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Levosimendan reduces plasma cell-free DNA levels in patients with ischemic cardiomyopathy
Apostolos Zaravinos1, Spiros Tzoras, Stavros Apostolakis
1Department of Clinical Virology, Medical School, University of Crete, Heraklion, Crete, Greece.
Insights
Cell-free DNA (cfDNA) levels decreased in heart failure (HF) patients after levosimendan treatment improved cardiac function. This suggests cfDNA may indicate reduced cardiac apoptosis and tissue injury in HF.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Heart failure (HF) involves cardiac myocyte and non-myocyte apoptosis.
- Elevated cell-free DNA (cfDNA) in plasma is linked to cell death and injury.
- The role of cfDNA as a marker for cardiac apoptosis in HF requires further investigation.
Purpose of the Study:
- To investigate plasma cfDNA levels in patients with ischemic heart failure (HF) and severe left ventricular (LV) systolic dysfunction.
- To determine if cfDNA levels change following treatment with levosimendan, a drug that improves myocardial performance.
- To explore the potential of cfDNA as a marker of cardiac apoptosis affected by improved cardiac function.
Main Methods:
- Plasma cfDNA was measured in 19 HF patients before and 12 hours after levosimendan infusion.
- Echocardiographic and biochemical markers assessed LV diastolic pressure and systolic function.
- Statistical analysis compared cfDNA levels pre- and post-treatment.
Main Results:
- Levosimendan significantly improved echocardiographic and biochemical indices of LV function.
- Plasma cfDNA levels were significantly reduced post-levosimendan treatment (P = 0.028).
- A reduction in cfDNA was observed in 15/19 patients, with >50% reduction in 12/19 patients.
Conclusions:
- Improvement in LV function following levosimendan treatment is associated with a reduction in plasma cfDNA.
- These findings suggest that plasma cfDNA may serve as a marker for reduced cardiac apoptosis and improved cell preservation in HF patients.
- Further research is warranted to validate the utility of plasma cfDNA as a biomarker in heart failure.
Abstract:
Heart failure (HF) is a condition associated with the apoptosis and cell death of both cardiac myocytes and cardiac non-myocytes. DNA fragments released from programmed cell death or acute cellular injury are the main sources of disease-associated elevation of cell-free (cf) DNA. We hypothesized that cfDNA could be a relevant marker of cardiac apoptosis in HF patients that could be affected by the improvement of myocardial performance. To test our hypothesis, we measured plasma cfDNA in 19 patients with ischemic HF and severe left ventricular (LV) systolic dysfunction before and 12 h after completion of levosimendan infusion. Echocardiographic and biochemical markers of LV diastolic pressure and LV systolic function were also assessed. In accordance with previous observations levosimendan improved echocardiographic and biochemical indices of LV function. Plasma cfDNA was significantly reduced in HF patients post-levosimendan treatment (median: 89.4, interquartile range: 87.1 to median: 25.9, interquartile range: 12.3, P = 0.028). Notably, in 15/19 patients there was a reduction in cfDNA levels post-levosimendan infusion; while in 12/19 patients, a more than 50% reduction in plasma cfDNA was observed. Since cfDNA is a marker of tissue injury and apoptosis these results indicate that improvement of LV function has a potential impact on cell preservation and survival. Further studies are needed to substantiate our promising results regarding the role of plasma cfDNA as a marker of HF.
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