Cardiotoxicity of anticancer treatment in patients with ovarian cancer

Česká verzia

Authors: I. Sedláková ¹; R. Pudil ²; R. Praus ²; V. Študent ¹; J. Špaček ¹
Authors place of work: Porodnická a gynekologická klinika LF UK a FN Hradec Králové ¹; I. interní kardioangiologická klinika LF UK a FN Hradec Králové ²
Published in the journal: Kardiol Rev Int Med 2017, 19(1): 14-21

Summary

Objective:
The objective of this study is to point out at the risk of cardiotoxicity of anticancer treatment in ovarian cancer patients.

Patients and Methods:
The study included 55 patients treated for epithelial ovarian cancer newly diagnosed in the period 7/2013–11/2015. Biochemical cardiotoxicity markers (NT-proBNP, cTnT, TnI, CK-MB, MYO, h-FABP, GPBB), echocardiography and electrocardiography were evaluated during primary anticancer treatment.

Results:
Chemotherapy with paclitaxel and carboplatin has an impact on the QT interval and its dispersion. Concentrations of FABP, troponin T and NT-proBNP increased with the total dose of first line cytostatic agents. We found elevated CK-myoglobin (P = 0.051) and troponin T (P = 0.53) especially in ovarian cancer patients after the administration of ten cycles of chemotherapy with paclitaxel and carboplatin and bevacizumab in comparison with ovarian cancer patients receiving standard chemotherapy only.

Conclusion:
Cardiac toxicity is one of the possible adverse events of oncology treatment. It is an interdisciplinary issue requiring close cooperation between the oncologist, cardiologist and specialist in clinical biochemistry. Therefore special attention should be paid to prevent cardiac damage or at least to its early identification and prompt treatment.

Keywords:
ovarian cancer – cardiotoxicity – electrocardiography – biochemical markers – echocardiography

Zdroje

1. Cibula D, Petruželka L a kol. Onkogynekologie. 1. vyd. Praha: Grada Publishing 2009: 614.

2. Talač R, Žaloudík J, Hajdúch M et al. Hodnocení lékové rezistence in vitro a její klinické implikace. Klin Onkol 2000; 13(Speciál2): 2– 3.

3. Michalová E, Poprach A, Němečková I et al. Predikce citlivosti nádorových buněk k chemoterapeutikům ex vivo – úskalí a limitace vlastní metody. Klin Onkol 2008; 21(3): 93– 97.

4. Elbl L. Kardiotoxicita protinádorové léčby. Postgraduál Med 2011; 13(7): 799– 806.

5. Dufek D, Stračina T, Nováková M. Kardiovaskulární nežádoucí účinky protinádorových léčiv. Onkologie 2014; 8(6): 264– 268.

6. Poprach A, Petráková K, Vyskočil J et al. Kardiotoxicita léků používaných v onkologii. Klin Onkol 2008; 21(5): 288– 293.

7. Rowinski EK, McGuire WP, Guarnieri T et al. Cardiac disturbances during the administrativ of taxol. J Clin Oncol 1991; 9(9): 1704– 1712.

8. Arbuck SG, Strauss H, Rowinski E et al. A reassessment of cardiac toxicity associated with taxol. J Natl Cancer Inst Monogr 1993; 15: 117– 130.

9. Ray A, Ray S, Koner BC. Hypertension, cancer and angiogenesis: relevant epidemiological and pharmacological aspects. Indian J Pharmacol 2004; 36(6): 341– 347.

10. Kamba T, McDonald DM. Mechanisms of adverse effects of anti-VEGF therapy for cancer. Br J Cancer 2007; 96(12): 1788– 1795.

11. D’Adamo DR, Anderson SE, Albritton K et al. Phase II study of doxorubicin and bevacizumab for patient with metastatic soft-tissue sarcomas. J Clin Oncol 2005; 23(28): 7135– 7142.

12. Choueiri TK, Mayer EL, Je Y et al. Congestive heart silure risk in patients with breast cancer treated with bevacizumab. J Clin Oncol 2011; 29(6): 632– 638. doi: 10.1200/ JCO.2010.31.9129.

13. Chu TF, Rupnick MA, Kerkela R et al. Cardiotoxicity associated with thyrosine kinase inhibitor sunitinib. Lancet 2007; 370(9604): 2011– 2019.

14. Scappaticci FA, Skillings JR, Holden SN et al. Arterial thromboembolic events in patients with metastatic carcinoma treated with chemotherapy and bevacizumab. J Natl Cancer Inst 2007; 99(16): 1232– 1239.

15. Elbl L, Hrstková H, Chaloupka V et al. Poškození srdce protinádorovou léčbou. 1. vyd. Praha: Grada Publishing 2002: 156.

16. Cardinale D. A new frontier: cardio-oncology. Cardiologia 1996; 41(9): 887– 881.

17. Yeh ET, Bickford CL. Cardiovascular complications of cancer therapy: incidence, pathogenesis, diagnosis, and management. J Am Coll Cardiol 2009; 53(24): 2231– 2247. doi: 10.1016/ j.jacc.2009.02.050.

18. Horáček JM, Pudil R, Tichý M et al. Využití biochemických markerů při hodnocení akutní a chronické kardiotoxicity antracyklinů u hematologických pacientů. Klin Biochem Metab 2007; 15(1): 43– 49.

19. Elbl L, Hrstková H, Chaloupka V et al. Diagnostické možnosti pozdních následků kardiotonické chemoterapie antracykliny. Vnitř Lék 2002; 48(10): 981– 988.

20. Yasue H, Yoshimura M, Sumida H et al. Localization and mechanism of secretion of B-type natriuretic peptide in comparison with those of A-type natriuretic peptide in normal subjects and patients with heart silure. Circulation 1994; 90(1): 195– 203.

21. Remme WJ, Swedberg K. Guidelines for the diagnosis and treatment of chronic heart silure. Eur Heart J 2001; 22(17): 1527– 1560.

22. Jabor A, Pavlisová M, Kluh T et al. Stanovení natriuretických peptidů umožňuje predikci srdečního selhávání. Klin Biochem Metab 1999; 7(28): 44– 48.

23. Bauch M, Ester A, Kimura B et al. Atrial natriuretic peptide as a marker for doxorubicin-induced cardiotoxic effects. Cancer 1992; 69(6): 1492– 1497.

24. Suzuki T, Hayashi D, Yamazaki T et al. Elevated B-type natriuretic peptide levels after anthracyclines administrativ. Am Heart J 1998; 136(2): 362– 363.

25. Nousiainen T, Jantunen E, Vanninen E et al. Acute neurohumoral and cardiovascular effects of idarubicin in leukemia patients. Eur J Haematol 1998; 61(5): 347– 353.

26. Okumura H, Iuchi K, Yoshida T et al. Brain natriuretic peptide is a predictor of anthracyclines-induced cardiotoxicity. Acta Haematol 2000; 104(4): 158– 163.

27. Sandri MT, Salvatici M, Cardinale D et al. N-terminal pro B-type natriuretic peptide after high-dose chemotherapy: a marker predictive of cardiac dysfunction? Clin Chem 2005; 51(8): 1405– 1410.

28. Niwa N, Watanabe E, Hamaguchi M et al. Early and late elevation of plasma atrial and brain natriuretic peptides in patients after bone marrow transplantation. Ann Hematol 2001; 80(8): 460– 465.