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Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease
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| Zeitschriftentitel: | Vascular Medicine |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , , , , |
| In: | Vascular Medicine, 17, 2012, 2, S. 101-107 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
SAGE Publications
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| Schlagwörter: |
| author_facet |
Tabit, Corey E Holbrook, Monica Shenouda, Sherene M Dohadwala, Mustali M Widlansky, Michael E Frame, Alissa A Kim, Brian H Duess, Mai-Ann Kluge, Matthew A Levit, Aaron Keaney, John F Vita, Joseph A Hamburg, Naomi M Tabit, Corey E Holbrook, Monica Shenouda, Sherene M Dohadwala, Mustali M Widlansky, Michael E Frame, Alissa A Kim, Brian H Duess, Mai-Ann Kluge, Matthew A Levit, Aaron Keaney, John F Vita, Joseph A Hamburg, Naomi M |
|---|---|
| author |
Tabit, Corey E Holbrook, Monica Shenouda, Sherene M Dohadwala, Mustali M Widlansky, Michael E Frame, Alissa A Kim, Brian H Duess, Mai-Ann Kluge, Matthew A Levit, Aaron Keaney, John F Vita, Joseph A Hamburg, Naomi M |
| spellingShingle |
Tabit, Corey E Holbrook, Monica Shenouda, Sherene M Dohadwala, Mustali M Widlansky, Michael E Frame, Alissa A Kim, Brian H Duess, Mai-Ann Kluge, Matthew A Levit, Aaron Keaney, John F Vita, Joseph A Hamburg, Naomi M Vascular Medicine Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease Cardiology and Cardiovascular Medicine |
| author_sort |
tabit, corey e |
| spelling |
Tabit, Corey E Holbrook, Monica Shenouda, Sherene M Dohadwala, Mustali M Widlansky, Michael E Frame, Alissa A Kim, Brian H Duess, Mai-Ann Kluge, Matthew A Levit, Aaron Keaney, John F Vita, Joseph A Hamburg, Naomi M 1358-863X 1477-0377 SAGE Publications Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1177/1358863x12440117 <jats:p>Inflammation is critical for atherosclerosis development and may be a target for risk-reduction therapy. In experimental studies, activation of the inflammatory regulator, nuclear factor kappa B (NFlB), contributes to endothelial activation and reduced nitric oxide production. We treated patients with coronary artery disease with sulfasalazine, an inhibitor of NFκB, and placebo in a randomized, double-blind, crossover study design. Brachial artery flow-mediated dilation (FMD) and digital vascular function were measured at baseline and after each 6-week treatment period. Of the 53 patients enrolled in the crossover study, 32 (age 60 ± 10, 22% female) completed all the visits, with a high rate of study withdrawal due to gastrointestinal side effects. In a subset of 10 participants, we compared the effects of 4 days of sulfasalazine treatment ( n = 5) to no treatment ( n = 5) on NFκB-regulated gene expression in peripheral blood mononuclear cells. Tumor necrosis factor α-stimulated expression of CD69 and NFlB subunit p50 was significantly blunted after 4 days of sulfasalazine treatment but not after no treatment. However, FMD and digital vasodilator response did not significantly change from baseline with long-term sulfasalazine treatment. Short-term sulfasalazine inhibited NFlB activity; however, long-term treatment was poorly tolerated and did not improve endothelial function. Our findings suggest that sulfasalazine therapy is not the optimal anti-inflammatory treatment for reversing endothelial dysfunction in cardiovascular disease. Further studies are warranted to investigate the potential for NFlB inhibition to reduce cardiovascular risk.</jats:p> Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease Vascular Medicine |
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| title |
Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_unstemmed |
Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_full |
Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_fullStr |
Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_full_unstemmed |
Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_short |
Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_sort |
effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
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Cardiology and Cardiovascular Medicine |
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http://dx.doi.org/10.1177/1358863x12440117 |
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2012 |
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101-107 |
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<jats:p>Inflammation is critical for atherosclerosis development and may be a target for risk-reduction therapy. In experimental studies, activation of the inflammatory regulator, nuclear factor kappa B (NFlB), contributes to endothelial activation and reduced nitric oxide production. We treated patients with coronary artery disease with sulfasalazine, an inhibitor of NFκB, and placebo in a randomized, double-blind, crossover study design. Brachial artery flow-mediated dilation (FMD) and digital vascular function were measured at baseline and after each 6-week treatment period. Of the 53 patients enrolled in the crossover study, 32 (age 60 ± 10, 22% female) completed all the visits, with a high rate of study withdrawal due to gastrointestinal side effects. In a subset of 10 participants, we compared the effects of 4 days of sulfasalazine treatment ( n = 5) to no treatment ( n = 5) on NFκB-regulated gene expression in peripheral blood mononuclear cells. Tumor necrosis factor α-stimulated expression of CD69 and NFlB subunit p50 was significantly blunted after 4 days of sulfasalazine treatment but not after no treatment. However, FMD and digital vasodilator response did not significantly change from baseline with long-term sulfasalazine treatment. Short-term sulfasalazine inhibited NFlB activity; however, long-term treatment was poorly tolerated and did not improve endothelial function. Our findings suggest that sulfasalazine therapy is not the optimal anti-inflammatory treatment for reversing endothelial dysfunction in cardiovascular disease. Further studies are warranted to investigate the potential for NFlB inhibition to reduce cardiovascular risk.</jats:p> |
