Browsing by Author "Nenezic, Dragoslav (9232882900)"

Background To date, all published studies analyzing simultaneous treatment of carotid and proximal atherosclerotic lesions are describing retrograde approach and several technical variations. In the presented study, for the first time, antegrade approach is described for simultaneous carotid endarterectomy (CEA) and associated brachiocephalic trunk (BCT) or common carotid artery (CCA) angioplasty in the hybrid operating room. Methods From January 2012 till January 2016, antegrade hybrid procedures were performed in 18 patients. All patients were admitted to our institute for elective supraaortic arch multidetector computed tomography angiography when significant simultaneous proximal and distal supraaortic arch lesions were revealed. After surgical exposure of carotid arteries, proximal lesions were crossed by antegrade approach. Prior to stent placement, internal carotid artery (ICA) is clamped at its origin with the guidewire placed in the external carotid artery (ECA). After primary stenting and control arteriography, CCA and ECA are clamped and the ICA clamp moved more distally. An arteriotomy is performed in the CCA, with flushing of possible debris and thrombus before performance of the eversion CEA, once again flushing before completion of the anastomosis. Follow-up ranged from 6 to 36 months with average follow-up of 22.15 ± 11.31 months. Results All procedures went uneventfully. Out of 18 patients, 11 were males and 7 females, mean age 66.6 ± 3.82 years. In 10 patients (55.5%), simultaneous CEA and CCA angioplasty was performed, in 7 patients (38.9%) CEA and BCT angioplasty, and in 1 patient (5.5%) tubular graft interposition between the CCA and the ICA and CCA angioplasty. In 6 patients (33.3%), CCA/BCT balloon angioplasty alone was performed simultaneously with CEA. None of the patient had postoperative transient ischemic attack, stroke, hematoma, dissection, myocardial infarction, or ischemia in the early postoperative period and during the follow-up. There were no lethal outcomes, neither in the early postoperative course nor during the follow-up. Conclusions Antegrade approach for simultaneous treatment of proximal CCA/BCT and distal carotid lesions with temporary ICA clamping is safe and feasible procedure that should be thought of in the future in addition to already described retrograde approach. © 2017 Elsevier Inc.

Vascular graft infection is a serious complication associated with high morbidity and mortality. Because of this, various graft preservation techniques have been increasingly utilized in an attempt to improve outcomes. When this devastating complication occurs several possibilities for treatment are available. The traditional treatment consists of graft excision and extra-anatomic reconstruction. Reconstruction can also be done in situ using homografts or autologous grafts, as well as new synthetic prostheses with antimicrobial properties. A more conservative approach and graft preservation may be indicated in some cases. This paper presents a case of successful graft preservation using a vacuum-assisted closure system.

Purpose: Carotid artery stenting (CAS) is an option for carotid restenosis (CR) treatment with favorable outcomes. However, CAS has also emerged as an alternative to carotid endarterectomy (CEA) for the management of patients with primary carotid stenosis. This study aimed to report CR rates after CAS was performed in patients with primary lesions versus restenosis after CEA, to identify predictors of CR, and to report both neurological and overall outcomes. Materials and methods: From January 2000 to September 2018, a total of 782 patients were divided into 2 groups: The CAS (prim) group consisted of 440 patients in whom CAS was performed for primary lesions, and the CAS (res) group consisted of 342 patients with CAS due to restenosis after CEA. Indications for CAS were symptomatic stenosis/restenosis >70% and asymptomatic stenosis/restenosis >85%. A color duplex scan (CDS) of carotid arteries was performed 6 months after CAS, after 1 year, and annually afterward. Follow-up ranged from 12 to 88 months, with a mean follow-up of 34.6±18.0 months. Results: There were no differences in terms of CR rate between the patients in the CAS (prim) and CAS (res) groups (8.7% vs 7.2%, χ2=0.691, p=0.406). The overall CR rate was 7.9%, whereas significant CR (>70%) rate needing re-intervention was 5.6%, but there was no difference between patients in the CAS (prim) and CAS (res) groups (6.4% vs 4.7%, p=0.351). Six independent predictors for CR were smoking, associated previous myocardial infarction and angina pectoris, plaque morphology, spasm after CAS, the use of FilterWire or Spider Fx cerebral protection devices, and time after stenting. A carotid restenosis risk index (CRRI) was created based on these predictors and ranged from –7 (minimal risk) to +10 (maximum risk); patients with a score >–4 were at increased risk for CR. There were no differences in terms of neurological and overall morbidity and mortality between the 2 groups. Conclusions: There was no difference in CR rate after CAS between the patients with primary stenosis and restenosis after CEA. A CRRI score >–4 is a criterion for identifying high-risk patients for post-CAS CR that should be tested in future randomized trials. © The Author(s) 2022.

