Abstract
Neuroendocrine/inflammatory and endothelial functions have been indicated as crucial for heart failure (HF) patients. We evaluated relation in HF patients among cytokines and asymmetric dimethylarginine (ADMA) and left ventricular ejection fraction (LVEF) at baseline and after long-term administration of carvedilol. Interleukin 10 (IL-10), interleukin 18 (IL-18), and ADMA were measured in 22 NYHA class II to IV HF patients at baseline and after 40 ± 14 months of carvedilol treatment. Patients were divided into 2 groups according to whether, after treatment with carvedilol, LVEF had increased at least 5% (responders) or less than 5% (non-responders). In responders (11 of 22 patients), LVEF increased from 38 ± 6% to 50 ± 7%, (P <0.001); in non-responders, it decreased from 36 ± 9% to 31 ± 6%, (P = 0.02); NYHA class significantly decreased in both groups. IL-18 decreased in responders (from 586.4 ± 128 to 183.13 ± 64.4 pg/mL; P <0.001) and in non-responders (from 529.3 ± 116.25 to 142.4 ± 58.9 pg/mL; P <0.001). IL-10 increased in responders (from 0.49 ± 0.25 to 2.01 ± 1.01 pg/mL; P <0.001) and in non-responders (from 0.64 ± 0.31 to 1.33 ± 0.59 pg/mL; P <0.001). Conversely, ADMA levels decreased only in responders (from 0.67 ± 0.16 to 0.44 ± 0.15 μmol/L; P <0.001), and an inverse correlation was observed between basal ADMA levels and changes in LVEF after treatment. In HF patients, carvedilol appears to reduce symptoms and the expression of inflammation, regardless of the LV functional response. In those patients showing improvement of LVEF, the reduction of inflammation is paralleled by a reduction of ADMA. We surmise that carvedilol could be effective at various independent levels as a result of possible pleiotropic effects of this agent.
| Original language | English |
|---|---|
| Pages (from-to) | 49-54 |
| Number of pages | 6 |
| Journal | Journal of Cardiovascular Pharmacology |
| Volume | 52 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jul 2008 |
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Keywords
- Carvedilol
- Endothelial function
- Heart failure
- Inflammation
ASJC Scopus subject areas
- Pharmacology
- Cardiology and Cardiovascular Medicine
Cite this
Differential long-term effects of carvedilol on proinflammatory and antiinflammatory cytokines, asymmetric dimethylarginine, and left ventricular function in patients with heart failure. / Alfieri, Anna B.; Briceno, Luis; Fragasso, Gabriele; Spoladore, Roberto; Palloshi, Altin; Bassanelli, Giorgio; Montano, Chiara; Arioli, Francesco; Cuko, Amarild; Ruotolo, Giacomo; Margonato, Alberto.
In: Journal of Cardiovascular Pharmacology, Vol. 52, No. 1, 07.2008, p. 49-54.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Differential long-term effects of carvedilol on proinflammatory and antiinflammatory cytokines, asymmetric dimethylarginine, and left ventricular function in patients with heart failure
AU - Alfieri, Anna B.
