TY  - JOUR
AU  - Rakočević, Jelena
AU  - Dobrić, Milan
AU  - Labudović-Borović, Milica
AU  - Milutinović, Katarina
AU  - Milenković, Sanela
AU  - Tomašević, Miloje
PY  - 2023
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4520
AB  - Inflammation plays an important role in all stages of atherosclerosis — from endothelial dysfunction, to formation of fatty streaks and atherosclerotic plaque, and its progression to serious complications, such as atherosclerotic plaque rupture. Although dyslipidemia is a key driver of atherosclerosis, pathogenesis of atherosclerosis is now considered interplay between cholesterol and inflammation, with the significant role of the immune system and immune cells. Despite modern therapeutic approaches in primary and secondary cardiovascular prevention, cardiovascular diseases remain the leading cause of mortality worldwide. In order to reduce residual cardiovascular risk, despite the guidelines-guided optimal medical therapy, novel therapeutic strategies are needed for prevention and management of coronary artery disease. One of the innovative and promising approaches in atherosclerotic cardiovascular disease might be inflammation-targeted therapy. Numerous experimental and clinical studies are seeking into metabolic pathways underlying atherosclerosis, in order to find the most suitable pathway and inflammatory marker/s that should be the target for anti-inflammatory therapy. Many anti-inflammatory drugs have been tested, from the well-known broad range anti-inflammatory agents, such as colchicine, allopurinol and methotrexate, to targeted monoclonal antibodies specifically inhibiting a molecule included in inflammatory pathway, such as canakinumab and tocilizumab. To date, there are no approved anti-inflammatory agents specifically indicated for silencing inflammation in patients with coronary artery disease. The most promising results came from the studies which tested colchicine, and studies where the inflammatory-target was NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome/interleukin-1 beta (IL-1β)/interleukin-6 (IL-6)/C-reactive protein (CRP) pathway. A growing body of evidence, along with the ongoing clinical studies, suggest that the anti-inflammatory therapy might become an additional strategy in treating atherosclerotic cardiovascular disease. Herein we present an overview of the role of inflammation in atherosclerosis, the most important inflammatory markers chosen as targets of anti-inflammatory therapy, along with the critical review of the major clinical trials which tested non-targeted and targeted anti-inflammatory drugs in patients with atherosclerotic cardiovascular disease.
PB  - IMR Press Limited
T2  - Reviews in Cardiovascular Medicine
T1  - Anti-Inflammatory Therapy in Coronary Artery Disease: Where Do We Stand?
VL  - 24
IS  - 1
DO  - 10.31083/j.rcm2401010
ER  - 

@article{
author = "Rakočević, Jelena and Dobrić, Milan and Labudović-Borović, Milica and Milutinović, Katarina and Milenković, Sanela and Tomašević, Miloje",
year = "2023",
abstract = "Inflammation plays an important role in all stages of atherosclerosis — from endothelial dysfunction, to formation of fatty streaks and atherosclerotic plaque, and its progression to serious complications, such as atherosclerotic plaque rupture. Although dyslipidemia is a key driver of atherosclerosis, pathogenesis of atherosclerosis is now considered interplay between cholesterol and inflammation, with the significant role of the immune system and immune cells. Despite modern therapeutic approaches in primary and secondary cardiovascular prevention, cardiovascular diseases remain the leading cause of mortality worldwide. In order to reduce residual cardiovascular risk, despite the guidelines-guided optimal medical therapy, novel therapeutic strategies are needed for prevention and management of coronary artery disease. One of the innovative and promising approaches in atherosclerotic cardiovascular disease might be inflammation-targeted therapy. Numerous experimental and clinical studies are seeking into metabolic pathways underlying atherosclerosis, in order to find the most suitable pathway and inflammatory marker/s that should be the target for anti-inflammatory therapy. Many anti-inflammatory drugs have been tested, from the well-known broad range anti-inflammatory agents, such as colchicine, allopurinol and methotrexate, to targeted monoclonal antibodies specifically inhibiting a molecule included in inflammatory pathway, such as canakinumab and tocilizumab. To date, there are no approved anti-inflammatory agents specifically indicated for silencing inflammation in patients with coronary artery disease. The most promising results came from the studies which tested colchicine, and studies where the inflammatory-target was NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome/interleukin-1 beta (IL-1β)/interleukin-6 (IL-6)/C-reactive protein (CRP) pathway. A growing body of evidence, along with the ongoing clinical studies, suggest that the anti-inflammatory therapy might become an additional strategy in treating atherosclerotic cardiovascular disease. Herein we present an overview of the role of inflammation in atherosclerosis, the most important inflammatory markers chosen as targets of anti-inflammatory therapy, along with the critical review of the major clinical trials which tested non-targeted and targeted anti-inflammatory drugs in patients with atherosclerotic cardiovascular disease.",
publisher = "IMR Press Limited",
journal = "Reviews in Cardiovascular Medicine",
title = "Anti-Inflammatory Therapy in Coronary Artery Disease: Where Do We Stand?",
volume = "24",
number = "1",
doi = "10.31083/j.rcm2401010"
}