Background: Changes in K+ channel expression/function are associated with disruption of vascular reactivity in several pathological conditions, including hypertension, diabetes, and atherosclerosis. Gasotransmitters achieve part of their effects in the organism by regulating ion channels, especially K+ channels. Their involvement in hydrogen sulfide (H2S)-mediated vasorelaxation is still unclear, and data about human vessels are limited. Objective: To determine the role of K+ channel subtypes in the vasorelaxant mechanism of H2S donor, sodium-hydrosulfide (NaHS), on isolated human internal mammary artery (HIMA). Results: NaHS (1 × 10−6–3 × 10−3 mol/L) induced a concentration-dependent relaxation of HIMA pre-contracted by phenylephrine and high K+. Among K+ channel blockers, iberiotoxin, glibenclamide, 4-aminopyridine (4-AP), and margatoxin significantly inhibited NaHS-induced relaxation of phenylephrine-contracted HIMA (P < 0.01), whereas in the presence of apamin/1-[(2-chlorophenyl) diphenylmethyl]-1H-pyrazole (TRAM-34) combination, the HIMA relaxation was partially reduced (P < 0.05). The effect of NaHS was antagonized by NO pathway inhibitors, L-NAME and KT5823, and by cyclo-oxygenase inhibitor, indomethacin (P < 0.01). Under conditions of blocked NO/prostacyclin synthesis and release, apamin/TRAM-34 and glibenclamide caused further decrease in NaHS-induced vasorelaxation (P < 0.01), while iberiotoxin, 4-AP, and margatoxin were without additional effect (P > 0.05). In the presence of nifedipine, NaHS induced partial relaxation of HIMA (P < 0.01). Conclusion: Our results demonstrated that H2S donor, NaHS, induced concentration-dependent relaxation of isolated HIMA. Vasorelaxant mechanisms of H2S included direct or indirect opening of different K+ channel subtypes, KATP, BKCa, SKCa/IKCa, and KV (subtype KV1.3), in addition to NO pathway activation and interference with extracellular Ca2+ influx. © 2024 Société Française de Pharmacologie et de Thérapeutique. Published by John Wiley & Sons Ltd.

Background: Changes in K+ channel expression/function are associated with disruption of vascular reactivity in several pathological conditions, including hypertension, diabetes, and atherosclerosis. Gasotransmitters achieve part of their effects in the organism by regulating ion channels, especially K+ channels. Their involvement in hydrogen sulfide (H2S)-mediated vasorelaxation is still unclear, and data about human vessels are limited. Objective: To determine the role of K+ channel subtypes in the vasorelaxant mechanism of H2S donor, sodium-hydrosulfide (NaHS), on isolated human internal mammary artery (HIMA). Results: NaHS (1 × 10−6–3 × 10−3 mol/L) induced a concentration-dependent relaxation of HIMA pre-contracted by phenylephrine and high K+. Among K+ channel blockers, iberiotoxin, glibenclamide, 4-aminopyridine (4-AP), and margatoxin significantly inhibited NaHS-induced relaxation of phenylephrine-contracted HIMA (P < 0.01), whereas in the presence of apamin/1-[(2-chlorophenyl) diphenylmethyl]-1H-pyrazole (TRAM-34) combination, the HIMA relaxation was partially reduced (P < 0.05). The effect of NaHS was antagonized by NO pathway inhibitors, L-NAME and KT5823, and by cyclo-oxygenase inhibitor, indomethacin (P < 0.01). Under conditions of blocked NO/prostacyclin synthesis and release, apamin/TRAM-34 and glibenclamide caused further decrease in NaHS-induced vasorelaxation (P < 0.01), while iberiotoxin, 4-AP, and margatoxin were without additional effect (P > 0.05). In the presence of nifedipine, NaHS induced partial relaxation of HIMA (P < 0.01). Conclusion: Our results demonstrated that H2S donor, NaHS, induced concentration-dependent relaxation of isolated HIMA. Vasorelaxant mechanisms of H2S included direct or indirect opening of different K+ channel subtypes, KATP, BKCa, SKCa/IKCa, and KV (subtype KV1.3), in addition to NO pathway activation and interference with extracellular Ca2+ influx. © 2024 Société Française de Pharmacologie et de Thérapeutique. Published by John Wiley & Sons Ltd.

