Impact of Ivabradine on Inflammatory Markers in Chronic Heart Failure.
Background. Inflammation plays a crucial role in the progression of chronic heart failure (CHF). Ivabradine is known to reduce the morbidity and mortality of patients with CHF under certain conditions. Beyond the reduction of heart rate, only limited knowledge exists about potential anti-inflammatory effects of ivabradine that might contribute to its benefit in CHF. Thus, the present study aimed to investigate the effect of ivabradine on systemic inflammation.Methods. In the present study, 33 patients with CHF due to dilated, ischemic, and hypertensive cardiomyopathy were treated with ivabradine according to the guidelines of the European Society of Cardiology (ESC). A number of circulating dendritic cells as well as inflammatory mediators were investigated using FACS analysis and ELISA, respectively, before and during ivabradine therapy.Results. Treatment with ivabradine resulted in a significant improvement of CHF symptoms as well as an increase in left ventricular ejection fraction. Moreover, ivabradine treatment led to a significant reduction of TNF-alpha (TNF-α) serum levels and a reconstitution of circulating dendritic cells which are known to be reduced in patients with CHF.Conclusion. We show that treatment with ivabradine in patients with CHF resulted in an improvement of HF symptoms and ejection fraction as well as a normalization of inflammatory mediators.
Department of Internal Medicine I, Friedrich-Schiller-University of Jena, Jena, Germany.
Ilonka
0000-0002-7727-8356
I
Rohm
Department of Internal Medicine I, Friedrich-Schiller-University of Jena, Jena, Germany.
Daniel
D
Kretzschmar
Department of Internal Medicine I, Friedrich-Schiller-University of Jena, Jena, Germany.
Rudin
R
Pistulli
Department of Internal Medicine I, Friedrich-Schiller-University of Jena, Jena, Germany.
Marcus
0000-0001-6543-4684
M
Franz
Department of Internal Medicine I, Friedrich-Schiller-University of Jena, Jena, Germany.
P Christian
PC
Schulze
Department of Internal Medicine II, Friedrich-Alexander University of Erlangen-Nuremberg, Erlangen, Germany.
Christian
C
Stumpf
Department of Internal Medicine II, Elisabeth Klinikum Schmalkalden, Schmalkalden, Germany.
Atilla
A
Yilmaz
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D001552:Benzazepines / Q000494:pharmacology / Q000627:therapeutic use*; D015415:Biomarkers; D002317:Cardiovascular Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002908:Chronic Disease; D015897:Comorbidity; D016207:Cytokines / Q000378:metabolism*; D004452:Echocardiography; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000175:diagnosis / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D000077550:Ivabradine; D008297:Male; D008875:Middle Aged; D011788:Quality of Life; D012307:Risk Factors; D016896:Treatment Outcome
D000319:Adrenergic beta-Antagonists; D001552:Benzazepines; D015415:Biomarkers; D002317:Cardiovascular Agents; D016207:Cytokines; D018836:Inflammation Mediators; D000077550:Ivabradine