Browsing by Author "Kanjuh, Vladimir (57213201627)"

[No abstract available]

The data that episodes and sequels of venous thromboembolism (VTE) are recorded in a significant percentage of patients receiving standard anticoagulants as VTE prophylaxis (unfractionated, low-molecular-weight heparin and vitamin K inhibitors) as well as the fact that these drugs have significant limitations and that they may cause serious side-effects in some patients indicate the need for the introduction of new anticoagulant drugs. Fondaparinux, a selective inhibitor of Factor Xa, administered following major orthopedic surgeries having a high risk for the development of VTE, is more efficient than enoxaparin sodium used in European and North-American approved doses. The increased incidence of major bleeding (excluding fatal) due to fondaparinux could be perhaps lowered by dosage reduction in patients with a mildly decreased creatinine clearance. Dabigatran, a peroral direct thrombin inhibitor, administered for VTE prophylaxis in elective hip and knee surgery, showed in to date studies the efficacy comparable (if dabigatran is given in both dosage regimes of 150 mg and 220 mg daily) or superior (if dabigatran is given at a dose of 220 mg daily) to enoxaparin administered in European-approved doses, while North American-approved doses of enoxaparin were superior than dabigatran in VTE reduction. No significant differences in bleeding rates were determined in any of the study groups. We consider that the introduction of new anticoagulants, including fondaparinux and dabigatran, will contribute to the establishment of a better safety profile and efficacy, and will also enable adequate therapy individualization for each patient depending on his/hers clinical characteristics. The introduction of novel peroral anticoagulants will, inter alia, significantly contribute to improvement in the quality of life, release the patient from numerous limitations in nutrition, interreaction, frequent laboratory monitoring, and also significantly improve therapeutic predictability. © 2015, Serbia Medical Society. All rights reserved.

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.

Cardiomyopathies are a heterogeneous group of heart muscle diseases and an important cause of heart failure (HF). Current knowledge on incidence, pathophysiology and natural history of HF in cardiomyopathies is limited, and distinct features of their therapeutic responses have not been systematically addressed. Therefore, this position paper focuses on epidemiology, pathophysiology, natural history and latest developments in treatment of HF in patients with dilated (DCM), hypertrophic (HCM) and restrictive (RCM) cardiomyopathies. In DCM, HF with reduced ejection fraction (HFrEF) has high incidence and prevalence and represents the most frequent cause of death, despite improvements in treatment. In addition, advanced HF in DCM is one of the leading indications for heart transplantation. In HCM, HF with preserved ejection (HFpEF) affects most patients with obstructive, and ∼10% of patients with non-obstructive HCM. A timely treatment is important, since development of advanced HF, although rare in HCM, portends a poor prognosis. In RCM, HFpEF is common, while HFrEF occurs later and more frequently in amyloidosis or iron overload/haemochromatosis. Irrespective of RCM aetiology, HF is a harbinger of a poor outcome. Recent advances in our understanding of the mechanisms underlying the development of HF in cardiomyopathies have significant implications for therapeutic decision-making. In addition, new aetiology-specific treatment options (e.g. enzyme replacement therapy, transthyretin stabilizers, immunoadsorption, immunotherapy, etc.) have shown a potential to improve outcomes. Still, causative therapies of many cardiomyopathies are lacking, highlighting the need for the development of effective strategies to prevent and treat HF in cardiomyopathies. © 2019 The Authors. European Journal of Heart Failure © 2019 European Society of Cardiology