Hydrogen sulfide (H2S) represents the third and the youngest member of the gaseous transmitters family. The dominant effect of H2S on isolated vessels is vasodilation. As the mechanism of H2S-induced relaxation in human vessels remains unclear, the present study aimed to investigate the effects of H2S donor, sodium hydrosulfide (NaHS), on isolated human saphenous vein (HSV) and to determine the mechanism of action. Our results showed that NaHS (1 µM–3 mM) induced a concentration-dependent relaxation of endothelium-intact HSV rings pre-contracted by phenylephrine. Pre-treatment with L-NAME, ODQ and KT5823 significantly inhibited NaHS-induced relaxation, while indomethacin induced partial inhibition. Among K+ channel blockers, the combination of apamin and TRAM-34 significantly affected the relaxation produced by NaHS, while iberiotoxin and glibenclamide only reduced maximal relaxation of HSV. NaHS partially relaxed endothelium-intact rings pre-contracted by high K+, as well as phenylephrine-contracted rings in the presence of nifedipine. Additionally, the incubation of HSV rings with NaHS increased NO production. These results demonstrate that NaHS produces the concentration- and endothelium-dependent relaxation of isolated HSV. Vasorelaxation to NaHS probably involves activation of NO/cGMP/PKG pathway and partially prostacyclin. In addition, different K+ channels subtypes, especially SKCa and IKCa, as well as BKCa and KATP channels in high concentrations of NaHS, probably participate in the NaHS-induced vasorelaxation. © 2021 Société Française de Pharmacologie et de Thérapeutique

Hydrogen sulfide (H2S) represents the third and the youngest member of the gaseous transmitters family. The dominant effect of H2S on isolated vessels is vasodilation. As the mechanism of H2S-induced relaxation in human vessels remains unclear, the present study aimed to investigate the effects of H2S donor, sodium hydrosulfide (NaHS), on isolated human saphenous vein (HSV) and to determine the mechanism of action. Our results showed that NaHS (1 µM–3 mM) induced a concentration-dependent relaxation of endothelium-intact HSV rings pre-contracted by phenylephrine. Pre-treatment with L-NAME, ODQ and KT5823 significantly inhibited NaHS-induced relaxation, while indomethacin induced partial inhibition. Among K+ channel blockers, the combination of apamin and TRAM-34 significantly affected the relaxation produced by NaHS, while iberiotoxin and glibenclamide only reduced maximal relaxation of HSV. NaHS partially relaxed endothelium-intact rings pre-contracted by high K+, as well as phenylephrine-contracted rings in the presence of nifedipine. Additionally, the incubation of HSV rings with NaHS increased NO production. These results demonstrate that NaHS produces the concentration- and endothelium-dependent relaxation of isolated HSV. Vasorelaxation to NaHS probably involves activation of NO/cGMP/PKG pathway and partially prostacyclin. In addition, different K+ channels subtypes, especially SKCa and IKCa, as well as BKCa and KATP channels in high concentrations of NaHS, probably participate in the NaHS-induced vasorelaxation. © 2021 Société Française de Pharmacologie et de Thérapeutique

