SavedAdd your journal

Journals / The Anatolian Journal of Cardiology / 2017 / Cilt: 18 - Sayı: 4

Effects of rivaroxaban on intimal hyperplasia and smooth muscle cell proliferation at the carotid artery anastomosis site in rabbits

Gökmen AKKAYA
Çağatay BİLEN
TUĞRA GENÇPINAR
PINAR AKOKAY
Baran UĞURLU
Pages
261–265
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)

When the section series were evaluated for media thickness, the thickness of group B was lesser than that of group A; the difference was statistically significant (p=0.002).Conclusion: This study may imply a potential midterm benefit of rivaroxaban following arterial anastomosis by reducing intimal proliferation and restenosis.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: This study aimed to assess the effect of new generation oral, direct factor Xa inhibitor rivaroxaban on intimal hyperplasia and smooth muscle cell proliferation at the carotid artery anastomosis site of rabbits.Methods: In total, 14 New Zealand male rabbits weighing 3-3.5 kg were randomized into two groups.
📊
Key Findings & Data:Group A (7 rabbits) served as the control group and received no medication.
💡
Conclusion & Impact:When the section series were evaluated for media thickness, the thickness of group B was lesser than that of group A; the difference was statistically significant (p=0.002).Conclusion: This study may imply a potential midterm benefit of rivaroxaban following arterial anastomosis by reducing intimal proliferation and restenosis.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: This study aimed to assess the effect of new generation oral, direct factor Xa inhibitor rivaroxaban on intimal hyperplasia and smooth muscle cell proliferation at the carotid artery anastomosis site of rabbits.Methods: In total, 14 New Zealand male rabbits weighing 3-3.5 kg were randomized into two groups. Group A (7 rabbits) served as the control group and received no medication. Rivaroxaban was perorally administered to group B (7 rabbits) mg/kg/day for 28 days. Following anesthesia induction, carotid arteries were dissected through a right neck incision. following heparinization at 100 IU/kg, vertical full thickness arteriotomy was performed, then was repaired continuously with 8-0 polypropylene. At day 28, all rabbits were sacrificed and the anastomosed carotid artery segments were analyzed using light microcopy. Hematoxylin-eosin and Masson's trichrome stained images were analyzed using a digital image analysis program, and lumen diameter, lumen area, intimal and medial thickness, and media areas were measured and results were compared.Results: In the serial sections, the average lumen diameter of group B was higher than that of group A (p=0.001). The lumen areas of group B were also higher than those of group A (p=0.004). The intimal thickness of group B was lower than that of group A (p=0.001). When the section series were evaluated for media thickness, the thickness of group B was lesser than that of group A; the difference was statistically significant (p=0.002).Conclusion: This study may imply a potential midterm benefit of rivaroxaban following arterial anastomosis by reducing intimal proliferation and restenosis.

🔖

Cite This Article

AKKAYA, G., BİLEN, Ç., GENÇPINAR, T., AKOKAY, P., UĞURLU, B. (2017). Effects of rivaroxaban on intimal hyperplasia and smooth muscle cell proliferation at the carotid artery anastomosis site in rabbits. The Anatolian Journal of Cardiology, Cilt: 18 - Sayı: 4, 261–265. https://ajindex.com/articles/367306

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (13)

  1. Wang B, Zhang M, Takayama T, Shi X, Roenneburg DA, Kent KC, et al Bromodomain Blockade Mitigates Intimal Hyperplasia in Rat Carotid Arteries. EbioMedicine 2015; 2: 1650-61
  2. Jukema JW, Ahmed TA, Verschuren JJ, Quax PH. Restenosis after PCI. Part 2: prevention and therapy. Nat Rev Cardiol 2012; 9: 79-90
  3. Hoffman M, Monroe DM 3rd. A cell-based model of hemostasis. Thromb Haemost 2001; 85: 958-65
  4. Herbert J, Bono F, Herault J, Avril C, Dol F, Mares A, et al. Effector protease receptor 1 mediates the mitogenic activity of factor Xa for vascular smooth muscle cells in vitro and in vivo. J Clin Invest 1998; 101: 993-1000
  5. Cirino G, Cicala C, Bucci M, Sorrentino L, Ambrosini G, DeDominicis G, et al. Factor Xa as an interface between coagulation and inflammation. Molecular mimicry of factor Xa association with effector cell protease receptor-1 induces acute inflammation in vivo. J Clin Invest 1997; 99: 2446-51
  6. Sharma A, Garg A, Borer JS, Krishnamoorthy P, Garg J, Lavie CJ, et al. Role of oral factor Xa inhibitors after acute coronary syndrome. Cardiology 2014; 129: 224-32
  7. Mustanoja S, Metso TM, Putaala J, Heikkinen N, Haapaniemi E, Salonen O, et al. Helsinki experience on nonvitamin K oral anticoagulants for treating cervical artery dissection. Brain Behav 2015; 5: e00349
  8. Seri A, Marta DS, Madalan A, Popescu M, Tiglea AI, Moldoveanu E. Lipoprotein-associated phospholipase A2, myeloperoxidase and vascular endothelial growth factor - predictors of high vascular risk in respiratory bacterial infections. J Med Life 2016 9: 429-33
  9. Bonetti PO, Lerman LO, Lerman A. Endothelial dysfunction: a marker of atherosclerotic risk. Arterioscler Thromb Vasc Biol 2003; 23: 168-75
  10. Cohn JN. Arterial compliance to stratify cardiovascular risk: more precision in therapeutic decision making. Am J Hypertens 2001; 14: 258-63
  11. Hara T, Fukuda D, Tanaka K, Higashikuni Y, Hirata Y, Nishimoto S, et al. Rivaroxaban, a novel oral anticoagulant, attenuates atherosclerotic plaque progression and destabilization in ApoE-deficient mice. Atherosclerosis 2015; 242: 639-46
  12. Wong PC, Crain EJ, Watson CA, Xin B. Favorable therapeutic index of the direct factor Xa inhibitors, apixaban and rivaroxaban, compared with the thrombin inhibitor dabigatran in rabbits. J Thromb Haemost 2009; 7: 1313-20
  13. Marcus AJ, Broekman MJ, Drosopoulos JH, Islam N, Alyonycheva TN, Safier LB, et al. The endothelial cell ecto -ADPase responsible for inhibition of platelet function is