Comprehension of the mesencephalic syndromes that affect oculomotor nerve fascicles requires a detailed knowledge of their relationship with the adjacent structures and the blood supply of the central midbrain region. This was the reasoning behind our study, which was performed in ten serially sectioned midbrains stained with cresyl violet and luxol fast blue, in three microdissected midbrains, and in two injected and cleared specimens. Three continuous groups of the intramesencephalic oculomotor nerve fascicles were distinguished: the caudal, intermediate and rostral. The caudal fascicles, which most likely innervate the superior rectus and the levator palpebrae superioris muscles, extend through the superior cerebellar peduncle just caudal to the red nucleus and close to the lateral lemniscus. The intermediate fascicles, devoted to the medial rectus and the inferior oblique muscles, always pass through the superior cerebellar peduncle, just medial to the caudal part of the red nucleus (60 %), and less frequently (40 %) through the nucleus itself. The rostral oculomotor fascicles, which terminate in the inferior rectus and sphincter pupillae muscles, course medial to the rostral part of the red nucleus. While the rostral and intermediate oculomotor fascicles are supplied only by the medial twigs of the paramedian mesencephalic perforating arteries, the caudal fascicles are also nourished by the lateral branches of the same perforating arteries. The data obtained form an important basis for the explanation of certain mesencephalic syndromes, and even anticipate some new syndromes not yet described in the literature. © Japanese Association of Anatomists 2012.

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.

Introduction. Atrial fibrillation (AF) is the major cause of stroke, particularly in older patients over 75 years of age. European Society of Cardiology guidelines recommend chronic anticoagulation therapy in patients with atrial fibrillation if CHA2DS2-VASc score is ≥ 1 [CHA2DS2-VASc score for estimating the risk of stroke in patients with nonrheumatic AF consisting of the first letters of patients condition: C – congestive heart failure; H – hypertension; A2 – age ≥ 75 years; D – diabetes mellitus; S2 – prior stroke, transitory ischaemic attack (TIA) or thrombolism; V – vascular disease; A – age 65–74 years; Sc – sex category]. However, a significant number of patients have a high bleeding risk, or are contraindicated for chronic oral anticoagulation, and present a group of patients in whom alternative treatment options for thromboembolic prevention are required. Transcatheter percutaneous left atrial appendage closure (LAAC) devices have been recommended in patients with contraindications for chronic anticoagulant therapy. Case report. We present our first three patients with nonvalvular AF and contraindications for chronic anticoagulant therapy who were successfully treated with implantation of LAAC Watchman device in Catheterization Laboratory of the Clinic for Cardiology, Clinical Center of Serbia in Belgrade Conclusion. Our initial results with Watchman LAAC device are promising and encouraging, providing real alternative in patients with non-valvular AF and contraindication for chronic anticoagulant therapy and high bleeding risk. © 2017, Institut za Vojnomedicinske Naucne Informacije/Documentaciju. All rights reserved.

After reviewing the general characteristics of lipids (LDL-C, VLDL-C, HDL-C) and atherothrombosis, including the I-VIII degrees of its histopathological arterial lesions (with contributions of J. E. Edwards and R. Virmani), the authors described the P. Libby's data on lipoprotein-associated phospholipaseA2 (Lp-PLA2) and its two inflammatory mediators: lysophosphatidylcholine and oxidized nonesterified fatty acids. They are involved in plaque progression and vulnerability. Lp-PLA2 is an emerging proinflammatory marker. The new drug darapladib inhibits Lp-PLA2 and acts against inflammation. LDL-C is present in the atherosclerotic plaque from the circulating blood in arterial lumen (through the dysfunctional endothelium) and vasa vasorum as well as after the decomposition of foam cells (monocytes-phagocytes, smooth muscle and dendritic cells) and outpoured erythrocytes (its membranes) after hemorrhage. The blood from the arterial lumen can also enter the atherosclerotic plaque through the lesions in its fibrous cap (erosion, fissure, rupture). Atherosclerosis as a disease or as an inevitable accompaniment of aging ("the senescence hypothesis"). The familial hypercholesterolemia is usually due to mutation of just one gene--a defective LDL-C receptor gene on chromosome 19. The accelerated and severe atherosclerosis very resistant to therapy occurs. The patients with homozygous familial hypercholesterolemia can die of myocardial infarction in early childhood. Therapeutic decrease of LDL-C and increase of HDL-C slows down the evolution of atherosclerosis, stabilizes the atherosclerotic plaques, and even brings about their partial regression. Statins, niacin, ezetimibe, LDL-C apheresis, and surgery: shunt between the portal and inferior caval veins, liver transplantation, and partial ileal bypass. The elevated LDL-C is the most established risk factor for atherosclerosis with impact on coronary heart disease mortality of 26%, and it should be the primary target of preventive and therapeutic efforts.