Anticoagulants are effective agents for the prevention and treatment of thrombosis and thromboembolic complications, which represent a common cause of morbidity and mortality. Despite their clinical efficiency, traditional anticoagulants are all associated with significant drawbacks. As a result, modulation of the coagulation process represents an important target in the development of new oral and parenteral anticoagulants today. The new oral anticoagulants selectively target thrombin (ximelagatran, dabigatran etexilate) or factor Xa (rivaroxaban, apixaban, edoxaban). Unlike the traditional anticoagulants, vitamin K antagonists, these drugs have rapid onset of action and a relatively wide therapeutic range, do not require routine prothrombin time (PT) monitoring and have low potential for food and drug interaction. The new parenteral anticoagulants achieve their effects through indirect (semuloparin, idrabiotaparinux) or direct inhibition of factor Xa (otamixaban), as well as through inhibition of coagulation factor IXa (RB006). The main characteristics of these agents are a rapid onset of action and a predictable anticoagulant effect, whereby the most of them can be rapidly neutralized by an adequate antidote.

We report a case of successful transcatheter arterial embolization of a pancreaticoduodenal artery pseudoaneurysm (PSA) caused by erosion of the pancreatic pseudocyst content near pancreaticoduodenal arteries. A 55-year-old man was admitted to a local hospital for investigation of severe, stabbing epigastric pain confined to the upper abdomen. He had a history of previous alcohol abuse, chronic pancreatitis, and a duodenal ulcer. Upper gastrointestinal endoscopy revealed narrowing in the pyloric channel along with an ulcer located at the first and second portions of the duodenum with oozing beneath an adherent cloth and duodenal distortion. Computed tomography additionally revealed an enlarged head of the pancreas with numerous spot calcifications and round cystic formation inside, with a diameter of 30 x 25 mm. Following two surgical procedures for duodenal ulcers, selective angiography revealed a PSA located inside the pancreas head and high-grade stenosis > 90% of the celiac trunk and hepatic artery that rose separately from the aorta. Fiber coil embolization was used to occlude the PSA sac successfully. There was no complication after completion of the last embolic procedure. The patient was doing well after 26 months. © BC Decker Inc. All rights reserved.

Background: The aim of this paper is to determine which therapy gives best results regarding process of healing of diabetic foot ulcers among three proposed: only negative pressure wound therapy, only hyperbaric oxygen therapy, and both when used in conjunction. Methods: This bicentric prospective study included 60 patients, and they were, consecutively, assigned to one of three groups. The first group consisted of 20 patients who were treated only by hyperbaric oxygen therapy, second group consisted of 20 patients treated with combined hyperbaric oxygen and negative pressure wound therapy, and third group consisted of 20 patients who were treated only by negative pressure wound therapy. In some cases, previous revascularization of lower limb was performed and patients with poor run-off, without possibility to perform revascularization, were excluded from the study. Results: Patients were predominantly men (56.7%) and mean age was 60.57 years. Majority of patients had ulcers of ischemic origin (45%), in 30% of cases, the reason of foot ulceration was neuropathy, and in 25% of patients, the etiology was combined. During the study, in three patients (5%), minor amputations were observed. Regarding Wagner classification of foot ulcers, most dominant was stage II (χ = 12.618, df = 4, p < 0.05). Statistically significant reduction of wound area was achieved when hyperbaric oxygen and negative pressure wound therapy were used in conjunction comparing to isolated use either of these two modalities of treatment (χ = 116.000, df = 44, p < 0.01). Conclusion: Our data suggests simultaneous use of hyperbaric oxygen therapy and negative pressure wound therapy in diabetic foot ulcer treatment in order to achieve best results. Of great importance is previous wound debridement and successful limb revascularization. © 2019, Research Society for Study of Diabetes in India.

