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UVOD: u atrijalnoj fibrilaciji (AF) povišen je rizik od tromboembolijskih (TE) komplikacija praćenih visokim mortalitetom ili trajnim invaliditetom. Poslednjih godina je pokazano da povišenom TE riziku, pored staze krvi u levoj pretkomori (LP), doprinose strukturne i funkcionalne promene endotela LP, kao i povišeni nivoi cirkulišućih medijatora koji odražavaju proinflamatorno (npr. C-reaktivni protein, CRP, fibrinogen), prokoagulantno (npr. D-dimer), prooksidativno stanje (npr. oksidisani lipoproteini male gustine, oxLDL) i neurohormonalnu aktivaciju (npr. B-tip natriuretskog peptida, BNP). Endotelno oštećenje je najčeće povezano sa povišenom koncetracijom von Willebrandovog faktora (vWF) u krvi, za koji se smatra da potiče iz oštećenog endokarda LP. Kod jednog broja obolelih, dokumentovani su i znaci disfunkcije endotela arterijskih krvnih sudova (snižena endotel-zavisna dilatacija, flow-mediated dilation, FMD), a pokazana je i povezanost endotelnog oštećenja, prokoagulantnih medijatora i remodelovanja LP. Međutim, ostalo je nerazjašnjeno da li je endotelna disfunkcija prisutna kod svih obolelih od AF (nezavisno od kliničkog tipa aritmije ili pridruženog kardiovaskularnog oboljenja), da li je endotelna disfunkcja ograničena na LP ili obuhvata i disfunkciju vaskularnog endotela i da li doprinosi prokoagulantnom, proinflamatornom i prooksidativnom stanju. Takođe, prognostički značaj endotelne (dis)funkcije u pogledu uticaja na morbiditet i mortalitet obolelih od AF nedovoljno je ispitan. CILJEVI ISTRAŽIVANJA: (I) Procena vaskularne endotelne funkcije ultrazvučnom metodom endotel-zavisne vazodilatcije brahijalne arterije (FMD) kod obolelih od AF sa i bez strukturnog srčanog oboljenja i kardiovaskularnih (KV) faktora rizika. (II) Poređenje pokazatelja endotelne funkcije obolelih od AF i zdravih osoba. (III) Procena povezanosti pokazatelja endotelne funkcije određenih pomoću FMD metode i laboratorijskih pokazatelja endotelnog oštećenja (vWF), inflamacije (CRP, fibrinogen), tromboze (D-dimer), neurohormonalne aktivacije (BNP) i oksidativnog stresa (oxLDL). (IV) Ispitivanje povezanosti endotelne funkcije (FMD i vWF) i remodelovanja LP, izraženog ehokardiografskom procenom volumena LP. (V) Ispitivanje značaja endotelne funkcije za prognozu različitih oblika AF (paroksizmalne, perzistentne, permanentne) kod osoba sa i bez strukturnog srčanog oboljenja... INTRODUCTION: atrial fibrillation (AF) confers an increased risk of thromboembolic (TE) complications, associated with high mortality and disability rates. Besides blood stasis in the left atrium (LA), recent evidence attributed increased TE risk in AF to the structural and functional changes of the atrial endocardium and to the raised blood levels of pro-inflammatory (i.e C-reactive protein, CRP, fibrinogen), pro-thrombotic (i.e D-dimer), and pro-oxidative (oxidized low density lipoprotein, oxLDL) mediators and increased neurohormonal activity (i.e. B-type natriuretic peptide, BNP). Endothelial dysfunction in AF was associated with increased plasma levels of von Willebrand factor (vWF), considered a marker of endocardial damage. In some instances, decreasedendothelium dependent vasodilation (FMD) was documented in the peripheral blood vessels of AF patients, accompanied by increased levels of procoagulant factors and evidence of LA remodeling. However, whether endothelial dysfunction is present in all AF subjects (regardless of AF type or associated comorbidities) and whether endothelial dysfunction is systemic or confined to the LA endocardium remains unclear. The association of endothelial dysfunction with markers of inflammation, oxidative and prothrombotic state and neurohormonal activation is also unclear. The prognostic significance of endothelial dysfunction in AF remained largely un-investigated. AIMS: (I) Assessment of brachial artery FMD by vascular ultrasound in AF patients with and without associated cardiovascular (CV) disease. (II) Comparison of FMD in AF patients with healthy controls in sinus rhythm. (III) Assessment of the association between markers of endothelial (dys)function (FMD, vWF) and biomarkers of inflammation (CRP, fibrinogen), thrombosis (D-dimer), oxidative stress (oxLDL) and neurohormonal activity (BNP). (IV) Assessment of the association of markers of endothelial (dys)function (FMD, vWF) with LA remodeling as evidenced by echocardiographic determination of the LA volume. (V) Evaluation of the prognostic significance of endothelial (dys)function for adverse vascular events in AF patients with and without CV disease...

