Browsing by Author "Stojanovic, Ivan (55014093700)"

Background and Objectives: There is a lack of data about the survival of patients after the implantation of sutureless relative to stented bioprostheses in middle-income settings. The objective of this study was to compare the survival of people with isolated severe aortic stenosis after the implantation of sutureless and stented bioprostheses in a tertiary referral center in Serbia. Materials and Methods: This retrospective cohort study included all people treated for isolated severe aortic stenosis with sutureless and stented bioprostheses from 1 January 2018 to 1 July 2021 at the Institute for Cardiovascular Diseases “Dedinje”. Demographic, clinical, perioperative and postoperative data were extracted from the medical records. The follow-up lasted for a median of 2 years. Results: The study sample comprised a total of 238 people with a stented (conventional) bioprosthesis and 101 people with a sutureless bioprosthesis (Perceval). Over the follow-up, 13.9% of people who received the conventional and 10.9% of people who received the Perceval valve died (p = 0.400). No difference in the overall survival was observed (p = 0.797). The multivariate Cox proportional hazard model suggested that being older, having a higher preoperative EuroScore II, having a stroke over the follow-up period and having valve-related complications were independently associated with all-cause mortality over a median of 2 years after the bioprosthesis implantation. Conclusions: This research conducted in a middle-income country supports previous findings in high-income countries regarding the survival of people with sutureless and stented valves. Survival after bioprosthesis implantation should be monitored long-term to ensure optimum postoperative outcomes. © 2023 by the authors.

We present a case of a 42-year-old man who suffered an iatrogenic injury to his left circumflex (Cx) coronary artery after mitral valve (MV) repair surgery. After the patient suffered from myocardial infarction without ST-segment elevation following minimally invasive MV surgery, we performed repeated coronary angiography and optical coherence tomography (OCT), which revealed severe coronary stenosis of the dominant Cx caused by intramural hematoma. In addition, we proceeded with percutaneous coronary intervention and stent implantation. 2023 Borzanovic, Ilic, Nikolic and Stojanovic.

The drug nicorandil is a vasodilator approved for the treatment of angina. In addition to its well-known effect on the opening of ATP-sensitive K +(K ATP) channels, nicorandil-induced vasorelaxation also involves the opening of Ca 2+-activated K + channels. The aim of this study was to investigate the effects of nicorandil on the isolated human internal mammary artery (HIMA) and the human saphenous vein (HSV) and to define the contribution of different K + channel subtypes in the nicorandil action on these arterial and venous grafts. Our results show that nicorandil induced a concentration-dependent relaxation of HSV and HIMA rings precontracted by phenylephrine. Glibenclamide, a selective K ATP channels inhibitor, partially inhibited the response to nicorandil in both HSV and HIMA. Iberiotoxin, a most selective blocker of large-conductance Ca 2+-activated K + (BK Ca) channels, partly antagonized relaxation of HIMA. A nonselective blocker of voltage-gated K + channels, 4-aminopyridine caused partial inhibition of the nicorandil-induced relaxation of HSV but did not antagonize relaxation of HIMA induced by nicorandil. Margatoxin, a potent inhibitor of K V1.3 channels, did not abolish the effect of nicorandil on HSV and HIMA. Our results showed that nicorandil induced strong endothelium-independent relaxation of HSV and HIMA contracted by phenylephrine. It seems that K ATP and 4-aminopyridine-sensitive K + channels located in the smooth muscle of HSV mediated relaxation induced by nicorandil. In addition, K ATP and BK Ca channels are probably involved in the nicorandil action on HIMA. © 2011 Lippincott Williams & Wilkins.

The drug nicorandil is a vasodilator approved for the treatment of angina. In addition to its well-known effect on the opening of ATP-sensitive K +(K ATP) channels, nicorandil-induced vasorelaxation also involves the opening of Ca 2+-activated K + channels. The aim of this study was to investigate the effects of nicorandil on the isolated human internal mammary artery (HIMA) and the human saphenous vein (HSV) and to define the contribution of different K + channel subtypes in the nicorandil action on these arterial and venous grafts. Our results show that nicorandil induced a concentration-dependent relaxation of HSV and HIMA rings precontracted by phenylephrine. Glibenclamide, a selective K ATP channels inhibitor, partially inhibited the response to nicorandil in both HSV and HIMA. Iberiotoxin, a most selective blocker of large-conductance Ca 2+-activated K + (BK Ca) channels, partly antagonized relaxation of HIMA. A nonselective blocker of voltage-gated K + channels, 4-aminopyridine caused partial inhibition of the nicorandil-induced relaxation of HSV but did not antagonize relaxation of HIMA induced by nicorandil. Margatoxin, a potent inhibitor of K V1.3 channels, did not abolish the effect of nicorandil on HSV and HIMA. Our results showed that nicorandil induced strong endothelium-independent relaxation of HSV and HIMA contracted by phenylephrine. It seems that K ATP and 4-aminopyridine-sensitive K + channels located in the smooth muscle of HSV mediated relaxation induced by nicorandil. In addition, K ATP and BK Ca channels are probably involved in the nicorandil action on HIMA. © 2011 Lippincott Williams & Wilkins.

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

Background: Our study aimed to evaluate the early outcomes of aortic valve replacement with Perceval S sutureless valve through the right anterior thoracotomy and upper hemisternotomy approaches, and to determine if there are any differences between these two approaches. Methods: We carried out a study using data from 174 patients who underwent minimally invasive Perceval S valve implantation for aortic valve stenosis between January 2018 and August 2023. This was a retrospective, single-center observational study. The patients were divided into two groups: the hemisternotomy group (n = 100) and the right anterior thoracotomy group (n = 74). Results: The overall in-hospital mortality was 1,7%. The cardiopulmonary bypass and cross-clamp times were longer in the right anterior thoracotomy group (p <.001). There were no statistically significant differences in terms of stroke, paravalvular leak, mechanical ventilation time, blood transfusion requirements, pacemaker implantation, reexploration for bleeding, conversion, wound infection, or in-hospital stay. Postoperative chest drainage was lower (p <.001) and postoperative atrial fibrillation occurred less frequently (p =.044) in the right anterior thoracotomy group. The median intensive care unit stay was shorter in the right anterior thoracotomy group (p =.018). Conclusion: Aortic valve replacement with the Perceval S valve through either an upper hemisternotomy or a right anterior thoracotomy is a procedure associated with low perioperative complication rates. Right anterior thoracotomy for an aortic valve replacement with the Perceval S valve was associated with lower postoperative bleeding, a lower postoperative atrial fibrillation incidence and a shorter intensive care unit stay compared to upper hemistornotomy. 2024 Okiljevic, Raickovic, Zivkovic, Vukovic, Milicic, Stojanovic, Milacic and Micovic.