Rakočević, J., Dobrić, M., Labudović-Borović, M., Milutinović, K., Milenković, S.,& Tomašević, M.. (2023). Anti-Inflammatory Therapy in Coronary Artery Disease: Where Do We Stand?. in Reviews in Cardiovascular Medicine
IMR Press Limited., 24(1).
https://doi.org/10.31083/j.rcm2401010

Rakočević J, Dobrić M, Labudović-Borović M, Milutinović K, Milenković S, Tomašević M. Anti-Inflammatory Therapy in Coronary Artery Disease: Where Do We Stand?. in Reviews in Cardiovascular Medicine. 2023;24(1).
doi:10.31083/j.rcm2401010 .

Rakočević, Jelena, Dobrić, Milan, Labudović-Borović, Milica, Milutinović, Katarina, Milenković, Sanela, Tomašević, Miloje, "Anti-Inflammatory Therapy in Coronary Artery Disease: Where Do We Stand?" in Reviews in Cardiovascular Medicine, 24, no. 1 (2023),
https://doi.org/10.31083/j.rcm2401010 . .

TY  - JOUR
AU  - Dobrić, Milan
AU  - Giga, Vojislav
AU  - Beleslin, Branko
AU  - Ignjatović, Svetlana
AU  - Paunović, Ivana
AU  - Stepanović, Jelena M.
AU  - Đorđević-Dikić, Ana
AU  - Kostić, Jelena
AU  - Nedeljković, Ivana
AU  - Nedeljković, Milan
AU  - Tesić, Milorad
AU  - Dajak, Marijana
AU  - Ostojić, Miodrag
PY  - 2013
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1868
AB  - Background: Glycogen phosphorylase BB (GPBB) is released from cardiac cells during myocyte damage. Previous studies have shown contradictory results regarding the relation of enzyme release and reversible myocardial ischemia. The aim of this study was to determine the plasma kinetics of GPBB as a response to the exercise stress echocardiographic test (ESET), and to define the relationship between myocardial ischemia and enzyme plasma concentrations. Methods: We studied 46 consecutive patients undergoing ESET, with recent coronary angiography. In all patients, a submaximal stress echo test according to Bruce protocol was performed. Concentration of GPBB was measured in peripheral blood that was sampled 5 min before and 10, 30 and 60 min after ESET. Results: There was significant increase of GPBB concentration after the test (p=0.021). Significant increase was detected 30 min (34.9% increase, p=0.021) and 60 min (34.5% increase, p=0.016) after ESET. There was no significant effect of myocardial ischemia on GPBB concentrations (p=0.126), and no significant interaction between sampling intervals and myocardial ischemia, suggesting a similar release profile of GPBB in ischemic and non-ischemic conditions (p=0.558). Patients in whom ESET was terminated later (stages 4 or 5 of standard Bruce protocol; n=13) had higher GPBB concentrations than patients who terminated ESET earlier (stages 1, 2 or 3; n=33) (p=0.049). Baseline GPBB concentration was not correlated to any of the patients' demographic, clinical and hemodynamic characteristics. Conclusions: GPBB plasma concentration increases after ESET, and it is not related to inducible myocardial ischemia. However, it seems that GPBB release during ESET might be related to exercise load/duration.
PB  - Walter de Gruyter Gmbh, Berlin
T2  - Clinical Chemistry and Laboratory Medicine
T1  - Glycogen phosphorylase isoenzyme BB plasma kinetics is not related to myocardial ischemia induced by exercise stress echo test
VL  - 51
IS  - 10
SP  - 2029
EP  - 2035
DO  - 10.1515/cclm-2013-0109
ER  - 