Data on the management of atrial fibrillation (AF) in the Balkan Region are limited. The Serbian AF Association (SAFA) prospectively investigated contemporary ‘real-world’ AF management in clinical practice in Albania, Bosnia&Herzegovina, Bulgaria, Croatia, Montenegro, Romania and Serbia through a 14-week (December 2014-February 2015) prospective, multicentre survey of consecutive AF patients. We report the results pertinent to stroke prevention strategies. Of 2712 enrolled patients, 2663 (98.2%) with complete data were included in this analysis (mean age 69.1 ± 10.9 years, female 44.6%). Overall, 1960 patients (73.6%) received oral anticoagulants (OAC) and 762 (28.6%) received antiplatelet drugs. Of patients given OAC, 17.2% received non-vitamin K antagonist oral anticoagulants (NOACs). CHA2DS2-VASc score was not significantly associated with OAC use. Of the ‘truly low-risk’ patients (CHA2DS2-VASc = 0 [males], or 1 [females]) 56.5% received OAC. Time in Therapeutic Range (TTR) was available in only 18.7% of patients (mean TTR: 49.5% ± 22.3%). Age ≥ 80 years, prior myocardial infarction and paroxysmal AF were independent predictors of OAC non-use. Our survey shows a relatively high overall use of OAC in AF patients, but with low quality of vitamin K antagonist therapy and insufficient adherence to AF guidelines. Additional efforts are needed to improve AF-related thromboprophylaxis in clinical practice in the Balkan Region.

Type 2 diabetes mellitus (T2DM) is common in patients with heart failure (HF) and associated with considerable morbidity and mortality. Significant advances have recently occurred in the treatment of T2DM, with evidence of several new glucose-lowering medications showing either neutral or beneficial cardiovascular effects. However, some of these agents have safety characteristics with strong practical implications in HF [i.e. dipeptidyl peptidase-4 (DPP-4) inhibitors, glucagon-like peptide-1 receptor agonists (GLP-1 RA), and sodium-glucose co-transporter type 2 (SGLT-2) inhibitors]. Regarding safety of DPP-4 inhibitors, saxagliptin is not recommended in HF because of a greater risk of HF hospitalisation. There is no compelling evidence of excess HF risk with the other DPP-4 inhibitors. GLP-1 RAs have an overall neutral effect on HF outcomes. However, a signal of harm suggested in two small trials of liraglutide in patients with reduced ejection fraction indicates that their role remains to be defined in established HF. SGLT-2 inhibitors (empagliflozin, canagliflozin and dapagliflozin) have shown a consistent reduction in the risk of HF hospitalisation regardless of baseline cardiovascular risk or history of HF. Accordingly, SGLT-2 inhibitors could be recommended to prevent HF hospitalisation in patients with T2DM and established cardiovascular disease or with multiple risk factors. The recently completed trial with dapagliflozin has shown a significant reduction in cardiovascular mortality and HF events in patients with HF and reduced ejection fraction, with or without T2DM. Several ongoing trials will assess whether the results observed with dapagliflozin could be extended to other SGLT-2 inhibitors in the treatment of HF, with either preserved or reduced ejection fraction, regardless of the presence of T2DM. This position paper aims to summarise relevant clinical trial evidence concerning the role and safety of new glucose-lowering therapies in patients with HF. G.A. reports personal fees from Angelini, Behring, Menarini, outside the submitted work. S.A. reports grants and personal fees from Vifor Int, Abbott Vascular, and personal fees from Bayer, Boehringer Ingelheim, Novartis, Servier, outside the submitted work. J.B. reports personal fees from Novartis, BMS, Pfizer, Servier, Orion, MSD, Boehringer Ingelheim, AstraZeneca, Abiomed, Abbott, and grants and personal fees from Vifor, Bayer, CvRX, Medtronic, outside the submitted work. O.C. reports grants from Servier, Novartis, Vifor, outside the submitted work. A.J.S.C reports personal fees from Actimed, AstraZeneca, Faraday, WL Gore, Menarini, Novartis, Nutricia, Respicardia, Servier, Stealth Peptides, Verona, Vifor, outside the submitted work. F.C. reports personal fees from Novo Nordisk, MSD, Pfizer, Mundipharma, Lilly, AstraZeneca, BMS, outside the submitted work. R.A.D.B reports grants from Abbott, AstraZeneca, Novo Nordisk, Novartis, Roche, and personal fees from