Heart electrical instability in patients with acute myeloid leukemia with anemic syndrome

1Lanovenko, II, 2Berezyuk, OM
1State Institution "Institute of Hematology and Blood Transfusion of the NAMS of Ukraine", Kyiv
2M. I. Pirogov Vinnytsia National Medical University
Dopov. Nac. akad. nauk Ukr. 2016, 11:104-111
Section: Medicine
Language: Ukrainian

In patients with acute myeloid leukemia with anemic syndrome (anemia of middle-level heaviness), the systemic electrosardiographic disorders are established. Before the carrying out chemotherapy, tachycardia, arrhythmia, deformation of the T wave, and a depression of segment ST are registered. After chemotherapy, the diffuse changes of the teeth, supraventricular arrhythmia, and damages in the conductivity and parameters of systole are revealed. With the deepening of anemia, the frequency of teeth deformations and violations of the interval and amplitude electroctrocardiographic parameters were increased. Combined disorders of automatism, of excitability, conductivity, and contractility suggest the development the syndrome of cardiac electrical instability in patients with acute myeloid leukemia. Increasing the amplitude of the P wave and the interval QT, diffuse violation of the T wave, ST segment depression to 1 mm should be viewed as predictors of fatal arrhythmias and acute coronary syndrome.

Keywords: acute myeloid leukemia, anemia syndrome, arrhythmia, electrocardiogram
  1. Harper P., Littlewood T. Oncology, 2005, 69, Suppl. 2: 2—7. doi: https://doi.org/10.1159/000088282, PMid:16244504
  2. Guide to Hematology, Ed. A.I. Vorobiev, Moscow: Nyudiamed, 2007 (in Russian).
  3. Lanovenko I.I., Berezyuk O.M. Reports of the National Academy of Sciences of Ukraine, 2010, 8: 200—207 (in Russian).
  4. Lanovenko I.I. Hematology and transfusiology news: Int. Collect. Peer Rev., 2007, Iss 6: 26—38 (in Russian).
  5. Semenza G.L. Physiology, 2009, 24, No 2: 97—106. doi: https://doi.org/10.1152/physiol.00045.2008, PMid:19364912
  6. Fisher J.W. Exp. Biol. Med., 2003, 228, No 1: 1—14.
  7. Moncada S., Palmer R.M.J., Higgs E.A. Pharmacol. Rev., 1991, 43, No 2: 109—142. PMid:1852778
  8. Lanovenko I.I. Hematology and Blood Transfusion: Int. Collect., 2008, Iss. 34, Vol. 1: 227—234 (in Ukrainian).
  9. Lanovenko I.I., Berezyuk O.M. Reports of the National Academy of Sciences of Ukraine, 2014, 12: 166—174 (in Ukrainian). doi: https://doi.org/10.15407/dopovidi2014.12.166
  10. Stockmann C., Fandrey G. Clin. Exp. Physiol. Pharmacol., 2006, 33, No 10: 968—979. doi: https://doi.org/10.1111/j.1440-1681.2006.04474.x, PMid:17002676
  11. Essop M. F. J. Physiol., 2007, 584, Pt. 3: 715—726. doi: https://doi.org/10.1113/jphysiol.2007.143511, PMid:17761770 PMCid:PMC2276994
  12. Guyton A.K., Hall J.E. Medical Physiology, Moscow: Logosfera, 2008 (in Russian).
  13. Naeije R. Prog. cardiovasc. Dis., 2010, 52, No 6: 456—466. doi: https://doi.org/10.1016/j.pcad.2010.03.004, PMid:20417339
  14. Brucks S., Little W.C., Chao T. et al. Am. J. Cardiol., 2004, 93, No 8 : 1055—1057. doi: https://doi.org/10.1016/j.amjcard.2003.12.062, PMid:15081458
  15. Naito Y., Tsujino T., Matsumoto M. et al. Am. J. Physiol. Heart Circ. Physiol., 2009, 296, No 3 : H585-593. doi: https://doi.org/10.1152/ajpheart.00463.2008, PMid:19136608