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Effects of Dapagliflozin on Novel Inflammatory Markers in Heart Failure Patients
1Department of Cardiology, Bakırcay University Cigli Training and Research Hospital, Izmir, Turkey.
Insights
Sodium-glucose cotransporter-2 (SGLT-2) inhibitors like dapagliflozin significantly reduce inflammation markers (SII and SIRI) in heart failure patients. This reduction in systemic inflammation may explain their cardiovascular benefits.
Area of Science:
- Cardiology
- Pharmacology
- Immunology
Background:
- Sodium-glucose cotransporter-2 (SGLT-2) inhibitors are known to reduce heart failure hospitalizations and cardiac death.
- The precise mechanisms underlying these benefits, particularly for dapagliflozin, remain under investigation.
- Potential anti-inflammatory and immunomodulatory effects of dapagliflozin are hypothesized to contribute to its cardioprotective actions.
Purpose of the Study:
- To investigate the impact of dapagliflozin on systemic inflammation markers in patients with heart failure.
- To explore whether changes in inflammation indices correlate with dapagliflozin's known cardiovascular benefits.
Main Methods:
- A cohort of 191 heart failure patients initiated on dapagliflozin were assessed.
- Systemic Immune-inflammation Index (SII) and Systemic Inflammation Response Index (SIRI) were calculated before and after 6 months of treatment.
- Echocardiographic parameters were also evaluated to assess cardiac function.
Main Results:
- Dapagliflozin treatment led to a significant reduction in both SII and SIRI (p < 0.001).
- No significant changes were observed in echocardiographic parameters (p > 0.05).
- The observed decrease in inflammation indices was consistent across all heart failure subtypes and in patients with or without diabetes mellitus.
Conclusions:
- Dapagliflozin treatment significantly decreases key systemic inflammation markers, SII and SIRI.
- These anti-inflammatory effects may represent a crucial mechanism mediating the cardiovascular advantages of dapagliflozin in heart failure.
- Further research is warranted to fully elucidate the role of inflammation modulation in dapagliflozin's efficacy.
Background:
Sodium-glucose cotransporter-2 (SGLT-2) inhibitors have been established to decrease hospitalizations and cardiac death within all heart failure groups. The exact mechanisms by which the oral antidiabetic medication dapagliflozin achieves this advantage are still unknown. The potential beneficial effects of dapagliflozin on inflammation and the immune system may contribute to these mechanisms.
Method:
The laboratory and echocardiographic data of 191 consecutive patients who were started on dapagliflozin due to heart failure were compared before and 6 months after the treatment began. The systemic immune-inflammation index (SII) and the systemic inflammation response index (SIRI) were calculated using the following formulae: (platelet × neutrophil)/lymphocyte and (neutrophil × monocyte)/lymphocyte, respectively.
Results:
The mean age of the patients included in the study was 66.17 ± 10.7 years. A total of 156 patients (81.7%) had diabetes mellitus. Seventy patients (36.6%) had heart failure with reduced ejection fraction (HFrEF), 31 (16.2%) had heart failure with mildly reduced ejection fraction (HFmrEF), and 90 (47.1%) had heart failure with preserved ejection fraction (HFpEF). While no significant change was observed in echocardiographic parameters with dapagliflozin treatment (p > 0.05), a significant decrease was detected in the SII and SIRI (1357.4 ± 1404.3 vs. 805.8 ± 586.7, p < 0.001 and 3.68 ± 3.6 vs. 2.19 ± 1.7, p < 0.001). In these indices, a consistently significant decrease was observed in all groups, irrespective of the type of heart failure and the presence of diabetes mellitus (p < 0.005).
Conclusion:
With dapagliflozin treatment, the most recent inflammation parameters, SII and SIRI, have significantly decreased. This effect may be one reason for the cardiovascular benefits of dapagliflozin treatment.
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