Browsing by Author "Todorovic, Z. (7004371236)"
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Publication Clopidogrel cessation triggers aspirin rebound in patients with coronary stent(2014) ;Djukanovic, N. (24722840600) ;Todorovic, Z. (7004371236) ;Obradovic, S. (6701778019) ;Njegomirovic, S. (50561884300) ;Zamaklar-Trifunovic, D. (9241771000) ;Protic̈, D. (18635502600)Ostojic, M. (34572650500)What is known and objective Premature discontinuation of clopidogrel in patients undergoing percutaneous coronary intervention is a significant risk factor for thrombotic adverse outcomes. However, recent studies indicate that even discontinuation of long-term use of clopidogrel may be associated with multiple adverse outcomes, that is, rebound phenomenon whose mechanism is not definitely clear. The aim of the study was to examine the effect of clopidogrel withdrawal in those on combined aspirin and clopidogrel therapy. Methods This prospective, multicenter study enrolled 200 patients who underwent coronary stent implantation and were on dual antiplatelet therapy (100 mg aspirin + 75 mg clopidogrel) 1 year after the stent placement. In all patients, we measured the platelet aggregation, by multiplate electrode aggregometry, using two agonists [adenosine diphosphate with PGE1 (ADPHS) and arachidonic acid (ASPI)] two times: on the day of cessation of clopidogrel and 90 days after clopidogrel was stopped. Results and discussion Following clopidogrel discontinuation, we registered an increase in ASPI values (P < 0·001), linear correlation between changes in ASPI and ADPHS values (P = 0·009) and significant difference in the values of ASPI first quartile of ADPHS compared with the other three (P < 0·001, P = 0·016, P < 0·001, I vs. II, I vs. III and I vs. IV quartile of ADPHS, respectively). What is new and conclusion Our findings show that cessation of clopidogrel causes loss of antiplatelet synergism with aspirin, leading to a weakening of the response to aspirin, which may be one explanation for the rebound after the clopidogrel cessation. Recent studies indicate that even discontinuation of long-term use of clopidogrel may be associated with multiple adverse outcomes, i.e. rebound phenomenon whose mechanism is not definitely clear. The aim of the study was to examine the effect of clopidogrel withdrawal in those on combined aspirin and clopidogrel therapy. Our findings show that cessation of clopidogrel causes loss of antiplatelet synergism with aspirin, leading to a weakening of the response to aspirin, which may be one explanation for the rebound after the clopidogrel cessation. © 2013 John Wiley & Sons Ltd. - Some of the metrics are blocked by yourconsent settings
Publication Clopidogrel cessation triggers aspirin rebound in patients with coronary stent(2014) ;Djukanovic, N. (24722840600) ;Todorovic, Z. (7004371236) ;Obradovic, S. (6701778019) ;Njegomirovic, S. (50561884300) ;Zamaklar-Trifunovic, D. (9241771000) ;Protic̈, D. (18635502600)Ostojic, M. (34572650500)What is known and objective Premature discontinuation of clopidogrel in patients undergoing percutaneous coronary intervention is a significant risk factor for thrombotic adverse outcomes. However, recent studies indicate that even discontinuation of long-term use of clopidogrel may be associated with multiple adverse outcomes, that is, rebound phenomenon whose mechanism is not definitely clear. The aim of the study was to examine the effect of clopidogrel withdrawal in those on combined aspirin and clopidogrel therapy. Methods This prospective, multicenter study enrolled 200 patients who underwent coronary stent implantation and were on dual antiplatelet therapy (100 mg aspirin + 75 mg clopidogrel) 1 year after the stent placement. In all patients, we measured the platelet aggregation, by multiplate electrode aggregometry, using two agonists [adenosine diphosphate with PGE1 (ADPHS) and arachidonic acid (ASPI)] two times: on the day of cessation of clopidogrel and 90 days after clopidogrel was stopped. Results and discussion Following clopidogrel discontinuation, we registered an increase in ASPI values (P < 0·001), linear correlation between changes in ASPI and ADPHS values (P = 0·009) and significant difference in the values of ASPI first quartile of ADPHS compared with the other three (P < 0·001, P = 0·016, P < 0·001, I vs. II, I vs. III and I vs. IV quartile of ADPHS, respectively). What is new and conclusion Our findings show that cessation of clopidogrel causes loss of antiplatelet synergism with aspirin, leading to a weakening of the response to aspirin, which may be one explanation for the rebound after the clopidogrel cessation. Recent studies indicate that even discontinuation of long-term use of clopidogrel may be associated with multiple adverse outcomes, i.e. rebound phenomenon whose mechanism is not definitely clear. The aim of the study was to examine the effect of clopidogrel withdrawal in those on combined aspirin and clopidogrel therapy. Our findings show that cessation of clopidogrel causes loss of antiplatelet synergism with aspirin, leading to a weakening of the response to aspirin, which may be one explanation for the rebound after the clopidogrel cessation. © 2013 John Wiley & Sons Ltd. - Some of the metrics are blocked by yourconsent settings
Publication The emergence of multi-drug-resistant bacteria causing healthcare-associated infections in COVID-19 patients: a retrospective multi-centre study(2023) ;Gajic, I. (55428924700) ;Jovicevic, M. (57223044336) ;Popadic, V. (57223264452) ;Trudic, A. (56748072700) ;Kabic, J. (57215669275) ;Kekic, D. (36696225200) ;Ilic, A. (59430649200) ;Klasnja, S. (57222576460) ;Hadnadjev, M. (55362426300) ;Popadic, D.J. (58260434300) ;Andrijevic, A. (57225223464) ;Prokic, A. (58259671600) ;Tomasevic, R. (6603547250) ;Ranin, L. (6602522806) ;Todorovic, Z. (7004371236) ;Zdravkovic, M. (24924016800)Opavski, N. (6507364674)Introduction: We evaluated the prevalence, aetiologies and antibiotic resistance patterns of bacterial infections in hospitalized patients with laboratory-confirmed SARS-CoV-2. We also investigated comorbidities, risk factors and the mortality rate in COVID-19 patients with bacterial infections. Methods: This retrospective observational study evaluated medical records of 7249 randomly selected patients with COVID-19 admitted to three clinical centres between 1st January 2021 and 16th February 2022. A total of 6478 COVID-19 patients met the eligibility criteria for analysis. Results: The mean age of the patients with SARS-CoV-2 and bacterial infections was 68.6 ± 15.5 years (range: 24–94 years). The majority of patients (68.7%) were older than 65 years. The prevalence of bacterial infections among hospitalized COVID-19 patients was 12.9%, most of them being hospital-acquired (11.5%). Bloodstream (37.7%) and respiratory tract infections (25.6%) were the most common bacterial infections. Klebsiella pneumoniae and Acinetobacter baumannii caused 25.2% and 23.6% of all bacterial infections, respectively. Carbapenem-resistance in Enterobacterales, A. baumannii and Pseudomonas aeruginosa were 71.3%, 93.8% and 69.1%, respectively. Age >60 years and infections caused by ≥3 pathogens were significantly more prevalent among deceased patients compared with survivors (P<0.05). Furthermore, 95% of patients who were intubated developed ventilator-associated pneumonia. The overall in-hospital mortality rate of patients with SARS-CoV-2 and bacterial infections was 51.6%, while 91.7% of patients who required invasive mechanical ventilation died. Conclusions: Our results reveal a striking association between healthcare-associated bacterial infections as an important complication of COVID-19 and fatal outcomes. © 2023 The Authors 