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: To evaluate the prevalence of metastatic tumors involving the myocardium and study their presentation in order to increase awareness to their existence. Methods: Pathological reports from Sheba Medical Center (Israel, January 1, 2010 through December 31, 2015) and medical records from The Institute for Cardiovascular Diseases of Vojvodina, Sremska Kamenica (Serbia, 23years period) were screened for cases of metastatic cardiac tumors. Medical, radiological and pathological data of identified cases was retrieved and reviewed. Results: Out of thousands of registered cardiac surgeries we found less than a dozen cases of metastatic cardiac tumors classified as melanoma, carcinomas of lung, colon and kidney and sarcomas of uterine origin. We found that metastatic cardiac tumors comprised 15.8% of all the cardiac tumors. Conclusions: Metastatic cardiac tumors are extremely rare. As new diagnostic technologies and improved survival of oncological patients may increase the incidence of metastatic cardiac tumors in the future, awareness to their existence and knowledge of their presentation are key factors in their timely recognition. © 2018 The Author(s).

Background: To evaluate the prevalence of metastatic tumors involving the myocardium and study their presentation in order to increase awareness to their existence. Methods: Pathological reports from Sheba Medical Center (Israel, January 1, 2010 through December 31, 2015) and medical records from The Institute for Cardiovascular Diseases of Vojvodina, Sremska Kamenica (Serbia, 23years period) were screened for cases of metastatic cardiac tumors. Medical, radiological and pathological data of identified cases was retrieved and reviewed. Results: Out of thousands of registered cardiac surgeries we found less than a dozen cases of metastatic cardiac tumors classified as melanoma, carcinomas of lung, colon and kidney and sarcomas of uterine origin. We found that metastatic cardiac tumors comprised 15.8% of all the cardiac tumors. Conclusions: Metastatic cardiac tumors are extremely rare. As new diagnostic technologies and improved survival of oncological patients may increase the incidence of metastatic cardiac tumors in the future, awareness to their existence and knowledge of their presentation are key factors in their timely recognition. © 2018 The Author(s).

Despite a myriad of causes, pericardial diseases present in few clinical syndromes. Acute pericarditis should be differentiated from aortic dissection, myocardial infarction, pneumonia/pleuritis, pulmonary embolism, pneumothorax, costochondritis, gastroesophageal reflux/neoplasm, and herpes zoster. High-risk features indicating hospitalization are: fever >38 °C, subacute onset, large effusion/tamponade, failure of non-steroidal anti-inflammatory drugs (NSAIDs), previous immunosuppression, trauma, anticoagulation, neoplasm, and myopericarditis. Treatment comprises 10-14-days NSAID plus 3 months colchicine (2 × 0.5 mg; 1 × 0.5 mg in patients <70 kg). Corticosteroids are avoided, except for autoimmunity, as they facilitate the recurrences. Echo-guided pericardiocentesis (±fluoroscopy) is indicated for tamponade and effusions >2 cm. Smaller effusions are drained if neoplastic, purulent or tuberculous etiology is suspected. In recurrent pericarditis, repeated testing for autoimmune and thyroid disease is appropriate. Pericardioscopy and pericardial/epicardial biopsy may clarify the etiology. Familial clustering was recently associated with tumor necrosis factor receptor-associated periodic syndrome (TNFRSF1A gene mutation). Treatment includes 10-14 days NSAIDs with colchicine 0.5 mg bid for up to 6 months. In non-responders, low-dose steroids, intrapericardial steroids, azathioprine, and cyclophosphamide can be tried. Successful management with interleukin-1 receptor antagonist (anakinra) was recently reported. Pericardiectomy remains the last option in >2 years severely symptomatic patients. In constriction, expansion of the heart is impaired by the rigid, chronically inflamed/thickened pericardium (no thickening ∼20 %). Chest radiography, echocardiography, computerized tomography, magnetic resonance imaging, hemodynamics, and endomyocardial biopsy indicate the diagnosis. Pericardiectomy is the only treatment for permanent constriction. Predictors of poor survival are prior radiation, renal dysfunction, high pulmonary artery pressures, poor left ventricular function, hyponatremia, age, and simultaneous HIV and tuberculous infection. © 2012 Springer Science+Business Media, LLC.