AU - Briceno, Luis
AU - Fragasso, Gabriele
AU - Spoladore, Roberto
AU - Palloshi, Altin
AU - Bassanelli, Giorgio
AU - Montano, Chiara
AU - Arioli, Francesco
AU - Cuko, Amarild
AU - Ruotolo, Giacomo
AU - Margonato, Alberto
PY - 2008/7
Y1 - 2008/7
N2 - Neuroendocrine/inflammatory and endothelial functions have been indicated as crucial for heart failure (HF) patients. We evaluated relation in HF patients among cytokines and asymmetric dimethylarginine (ADMA) and left ventricular ejection fraction (LVEF) at baseline and after long-term administration of carvedilol. Interleukin 10 (IL-10), interleukin 18 (IL-18), and ADMA were measured in 22 NYHA class II to IV HF patients at baseline and after 40 ± 14 months of carvedilol treatment. Patients were divided into 2 groups according to whether, after treatment with carvedilol, LVEF had increased at least 5% (responders) or less than 5% (non-responders). In responders (11 of 22 patients), LVEF increased from 38 ± 6% to 50 ± 7%, (P <0.001); in non-responders, it decreased from 36 ± 9% to 31 ± 6%, (P = 0.02); NYHA class significantly decreased in both groups. IL-18 decreased in responders (from 586.4 ± 128 to 183.13 ± 64.4 pg/mL; P <0.001) and in non-responders (from 529.3 ± 116.25 to 142.4 ± 58.9 pg/mL; P <0.001). IL-10 increased in responders (from 0.49 ± 0.25 to 2.01 ± 1.01 pg/mL; P <0.001) and in non-responders (from 0.64 ± 0.31 to 1.33 ± 0.59 pg/mL; P <0.001). Conversely, ADMA levels decreased only in responders (from 0.67 ± 0.16 to 0.44 ± 0.15 μmol/L; P <0.001), and an inverse correlation was observed between basal ADMA levels and changes in LVEF after treatment. In HF patients, carvedilol appears to reduce symptoms and the expression of inflammation, regardless of the LV functional response. In those patients showing improvement of LVEF, the reduction of inflammation is paralleled by a reduction of ADMA. We surmise that carvedilol could be effective at various independent levels as a result of possible pleiotropic effects of this agent.
AB - Neuroendocrine/inflammatory and endothelial functions have been indicated as crucial for heart failure (HF) patients. We evaluated relation in HF patients among cytokines and asymmetric dimethylarginine (ADMA) and left ventricular ejection fraction (LVEF) at baseline and after long-term administration of carvedilol. Interleukin 10 (IL-10), interleukin 18 (IL-18), and ADMA were measured in 22 NYHA class II to IV HF patients at baseline and after 40 ± 14 months of carvedilol treatment. Patients were divided into 2 groups according to whether, after treatment with carvedilol, LVEF had increased at least 5% (responders) or less than 5% (non-responders). In responders (11 of 22 patients), LVEF increased from 38 ± 6% to 50 ± 7%, (P <0.001); in non-responders, it decreased from 36 ± 9% to 31 ± 6%, (P = 0.02); NYHA class significantly decreased in both groups. IL-18 decreased in responders (from 586.4 ± 128 to 183.13 ± 64.4 pg/mL; P <0.001) and in non-responders (from 529.3 ± 116.25 to 142.4 ± 58.9 pg/mL; P <0.001). IL-10 increased in responders (from 0.49 ± 0.25 to 2.01 ± 1.01 pg/mL; P <0.001) and in non-responders (from 0.64 ± 0.31 to 1.33 ± 0.59 pg/mL; P <0.001). Conversely, ADMA levels decreased only in responders (from 0.67 ± 0.16 to 0.44 ± 0.15 μmol/L; P <0.001), and an inverse correlation was observed between basal ADMA levels and changes in LVEF after treatment. In HF patients, carvedilol appears to reduce symptoms and the expression of inflammation, regardless of the LV functional response. In those patients showing improvement of LVEF, the reduction of inflammation is paralleled by a reduction of ADMA. We surmise that carvedilol could be effective at various independent levels as a result of possible pleiotropic effects of this agent.
KW - Carvedilol
KW - Endothelial function
KW - Heart failure
KW - Inflammation
UR - http://www.scopus.com/inward/record.url?scp=55949108230&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=55949108230&partnerID=8YFLogxK
U2 - 10.1097/FJC.0b013e31817e0edd
DO - 10.1097/FJC.0b013e31817e0edd
M3 - Article
C2 - 18594474
AN - SCOPUS:55949108230
VL - 52
SP - 49
EP - 54
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
SN - 0160-2446
IS - 1
ER -