Influence of previous long-term treatment with aspirin on clinical progression of an acute coronary syndrome

Czech version

Authors: J. Špác ¹; J. Pařenica ²
Authors‘ workplace: II. interní klinika Lékařské fakulty MU a FN u sv. Anny, Brno, přednosta doc. MUDr. Miroslav Souček, CSc. ¹; Interní kardiologická klinika Lékařské fakulty MU a FN Brno, pracoviště Bohunice, přednosta prof. MUDr. Jiří Špinar, CSc., FESC ²
Published in: Vnitř Lék 2005; 51(6): 664-670
Category: Original Contributions

Overview

There is a failure of antiaggregation treatment in a large group of patients with chronic forms of ischaemic disease leading to recurrence of ischaemic events. The objective of this paper is to analyse the influence of previous long-term antiaggregation treatment on clinical progression of an acute coronary syndrome.

Method:
The importance of previous treatment has been evaluated in 726 patients admitted into 38 hospitals in Czech Republic for acute coronary syndrome (ACS) without ST segment elevations inthe year 2000. 396 patients were treated with aspirin (group A) on a long-term basis before admission and 330 patients were without aspirin treatment before the admission into hospital (group B).

Results:
Patients in group A showed less frequently signs of myocardial infarction (MI) without ST segment elevations (21.8% versus 26.9%, NS) on admission and a progression of acute coronary syndrome into Q wave MI was less frequent in this group (5% versus 10.6%, p < 0.005) compared to patients in group B. However patients in group A had more frequently the incidence of recurrent angina pain (24.8% versus 13.9%, p < 0.005) and intervention methods of treatment were used more frequently in this group due to failure of a response to conservative treatment (coronarography – 30% versus 22.7%, p < 0.05, PTCA - 10% versus 8.2%, NS, and CABG – 10.2% and 4.2%, p < 0.005 versus group B). There were no differences in using of other methods of pharmacological medication between groups. The analysis demonstrated that even previous history of ACS does not influence the results.

Conclusion:
Patients with long-term antiaggregation treatment exhibit manifestations of less severe forms of acute coronary syndrome during the development of ACS but they respond worse to the conservative treatment in furtherprogression of the disease and they need to be treated with intervention methods more frequently. The mechanism responsible for these facts is thought to be an occurrence of inadequate response to the aspirin treatment. One of the approaches to improve this situation is using of quantitatively evaluated targeted antiaggregation treatment tailored to individual patients.

Key words:
acute coronary syndrome – aspirin treatment

Sources

1. Alexander JH, Harrington RA, Tuttle RH et al. Prior aspirin use predicts worse outcomes in patients with non-ST-elevation acute coronary syndromes. PURSUIT Investigators. Platelet IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy. Am J Cardiol 1999; 83: 1147–1151.

2. Antithrombotic Trialists’ Collaboration: Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction and stroke in high risk patients. British Medical Journal 2002; 324: 71–86.

3. Braunwald E et al. Heart disease. 5. ed. Philadelphia: WB Saunders Company 1997: 1184–1289.

4. Diener HC, Cunha L, Forbes C, et al. European Stroke Prevention Study 2. Dipyridamole plus acetylsalicylic acid in the secondary prevention of stroke. Journal of Neurologic Science 1996; 143: 1–13.

5. Diener HC, Bogousslavsky J, Brass LM et al. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. Journal of the American College of Cardiology 2004; 364: 331–337.

6. Eikelboom JW, Hirsh J, Weitz JI et al. Aspirin-resistant thromboxane biosynthesis and the risk of myocardial infarction, stroke, or cardiovascular death in patients at high risk for cardiovascular events. Circulation 2002; 105: 1650–1655.

7. Eikelboom JW, Hankey GJ. Aspirin resistance: A new independent predictor of vascular events? Journal of the American College of Cardiology 2003; 41: 966–968.

8. Garcia–Dorado D, Theroux P, Tornos P et al. Previous aspirin use may attenuate the severity of the manifestation of acute ischemic syndromes. Circulation 1995; 92:1743–1748.

9. Gum PA, Kottke-Marchant K, Welsh PA et al. A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease. Journal of the American College of Cardiology, 2003; 41: 961–965.

10. Gum PA, Kottke-Marchant K., Poggio ED et al. Profile and prevalence of aspirine resistance in patients with cardiovascular disease. Am J Cardiol 2001; 88: 230–235.

