Klemen Steblovnik

Dr. Klemen Steblovnik

University Medical Center Ljubljana, Ljubljana, Slovenia
orcid

Research Focus & Metrics

Academic Career Length

24Years (2003-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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20 December 2016 in Circulation
Verified
Journal Article
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Klemen SteblovnikKlemen Steblovnik
Klemen Steblovnik
ABAles Blinc
Ales Blinc
MMMojca Bozic Mijovski
Mojca Bozic Mijovski
MFMisa Fister
Misa Fister
UMUrsa Mikuz
Ursa Mikuz
MNMarko Noc
Marko Noc

20 June 2022 in JACC: Cardiovascular Interventions
Verified
Journal Article
Closed access
GWGuy Witberg
Guy Witberg
ULUri Landes
Uri Landes
YTYeela Talmor-Barkan
Yeela Talmor-Barkan
IRIlan Richter
Ilan Richter
MBMarco Barbanti
Marco Barbanti
RKRan Kornowski
Ran Kornowski

1 December 2003 in Klinische Monatsblätter für Augenheilkunde
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Journal Article
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MPMojca Globočnik Petrovič
Mojca Globočnik Petrovič
Klemen SteblovnikKlemen Steblovnik
Klemen Steblovnik
BPBorut Peterlin
Borut Peterlin
DPDaniel Petrovič
Daniel Petrovič
Hintergrund: Das Ziel dieser Studie war die Untersuchung der Beziehung zwischen den - 429 T/C und - 374 T/A Genpolymorphismen der Rezeptoren vom „advanced glycation end products” (RAGE)-Gen und der Entwicklung der diabetischen Retinopathie bei Kaukasiern mit Diabetes Typ II. Material und Methoden: 116 Patienten mit Diabetes Typ II und diabetischer Retinopathie wurden verglichen mit 70 Diabetikern ohne diabetische Retinopathie. Weiterhin wurden 76 Patienten mit proliferativer diabetischer Retinopathie (eine Untergruppe der diabetischen Retinopathie) verglichen mit 70 Diabetikern ohne diabetische Retinopathie. Ergebnisse: Die - 429 T/C und die - 374 T/A RAGE-Genverteilung bei Patienten mit diabetischer Retinopathie (- 429 T/C: CC 0,9 %, TC 29,9 %, TT 73 %, - 374 % T/A: AA 9,5 %, TA 47,4 %, TT 43,11) war nicht signifikant verschieden von der bei Diabetikern ohne diabetische Retinopathie (- 4,29 T/C: CC: 01, TC 25,71, TT 74,31; - 374 T/A: AA 15,71, TA 42,91, TT 41,41). Weiterhin war die - 429 T/C und die - 374 T/A RAGE-Gen-Verteilung bei Patienten mit proliferativer diabetischer Retinopathie statistisch nicht signifikant verschieden von der bei Diabetikern ohne Retinopathie. Schlussfolgerungen: Unsere Studie konnte keine Assoziation zwischen den - 429 T/C- bzw. - 374 T/A-Genpolymorphismus des RAGE-Gens und diabetischer Retinopathie bei Kaukasiern mit Diabetes Typ II feststellen. Ebenso konnte keine Assoziation zwischen - 429 T/C- bzw. - 374 T/A-Genpolymorphismus des RAGE-Gens und der proliferativen diabetischen Retinopathie bei Kaukasiern mit Diabetes Typ II aufgezeigt werden. Objective: The aim of this study was to look for a relationship between the - 429 T/C and the - 374 T/A gene polymorphisms of the receptor of advanced glycation end products (RAGE) gene and the development of diabetic retinopathy in Caucasians with type 2 diabetes. Materials and methods: One hundred and sixteen subjects with type 2 diabetes and diabetic retinopathy were compared to 70 diabetic subjects without diabetic retinopathy. Additionally, 76 subjects with proliferative diabetic retinopathy (a subgroup of diabetic retinopathy) were compared to 70 diabetic subjects without diabetic retinopathy. Results: The - 429 T/C and the - 374 T/A RAGE gene distributions in patients with diabetic retinopathy (- 429 T/C: CC 0.9 %, TC 25.9 %, TT 73.2 %; - 374 T/A: AA 9.5 %, TA 47.4 %, TT 43.1 %) were not significantly different from those of diabetic subjects without retinopathy (- 429 T/C: CC 0 %, TC 25.7 %, TT 74.3 %; - 374 T/A: AA 15.7 %, TA 42.9 %, TT 41.4 %). Moreover, the - 429 T/C and the - 374 T/A RAGE gene distributions in patients with proliferative diabetic retinopathy were not statistically significantly different from those in diabetic subjects without retinopathy. Conclusion: Our study failed to demonstrate an association between either - 429 T/C or - 374 T/A gene polymorphism of the RAGE gene and diabetic retinopathy in Caucasians with type 2 diabetes. Additionally, we failed to demonstrate an association between either - 429 T/C or - 374 T/A gene polymorphism of the RAGE gene and proliferative diabetic retinopathy in Caucasians with type 2 diabetes.

