Skip to main content

Advertisement

Log in

Prevention of Peri-procedural Myocardial Injury Using a Single High Loading Dose of Rosuvastatin

  • Published:
Cardiovascular Drugs and Therapy Aims and scope Submit manuscript

Abstract

Background

Extensively used lipid-lowering statins have also non-lipid-lowering, pleiotropic effects. Previous studies have demonstrated that a pre-procedural single dose of atorvastatin is associated with reduced peri-procedural myocardial injury.

Aim

The aim of the present study was to demonstrate the effect of a single high loading dose (40 mg) of rosuvastatin on peri-procedural myocardial injury.

Methods

Two hundred ninety nine statin-naive patients with stable angina and de novo lesions eligible for PCI were randomized to a rosuvastatin-treatment (n = 153) and to a no-treatment (n = 146) group. A 40 mg loading dose of rosuvastatin was administrated 24 h before the PCI. CK-MB and cTnI levels were measured before and 12 h after the procedure.

Results

Baseline characteristics were fairly similar between the two arms. The incidence of a CK-MB and cTnI elevation >3× ULN in the rosuvastatin group was significantly lower compared to the control group (0.7% vs. 11.0%, p < 0.001 and 10.5% vs. 39.0%, p < 0.001, respectively). Similarly, the incidence of any CK-MB and cTnI elevation > ULN in the rosuvastatin group was significantly lower compared to the control group (10.5% vs. 34.2%, p < 0.001 and 20.9% vs. 61.6%, p < 0.001, respectively). In addition, CK-MB and cTnI values 12 h after the PCI were significantly lower in the rosuvastatin group compared to the control group (20.13 ± 7.24 U/L vs. 27.02 ± 18.64 U/L, p < 0.001 and 0.14 ± 0.34 ng/ml vs. 0.35 ± 0.40 ng/ml, p < 0.001, respectively).

Conclusion

A single high loading dose of rosuvastatin reduces the incidence of peri-procedural myocardial necrosis and infarction effectively.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1
Fig. 2

Similar content being viewed by others

References

  1. Thygesen K, Alpert JS, White HD. Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. J Am Coll Cardiol. 2007;50:2173–95.

    Article  PubMed  Google Scholar 

  2. Wu AH, Boden WE, McKay RG. Long-term follow-up of patients with increased cardiac troponin concentrations following percutaneous coronary intervention. Am J Cardiol. 2002;89:1300–2.

    Article  CAS  PubMed  Google Scholar 

  3. Ricciardi MJ, Davidson CJ, Gubernikoff G, et al. Troponin I elevation and cardiac events after percutaneous coronary intervention. Am Heart J. 2003;145:522–8.

    Article  CAS  PubMed  Google Scholar 

  4. Tardiff BE, Califf RM, Tcheng JE, et al. Clinical outcomes after detection of elevated cardiac enzymes in patients undergoing percutaneous intervention. IMPACT-II Investigators. Integrilin (eptifibatide) to Minimize Platelet Aggregation and Coronary Thrombosis-II. J Am Coll Cardiol. 1999;33:88–96.

    Article  CAS  PubMed  Google Scholar 

  5. Kong TQ, Davidson CJ, Meyers SN, et al. Prognostic implication of creatine kinase elevation following elective coronary artery interventions. JAMA. 1997;277:461–6.

    Article  CAS  PubMed  Google Scholar 

  6. Abdelmeguid AE, Topol EJ, Whitlow PL, et al. Significance of mild transient release of creatine kinase-MB fraction after percutaneous coronary interventions. Circulation. 1996;94:1528–36.

    CAS  PubMed  Google Scholar 

  7. Abdelmeguid AE, Ellis SG, Sapp SK, et al. Defining the appropriate threshold of creatine kinase elevation after percutaneous coronary interventions. Am Heart J. 1996;131:1097–105.

    Article  CAS  PubMed  Google Scholar 

  8. Davignon J. Beneficial cardiovascular pleiotropic effects of statins. Circulation. 2004;109:III39–43.

    PubMed  Google Scholar 

  9. Pasceri V, Patti G, Nusca A. et al; ARMYDA Investigators. Randomized trial of atorvastatin for reduction of myocardial damage during coronary intervention: results from the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) study. Circulation. 2004;110:674–8.