Numerous limitations and side effects of standard anticoagulants require administering new anticoagulant drugs. New peroral anticoagulants of Factor Xa inhibitor group have more advantages, the key ones being: Substantial reductions in specific nutrition limitations and drug interaction, no need for routine laboratory monitoring and greatly improved therapy predictability. Rivaroxaban, a selective peroral Factor Xa inhibitor is more effective compared with enoxaparin for venous thromboembolism (VTE) prophylaxis in major orthopedic interventions. Though several single trials demonstrated no difference in hemorrhagic complications, certain meta-analyses with rivaroxaban showed a higher incidence of hemorrhage. Apixaban, a peroral reversible inhibitor of factor Xa approved for the prevention of VTE, compared with European-approved doses of enoxaparin has the efficacy almost equal to the North-American-approved enoxaparin doses without a significant difference in bleeding rates, though АDVANCE I study points towards lower bleeding rates in patients treated with apixaban. To clarify the contradictory results of the recent meta-analysis related to the comparison between the stated factor X inhibitors and various comparator enoxaparin regimens as well as related to the risk for symptomatic PTE and total bleeding events following major orthopedic surgery, new research will be required. Specificities of rivaroxaban and apixaban, already constituting, according to modern recommendations, an integral part of the VTE prophylaxis protocols after major orthopedic interventions, will enable the establishment of personalized protocols aimed at developing an improved safety profile of each individual patient. © 2020, Serbia Medical Society. All rights reserved.

Sudden death is a major health problem all over the world. The most common causes of sudden death are cardiac but there are also other causes such as neurological conditions (stroke, epileptic attacks and brain trauma), drugs, catecholamine toxicity, etc. A common feature of all these diverse pathologies underlying sudden death is the imbalance of the autonomic nervous system control of the cardiovascular system. This paper reviews different pathologies underlying sudden death with emphasis on the autonomic nervous system contribution, possibilities of early diagnosis and prognosis of sudden death using various clinical markers including autonomic markers (heart rate variability and baroreflex sensitivity), present possibilities of management and promising prevention by electrical neuromodulation. © The European Society of Cardiology 2017.

The concept of diversity, equity, inclusion and belonging is essential for research and academic programs and institutions worldwide, but although women do not lag behind men at entry and graduation from Serbian universities, equitable leadership does and it further hinders outcomes in every way: from translational science via healthcare up to legislative efforts to protect children, women and elderly. Although all these may seem as l’art-pour-l’art issues when compared to mere survival in war zones on two continents and all issues women face under circumstances of displacement and bans on rights to education, healthcare and sounds of their own voices in public, still it is the ongoing fight for rights lost in silence and where one least expects it that has to push every human being to fight for the oppressed and underprivileged. © 2024, Serbia Medical Society. All rights reserved.

Cardiovascular and reproductive health of women have been going hand in hand since the dawn of time, however, their links have been poorly studied and once the basis of their connections started to be established in late 20th century, it depended on local regional abilities and the level of progressive thinking to afford comprehensive women’s care beyond the “bikini medicine”. Further research identified different associations rendering more conditions sex-specific and launching therefore a slow, yet initial turn around in clinical trials’ concept as the majority of global cardiovascular guidelines rely on the results of research conducted on a very modest percentage of women and even less on the women of color. Currently, the concept of women’s heart centers varies depending on the local demographics’ guided needs, available logistics driven by budgeting and societal support of a broad-minded thinking environment, free of bias for everyone: from young adults questioning their gender identity, via women of reproductive age both struggling to conceive or keep working part time when healthy and line of work permits it during pregnancy, up to aging and the elderly. Using “Investigate-Educate-Advocate-Legislate” as the four pillars of advancing cardiovascular care of women, we aimed to sum-marize standing of women’s health in Serbia, present ongoing projects and propose actionable solutions for the future. © 2021, Serbia Medical Society. All rights reserved.