1 December 2016 in EuroIntervention
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Journal Article
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TGTomaž Goslar
Tomaž Goslar
RKRihard Knafelj
Rihard Knafelj
PRPeter Radsel
Peter Radsel
MFMisa Fister
Misa Fister
AGAlenka Golicnik
Alenka Golicnik
MNMarko Noc
Marko Noc
The Official Journal of EuroPCR and the European Association of Percutaneous Cardiovascular Interventions (EAPCI)

1 April 2015 in EuroIntervention
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Journal Article
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Klemen SteblovnikKlemen Steblovnik
Klemen Steblovnik
ABAles Blinc
Ales Blinc
Mojca Bozic MijovskiMojca Bozic Mijovski
Mojca Bozic Mijovski
IKIgor Kranjec
Igor Kranjec
EMEnver Melkic
Enver Melkic
MNMarko Noc
Marko Noc
To investigate the effects of clopidogrel and eptifibatide on platelet reactivity in patients resuscitated from cardiac arrest undergoing percutaneous coronary intervention (PCI) and hypothermia. VerifyNow® and Multiplate® aggregometry were used before, and 4, 12, 22 and 48 hours after 600 mg clopidogrel treatment in 28 post-cardiac arrest hypothermic patients and in 14 normothermic patients with acute coronary syndrome. Basal platelet reactivity after stimulation with iso-thrombin receptor-activating peptide (TRAP) and PAR4-activating peptide (BASE) was significantly lower in the post-cardiac arrest group and persisted up to 48 hours. The antiplatelet effect of clopidogrel measured by VerifyNow and expressed as % inhibition was significantly lower in the post-cardiac arrest group. It was close to zero with an increase to only around 10% after 48 hours. Post-cardiac arrest patients receiving eptifibatide showed profound platelet inhibition measured by both VerifyNow IIb/IIIa and Multiplate TRAP tests for at least 22 hours after administration. Post-resuscitation syndrome with ongoing hypothermia is associated with decreased platelet reactivity. Clopidogrel loading does not significantly affect platelet function during the first 48 hours. This is in contrast with eptifibatide which produces profound platelet inhibition, and may be used to bridge insufficient inhibition by clopidogrel.

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Klemen SteblovnikKlemen Steblovnik
Klemen Steblovnik
Matjaz BuncMatjaz Bunc
Matjaz Bunc
Aortic stenosis is the most common valve disease requiring surgery or percutaneous treatment. Since the first-in-man implantation in 2002 we have witnessed incredible progress in transcatheter aortic valve implantation (TAVI). In this article, we review the technical aspects of TAVI development with a look at the future. Durability, low thrombogenicity, good hydrodynamics, biocompatibility, low catheter profile, and deployment stability are the attributes of an ideal TAVI device. Two main design types exist—balloon-expandable and self-expanding prostheses. Balloon-expandable prostheses use a cobalt-chromium alloy frame providing high radial strength and radiopacity, while the self-expanding prostheses use a nickel-titanium (Nitinol) alloy frame, which expands to its original shape once unsheathed and heated to the body temperature. The valve is sewn onto the frame and consists of the porcine or bovine pericardium, which is specially treated to prevent calcinations and prolong durability. The lower part of the frame can be covered by polyethylene terephthalate fabric or a pericardial skirt, providing better sealing between the frame and aortic annulus. The main future challenges lie in achieving lower rates of paravalvular leaks and new pacemaker implantations following the procedure, lower delivery system profiles, more precise positioning, longer durability, and a good hemodynamic profile. Patient-specific design and the use of autologous tissue might solve these issues.