1992:113. Alexander RW. Hurst's The Heart (8th edition). The coronary ischemic syndromes: Relationship to the biology of atherosclerosis. 1994:1021. Ambrose JA, Winters SL, Stern A, et al. Angiographic morphology and the pathogenesis of unstable angina pectoris. J Am Coll Cardiol 1985; 5: 609-16. Faik E. Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death: autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion. Circulation 1985;71:699-708.
  2. Hirsch PD, Hillis LD, Campbell WB, Firth BG, Willerson JT. Release of prostaglandins and thromboxane intso the coronary circulation in patients with ischemic heart disease. N Eng J Med 1981; 304:685-91.
  3. Ardissino D, Merlini PA, Ariens R, et al. Tissue-factor antigen i activity in human coronary atherosclerotic plaques. Lancet 37;349:769-71.
  4. Toschi V, Gallo R, Lettino M, et al. Tissue factor modulates i thrombogenicity of human atherosclerotic plaques, culation 1997; 95:594-9. Weitz Jl. Activation of blood coagulation by plaque rupture: ichanisms and prevention. Am J Cardiol 1995; 75:23-5.
  5. Buchanan MR, Brister SJ. Individual variation in the effects ASA on platalet function: implications for the use of aspirin ıically. Can J Cardiol 1995; 11:221 -7. Fragmin during Instability in Coronary Artery Disease RISC) study group. Low molecular weight heparin during tability in coronary artery disease. Lancet 1996; 347:561-8.
  6. Sixma JJ, Wester J. The hemostatic plug. Semin Hematol 77; 14:265-99.
  7. Charo IF, Feinman RD, Detwiller TC. Interrelations of platelet gregation and secretion. J Clin Invest 1977; 60:866-73.
  8. Stenberg PE, Baintc/n DF. Storage organelles in platelets and igakaryocytes, in Phillips DR, Shuman MA (edds). Biochemistry Daltelets. Orlando, Fla., Academic Press, 1986:257-94.
  9. Helgason CM, Tortorice KL, Winkler SR, et al. Aspirin res-nce and failure in cerebral infarction. Stroke 1993; 24:345-50.
  10. Helgason CM, Bolin KM, Hoff JA, et al. Development of Dirin resistance in persons with previous ischemic stroke, oke 1994; 25:2331-6.
  11. Grotemeyer KH, Scharafinski HW, Husstedt IW. Two-year ow-up of aspirin responder and aspirin non responders. A Dt-study including 180 post-stroke patients. Thromb Res 1993;:397-403.
  12. Buchanan MR, Hirsh J. Effect of aspirin on hemostasi