11. Hennekens CH, Sacks FM, Tonkin A et al. Additive benefits of pravastatin and aspirin to decrease risks of cardiovascular disease: Randomized and observational comparisons of secondary prevention trials and their meta-analyses. Arch Intern Med 2004; 164: 40–44.

12. Hirmerová, J., Filipovský J. Klinický význam aspirinové rezistence. Vnitř Lék 2004; 50: 462–469.

13. Horie T, Sekiguchi M, Hirosawa K. Coronary thrombosis in pathogenesis of acute myocardial infarction: histoptahological study of coronary arteries in 108 necropsied cases using serial section. Br Heart J 1978; 40: 153–161.

14. Jurrien M ten Berg, Wim-Gerritsen BM, Haas FJLM et al. Daily Aspirin Does Not Guarantee Complete Inhibition of Platelet Function and Activation During Coronary Angioplasty: The Effect of an Additional Bolus of High-Dose Aspirin. Journal of the American College of Cardiology 2001; 37(Suppl A): 640A (abstract 885).

15. Kennon SRO, Price ChP, Ranjadayalan K et al. The effect of aspirin on C-reactive protein as a marker of risk in unstable angina pectoris. Journal of the American College of Cardiology 2001; 37(Suppl A): 640A (abstrakt 1185).

16. Kiss RG, Kerecsen G, Bato Z et al. Aspirin resistance is associated with platelet GP IIb/IIIa receptor polymorphism PLA2 and thrombotic events in coronary heart disease patients undergoing percutaneous coronary procedures. European Heart Journal 2000; 21(Suppl): 648.

17. Kurth T, Glynn JR, Walker AM et al. Inhibition of clinical benefits of aspirin on first myocardial infarction by nonsterouidel antiinflammatory drugs. Circulation 2003; 108: 1191–1195.

18. Lancaster GI, Lancaster CJ, Radley D et al. Prior aspirin use in unstable angina predisposes to higher risk: the aspirin paradox. International Journal Cardiology 2001; 80: 201–207.

19. Malý M, Vojáček J, Hadačová I et al. Stanovení rychlosti nástupu účinku protidestičkového vlivu dvou různých dávek kyseliny acetylsalicylové agregometrickou metodou. Vnitř Lék 2004; 50: 428–433.

20. Nawarskas JJ, Anderson JR, Raizada V. Whole Blood Aggregometry as a Potential Method of Detecting Aspirin Resistance. Journal of the American College of Cardiology 2003; 41(Suppl A): abstract 1009–119.

21. Peters RJ, Mehta SR, Fox KA et al. Effects of aspirin dose when used alone or in combination with clopidogrel in patients with acute coronary syndromes: observations from the Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) study. Circulation 2003; 108: 1682–1687.

22. Petrželová A, Stejskal D, Prošková J et al. První zkušenosti s využitím katonického propylgallátu jako induktoru agregace trombocytů v hodnocení účinnosti agregační terapie. Vnitř Lék 2001; 47: 747–752.

23. Pulcinelli FM, Pignatelli P, Celistini A et al. Inhibition of platelet aggregation by aspirin progressively decreases in long–term treated patients. Journal of the American College of Cardiology 2004; 43: 979–984.

24. Quinn MJ, Aronow HD, Califf RM et al. Aspirin dose and six month outcome after an acute coronary syndrome. Journal of the American College of Cardiology 2004; 43: 972–978.

25. Santopinto J, Gurfinkel EP, Torres V et al. Prior aspirin users with acute non-ST-elevation coronary syndromes are at increased risk of cardiac events and benefit from enoxaparin. Am Heart J 2001; 141: 566–572.

26. Sharis PJ, Cannon ChP, McCabe CH et al. Prior aspirin use is a univariate, but not a multivariate predcitor of 1 year mortality in 10 302 patients with acute coronary syndromes: results from OPUSTIMI 16. Journal of the American College of Cardiology 2000; 35(Suppl A): 391.

27. Spencer FA, Santopinto JJ, Gore JM et al. Impact of aspirin on presentation and hospital outcomes in patients with acute coronary syndromes (The Global Registry of Acute Coronary Events [GRACE]). Am J Cardiol 2002; 90: 1056–1061.

28. Špác J, Pařenica J, Partišová M et al. Nemocní s nestabilní anginou pectoris – jaká byla skutečnost v českých a moravských nemocnicích v roce 2000. Vnitř Lék 2003; 49: 603–609.

30. Špinar J, Vítovec J. ASA – je nám vše jasné? Vnitř Lék 2002; 48: 781–790.