Background: Inflammation is one of the mechanisms that leads to carotid restenosis (CR). The aim of this study was to examine the influence of increased values of inflammation markers (high-sensitivity C-reactive protein [hs-CRP], C3 complement, and fibrinogen) on CR development after eversion carotid endarterectomy (CEA). Methods: A consecutive 300 patients were included in the study, in which eversion CEA was performed between March 1 and August 1, 2010. Demographic data, atherosclerosis risk factors, comorbidities, and ultrasound plaque characteristics were listed in relation to potential risk factors for CR. Serum concentrations of hs-CRP, fibrinogen, and C3 complement were taken just before surgery (6 hours); 48 hours after CEA; and during regular checkups at 1 month, 6 months, 1 year, and 2 years. An “inflammatory score” was also created, which consisted of six predictive values of inflammatory markers (hs-CRP just before and just after CEA, fibrinogen just before and just after CEA, and C3 complement just before and just after CEA) with a maximum score of 6 and a minimum score of 0. At every follow-up visit to the outpatient clinic, ultrasound assessment of the carotid artery for restenosis was done. Results: Our results showed an increased risk of early CR within 1 year in patients with increased hs-CRP before CEA (6 hours) and increased fibrinogen 48 hours after surgery and in patients not taking aspirin after CEA. Sex was determined to be an independent predictor of CR, with female patients having a higher risk (P =.002). Male patients taking aspirin with an inflammatory score >2 had an increased risk for restenosis compared with male patients with inflammatory score <2. Not taking aspirin after CEA and fibrinogen (48 hours) were the strongest predictors, and the Fisher equation incorporating these predictors was used to predict CR. A computer program was created to calculate whether the patient was at high or low risk for CR by selecting whether the patient was taking aspirin (yes or no) and whether fibrinogen was increased 48 hours after CEA (yes or no) and to display the recommended therapeutic algorithm consisting of aspirin, clopidogrel, cilostazol, and statins. Conclusions: Increased hs-CRP before CEA, increased fibrinogen 48 hours after CEA, and not taking aspirin were the main predictors of early CR. With the clinical implementation of the Fisher equation, it is possible to identify patients at high risk for early CR and to apply an aggressive therapeutic algorithm, finally leading to a decreased CR rate. © 2017 Society for Vascular Surgery

The aim of this article is to review our experience in surgical treatment of carotid atherosclerosis using eversion carotid endarterectomy (ECEA) in 5,034 patients, with particular attention to temporal changes in patients' characteristics, diagnostic approach, surgical technique, medical therapy, and outcome in the early (group A, 1991-1997) versus fate (group B 1998-2004) period of ECEA. From January 1991 to December 2004, 5,034 primary ECEAs were performed for high-grade carotid stenosis. Patients treated for restenosis after previous carotid surgery were excluded from the analysis. Group A consisted of 1,714 patients who underwent surgery between 1991 and 1997, and group B consisted of 3,320 patients who underwent surgery between 1998 and 2004. Follow-up included routine clinical evaluation and noninvasive surveillance, with duplex scanning at 1 month after surgery, after 6 months, and annually afterward. Only 3% of patients in group A and 0.6% in group B were asymptomatic, with 23% and 47% of them having preoperative stroke, respectively. In group A, angiography was used for the final diagnosis in 78% of patients. In group B, duplex scanning was performed in 82% of patients and angiography in only 18% (p < .001). Clamping time was shorter in the latter group (12.4 ± 3.1 vs 14.5 ± 4.1 min, p < .01). Introperative shunting and regional anesthesia were rarely performed in both groups (1.4% vs. 0.4%, p < .01, and 2% vs 0.3%, p < .001). Total and neurologic morbidity was significantly higher in group A than in group B (6.41% ± 0.47% vs 4.81% ± 0.53%, p < .001, and 2.14% ± 0.31% vs 1.23% ± 0.29%, p < .001, respectively). Total mortality was also higher in group A than in group B (1.92% ± 0.24% vs 1.36% ± 0.50%, p < .05), but although there was a trend toward lower neurologic mortality, it did not reach statistical significance (1.04% ± 0.5% vs 0.57% ± 0.25%, p = .074). There was a lower rate of nonsignificant restenosis (< 50%) in group B (2% vs 5%, p < .01), but the incidence of restenosis a 50% was identical between the groups (5.5% for both). Our data show that ECEA is a reliable surgical technique for the treatment of atherosclerotic carotid disease. Temporal trends in our patients demonstrated a decline in periopertive mortality and morbidity, despite a higher incidence of preoperative stroke. © BC Decker Inc. All rights reserved.