Genome instability in peripheral blood lymphocytes of patients with heart failure and reduced ejection fraction

Author:

Tubić Vukajlović Jovana1,Simić Ivan23,Smiljanić Zorica3,Grujičić Darko1,Milošević-Djordjević Olivera14

Affiliation:

1. University of Kragujevac, Faculty of Science, Department of Biology and Ecology , 34000 Kragujevac , Serbia

2. University of Kragujevac, Faculty of Medical Sciences, Department of Internal Medicine , 34000 Kragujevac , Serbia

3. University Clinical Center Kragujevac, Department of Cardiology , 34000 Kragujevac , Serbia

4. University of Kragujevac, Faculty of Medical Sciences, Department of Genetics , 34000 Kragujevac , Serbia

Abstract

Abstract Heart failure (HF) is a complex clinical condition characterized by functional and structural defects of the myocardium, but genetic and environmental factors are considered to play an important role in the development of the disease. In the present study, we investigated the genome instability (DNA and chromosomal damage) in patients with heart failure with reduced ejection fraction (HFrEF) ≤40% and its association with risk factors. The studied population included 48 individuals, of which 29 HFrEF patients (mean age 57.41 ± 5.74 years) and 19 healthy controls (mean age 57.63 ± 6.09 years). The genetic damage index in peripheral blood lymphocytes was analyzed using the comet assay, while micronuclei frequency and nuclear division index were analyzed using the cytokinesis-block micronucleus assay. Our results showed that HFrEF patients had a significantly higher genetic damage index compared with the healthy controls (P < .001). Cytokinesis-block micronucleus assay showed that the average micronucleus frequency in peripheral blood lymphocytes of patients was significantly higher, while the nuclear division index values were significantly lower than in controls (P < .01). Using multiple linear regression analysis, pathological state, ejection fraction, creatinine, glucose, associated disease, residence, proBNP, troponin, urea, ACE-inhibitors, and length of the drug therapy were identified as predictors of DNA and/or chromosomal damage in HF patients. We can conclude that DNA and chromosomal damage was increased in patients with HF, which may be a consequence of disease and/or drug therapy.

Funder

Ministry of Education, Science and Technological Development of the Republic of Serbia

Publisher

Oxford University Press (OUP)

Subject

Health, Toxicology and Mutagenesis,Genetics (clinical),Toxicology,Genetics

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