    Article  CAS  PubMed  Google Scholar 

  10. Patti G, Pasceri V, Colonna G, et al. Atorvastatin pretreatment improves outcomes in patients with acute coronary syndromes undergoing early percutaneous coronary intervention: results of the ARMYDA ACS randomized trial. J Am Coll Cardiol. 2007;49:1272–8.

    Article  CAS  PubMed  Google Scholar 

  11. Di Sciascio G, Patti G, Pasceri V, et al. Efficacy of atorvastatin reload in patients on chronic statin therapy undergoing percutaneous coronary intervention: results of the ARMYDA-RECAPTURE (Atorvastatin for Reduction of Myocardial Damage During Angioplasty) Randomized Trial. J Am Coll Cardiol. 2009;54:558–65.

    Article  PubMed  Google Scholar 

  12. Briguori C, Visconti G, Focaccio A, et al. Novel Approaches for Preventing or Limiting Events (Naples) II Trial Impact of a Single High Loading Dose of Atorvastatin on Periprocedural Myocardial Infarction. J Am Coll Cardiol. 2009 Aug 3.

  13. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem. 1972;18:499–502.

    CAS  PubMed  Google Scholar 

  14. Bell RM, Yellon DM. Atorvastatin, administrated at the onset of reperfusion, and independent of lipid lowering, protects the myocardium by up-regulating a pro-survival pathway. J Am Coll Cardiol. 2003;41:508–15.

    Article  CAS  PubMed  Google Scholar 

  15. Mannacio VA, Iorio D, De Amicis V, Di Lello F, Musumeci F. Effect of rosuvastatin pretreatment on myocardial damage after coronary surgery: a randomized trial. J Thorac Cardiovasc Surg. 2008;136:1541–8.

    Article  PubMed  Google Scholar 

  16. Bellosta S. Direct vascular effects of HMG-CoA reductase inhibitors. Atherosclerosis. 1998;137:S101–9.

    Article  CAS  PubMed  Google Scholar 

  17. Essig M. 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors increase fibrinolytic activity in rat aortic endothelial cells. Role of geranylgeranylation and Rho proteins. Circ Res. 1998;83:683–90.

    CAS  PubMed  Google Scholar 

  18. Colli S. Vastatins inhibit tissue factor in cultured human macrophages. A novel mechanism of protection against atherothrombosis. Arterioscler Thromb Vasc Biol. 1997;17:265–72.

    CAS  PubMed  Google Scholar 

  19. Stalker T, Lefer A, Scalia R. A new HMG-CoA reductase inhibitor, rosuvastatin, exerts anti inflammatory effects on the microvascular endothelium: the role of mevalonic acid. Br J Pharmacol. 2001;133:406–12.

    Article  CAS  PubMed  Google Scholar 

  20. Laheta V, Goicoechea M, Garcia de Vinuesa S, et al. Endothelial dysfunction, oxidative stress and inflammation in atherosclerosis: beneficial effects of statins. Curr Med Chem. 2007;14:243–8.

    Article  Google Scholar 

  21. Laufs U, La Fata V, Plutzky J, et al. Upregulation of endothelial nitric oxide synthase by HMG CoA reductase inhibitors. Circulation. 1998;97:1129–35.

    CAS  PubMed  Google Scholar 

  22. Undas A, Brummel KE, Musial J, et al. Simvastatin depresses blood clotting by inhibiting activation of prpthrombin, factor V, and factor XIII and by enhancing factor Va inactivation. Circulation. 2001;103:2248–53.

    CAS  PubMed  Google Scholar 

  23. Meijer P, Oyen WJ, Dekker D, et al. Rosuvastatin increases extracellular adenosine formation in humans in vivo: a new perspective on cardiovascular protection. Arterioscler Thromb Vasc Biol. 2009;29:963–8.

    Article  CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Serkan Cay.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Cay, S., Cagirci, G., Sen, N. et al. Prevention of Peri-procedural Myocardial Injury Using a Single High Loading Dose of Rosuvastatin. Cardiovasc Drugs Ther 24, 41–47 (2010). https://doi.org/10.1007/s10557-010-6224-1

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s10557-010-6224-1

Key words

Navigation