@article{
author = "Dobrić, Milan and Giga, Vojislav and Beleslin, Branko and Ignjatović, Svetlana and Paunović, Ivana and Stepanović, Jelena M. and Đorđević-Dikić, Ana and Kostić, Jelena and Nedeljković, Ivana and Nedeljković, Milan and Tesić, Milorad and Dajak, Marijana and Ostojić, Miodrag",
year = "2013",
abstract = "Background: Glycogen phosphorylase BB (GPBB) is released from cardiac cells during myocyte damage. Previous studies have shown contradictory results regarding the relation of enzyme release and reversible myocardial ischemia. The aim of this study was to determine the plasma kinetics of GPBB as a response to the exercise stress echocardiographic test (ESET), and to define the relationship between myocardial ischemia and enzyme plasma concentrations. Methods: We studied 46 consecutive patients undergoing ESET, with recent coronary angiography. In all patients, a submaximal stress echo test according to Bruce protocol was performed. Concentration of GPBB was measured in peripheral blood that was sampled 5 min before and 10, 30 and 60 min after ESET. Results: There was significant increase of GPBB concentration after the test (p=0.021). Significant increase was detected 30 min (34.9% increase, p=0.021) and 60 min (34.5% increase, p=0.016) after ESET. There was no significant effect of myocardial ischemia on GPBB concentrations (p=0.126), and no significant interaction between sampling intervals and myocardial ischemia, suggesting a similar release profile of GPBB in ischemic and non-ischemic conditions (p=0.558). Patients in whom ESET was terminated later (stages 4 or 5 of standard Bruce protocol; n=13) had higher GPBB concentrations than patients who terminated ESET earlier (stages 1, 2 or 3; n=33) (p=0.049). Baseline GPBB concentration was not correlated to any of the patients' demographic, clinical and hemodynamic characteristics. Conclusions: GPBB plasma concentration increases after ESET, and it is not related to inducible myocardial ischemia. However, it seems that GPBB release during ESET might be related to exercise load/duration.",
publisher = "Walter de Gruyter Gmbh, Berlin",
journal = "Clinical Chemistry and Laboratory Medicine",
title = "Glycogen phosphorylase isoenzyme BB plasma kinetics is not related to myocardial ischemia induced by exercise stress echo test",
volume = "51",
number = "10",
pages = "2029-2035",
doi = "10.1515/cclm-2013-0109"
}

Dobrić, M., Giga, V., Beleslin, B., Ignjatović, S., Paunović, I., Stepanović, J. M., Đorđević-Dikić, A., Kostić, J., Nedeljković, I., Nedeljković, M., Tesić, M., Dajak, M.,& Ostojić, M.. (2013). Glycogen phosphorylase isoenzyme BB plasma kinetics is not related to myocardial ischemia induced by exercise stress echo test. in Clinical Chemistry and Laboratory Medicine
Walter de Gruyter Gmbh, Berlin., 51(10), 2029-2035.
https://doi.org/10.1515/cclm-2013-0109

Dobrić M, Giga V, Beleslin B, Ignjatović S, Paunović I, Stepanović JM, Đorđević-Dikić A, Kostić J, Nedeljković I, Nedeljković M, Tesić M, Dajak M, Ostojić M. Glycogen phosphorylase isoenzyme BB plasma kinetics is not related to myocardial ischemia induced by exercise stress echo test. in Clinical Chemistry and Laboratory Medicine. 2013;51(10):2029-2035.
doi:10.1515/cclm-2013-0109 .

Dobrić, Milan, Giga, Vojislav, Beleslin, Branko, Ignjatović, Svetlana, Paunović, Ivana, Stepanović, Jelena M., Đorđević-Dikić, Ana, Kostić, Jelena, Nedeljković, Ivana, Nedeljković, Milan, Tesić, Milorad, Dajak, Marijana, Ostojić, Miodrag, "Glycogen phosphorylase isoenzyme BB plasma kinetics is not related to myocardial ischemia induced by exercise stress echo test" in Clinical Chemistry and Laboratory Medicine, 51, no. 10 (2013):2029-2035,
https://doi.org/10.1515/cclm-2013-0109 . .