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| author | Tabit, Corey E, Holbrook, Monica, Shenouda, Sherene M, Dohadwala, Mustali M, Widlansky, Michael E, Frame, Alissa A, Kim, Brian H, Duess, Mai-Ann, Kluge, Matthew A, Levit, Aaron, Keaney, John F, Vita, Joseph A, Hamburg, Naomi M |
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| description | <jats:p>Inflammation is critical for atherosclerosis development and may be a target for risk-reduction therapy. In experimental studies, activation of the inflammatory regulator, nuclear factor kappa B (NFlB), contributes to endothelial activation and reduced nitric oxide production. We treated patients with coronary artery disease with sulfasalazine, an inhibitor of NFκB, and placebo in a randomized, double-blind, crossover study design. Brachial artery flow-mediated dilation (FMD) and digital vascular function were measured at baseline and after each 6-week treatment period. Of the 53 patients enrolled in the crossover study, 32 (age 60 ± 10, 22% female) completed all the visits, with a high rate of study withdrawal due to gastrointestinal side effects. In a subset of 10 participants, we compared the effects of 4 days of sulfasalazine treatment ( n = 5) to no treatment ( n = 5) on NFκB-regulated gene expression in peripheral blood mononuclear cells. Tumor necrosis factor α-stimulated expression of CD69 and NFlB subunit p50 was significantly blunted after 4 days of sulfasalazine treatment but not after no treatment. However, FMD and digital vasodilator response did not significantly change from baseline with long-term sulfasalazine treatment. Short-term sulfasalazine inhibited NFlB activity; however, long-term treatment was poorly tolerated and did not improve endothelial function. Our findings suggest that sulfasalazine therapy is not the optimal anti-inflammatory treatment for reversing endothelial dysfunction in cardiovascular disease. Further studies are warranted to investigate the potential for NFlB inhibition to reduce cardiovascular risk.</jats:p> |
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| spelling | Tabit, Corey E Holbrook, Monica Shenouda, Sherene M Dohadwala, Mustali M Widlansky, Michael E Frame, Alissa A Kim, Brian H Duess, Mai-Ann Kluge, Matthew A Levit, Aaron Keaney, John F Vita, Joseph A Hamburg, Naomi M 1358-863X 1477-0377 SAGE Publications Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1177/1358863x12440117 <jats:p>Inflammation is critical for atherosclerosis development and may be a target for risk-reduction therapy. In experimental studies, activation of the inflammatory regulator, nuclear factor kappa B (NFlB), contributes to endothelial activation and reduced nitric oxide production. We treated patients with coronary artery disease with sulfasalazine, an inhibitor of NFκB, and placebo in a randomized, double-blind, crossover study design. Brachial artery flow-mediated dilation (FMD) and digital vascular function were measured at baseline and after each 6-week treatment period. Of the 53 patients enrolled in the crossover study, 32 (age 60 ± 10, 22% female) completed all the visits, with a high rate of study withdrawal due to gastrointestinal side effects. In a subset of 10 participants, we compared the effects of 4 days of sulfasalazine treatment ( n = 5) to no treatment ( n = 5) on NFκB-regulated gene expression in peripheral blood mononuclear cells. Tumor necrosis factor α-stimulated expression of CD69 and NFlB subunit p50 was significantly blunted after 4 days of sulfasalazine treatment but not after no treatment. However, FMD and digital vasodilator response did not significantly change from baseline with long-term sulfasalazine treatment. Short-term sulfasalazine inhibited NFlB activity; however, long-term treatment was poorly tolerated and did not improve endothelial function. Our findings suggest that sulfasalazine therapy is not the optimal anti-inflammatory treatment for reversing endothelial dysfunction in cardiovascular disease. Further studies are warranted to investigate the potential for NFlB inhibition to reduce cardiovascular risk.</jats:p> Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease Vascular Medicine |
| spellingShingle | Tabit, Corey E, Holbrook, Monica, Shenouda, Sherene M, Dohadwala, Mustali M, Widlansky, Michael E, Frame, Alissa A, Kim, Brian H, Duess, Mai-Ann, Kluge, Matthew A, Levit, Aaron, Keaney, John F, Vita, Joseph A, Hamburg, Naomi M, Vascular Medicine, Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease, Cardiology and Cardiovascular Medicine |
| title | Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_full | Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_fullStr | Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_full_unstemmed | Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_short | Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_sort | effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| title_unstemmed | Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease |
| topic | Cardiology and Cardiovascular Medicine |
| url | http://dx.doi.org/10.1177/1358863x12440117 |