Abbott, AstraZeneca, MandalMed, Inc., Novartis, Roche, outside the submitted work. G.F. reports he was Committee member of trials and registries sponsored by Byer, Novartis, Servier, Vifor, Medtronic, Boehringer Ingelheim, outside the submitted work. L.H. reports personal fees from Novartis, during the conduct of the study. M.H. reports grants from Roche Diagnostics, and personal fees from Boerhinger, AstraZeneca during the conduct of the study. P.S.J. reports other from AstraZeneca, personal fees from Novartis, grants from Boehringer Ingelheim, during the conduct of the study; personal fees from Cytokinetics, outside the submitted work. M.K. reports personal fees from Novartis, Servier, BMS, Torrent, Sanofi, AstraZeneca, MSD, Novo Nordisk, outside the submitted work. Y.L. reports personal fees from Servier, Novartis, Boehringer Ingelheim, during the conduct of the study. L.H.L. reports personal fees from Merck, Sanofi, Bayer, Pharmacosmos, Abbott, Medscape; grants from Boehringer Ingelheim, Boston Scientific; grants and personal fees from Vifor-Fresenius, AstraZeneca, Relypsa, Novartis, Mundipharma, outside the submitted work. A.L. reports personal fees from Servier; grants and personal fees from Pfizer; personal fees from Novartis, Roche, Takeda, Boehringer Ingelheim, Amgen, Clinigen Group, Ferring Pharmaceuticals, Eli Lily, BMS, Eisai Ltd, outside the submitted work. M.M. reports grants from European Community during the conduct of the study and personal fees from Bayer, Novartis, and Servier outside the submitted work. W.M. has nothing to disclose. M.C.P. reports personal fees and other from AstraZeneca; personal fees from Novartis, Novo Nordisk, Lilly, Bayer; grants and personal fees from Beohringer Ingelheim, during the conduct of the study.; personal fees from Maquet, Takeda, null, outside the submitted work. M.P. has nothing to disclose. M.M.P. has nothing to disclose. P.P. has nothing to disclose. G.M.C.R. has nothing to disclose. I.S. has nothing to disclose. J.S. has nothing to disclose. P.M.S. received grants/research supports: Ministry of Education, Science and Technological Development of Republic of Serbia; receipt of honoraria or consultation fees from Servier, Boehringher Ingelheim, Hemofarm, Novartis, AstraZeneca; participation in a company sponsored speaker's bureau: Fondazione Internazionale Menarini. T.T. reports personal fees from Cardior Pharmaceuticals GmbH, outside the submitted work. M.V. reports personal fees from Servier during the conduct of the study. Seferovic, PM (reprint author), Univ Belgrade, Fac Med, 8 Koste Todorovica, Belgrade 11000, Serbia, Univ Belgrade, Med Ctr, Heart Failure Ctr, 8 Koste Todorovica, Belgrade 11000, Serbia. seferovic.petar@gmail.com

Aims Since its emergence in early 2020, the novel severe acute respiratory syndrome coronavirus 2 causing coronavirus disease 2019 (COVID-19) has reached pandemic levels, and there have been repeated outbreaks across the globe. The aim of this two part series is to provide practical knowledge and guidance to aid clinicians in the diagnosis and management of cardiovascular (CV) disease in association with COVID-19. Methods and results A narrative literature review of the available evidence has been performed, and the resulting information has been organized into two parts. The first, which was reported previously, focused on the epidemiology, pathophysiology, and diagnosis of CV conditions that may be manifest in patients with COVID-19. This second part addresses the topics of: care pathways and triage systems and management and treatment pathways, both of the most commonly encountered CV conditions and of COVID-19; and information that may be considered useful to help patients with CV disease (CVD) to avoid exposure to COVID-19. Conclusion This comprehensive review is not a formal guideline but rather a document that provides a summary of current knowledge and guidance to practicing clinicians managing patients with CVD and COVID-19. The recommendations are mainly the result of observations and personal experience from healthcare providers. Therefore, the information provided here may be subject to change with increasing knowledge, evidence from prospective studies, and changes in the pandemic. Likewise, the guidance provided in the document should not interfere with recommendations provided by local and national healthcare authorities., Graphical Abstract Graphical Abstract