Υπό την αιγίδα της Ευρωπαϊκής Εταιρείας...

ΣΥΝΕΔΡΙΟΓΛΑΥΚΩΜΑΤΟΣΥπό την αιγίδατης ΕυρωπαϊκήςΕταιρείας Γλαυκώματος

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6-8 ΑΠΡΙΛΙΟΥ 2017

ΔΙΟΙΚΗΤΙΚΟ ΣΥΜΒΟΥΛΙΟ

ΠΡΟΕΔΡΟΣΓ. ΜΑΓΚΟΥΡΙΤΣΑΣ

ΑΝΤΙΠΡΟΕΔΡΟΣΑ. ΚΩΝΣΤΑΣ

ΓΕΝ. ΓΡΑΜΜΑΤΕΑΣΦ. ΤΟΠΟΥΖΗΣ

ΤΑΜΙΑΣΑ. ΔΙΑΓΟΥΡΤΑΣ

ΕΙΔ. ΓΡΑΜΜΑΤΕΑΣΘ. ΚΑΡΜΙΡΗΣ

ΜΕΛΗΔ. ΠΑΠΑΚΩΝΣΤΑΝΤΙΝΟΥΙ. ΧΑΛΚΙΑΔΑΚΗΣ

ΑΘΗΝΑ, Ξενοδοχείο «Grande Bretagne»ΠΡΟΓΡΑΜΜΑ ΣΥΝΕΔΡΙΟΥΥΠΕΥΘΥΝΗ ΓΡΑΜΜΑΤΕΙΑΣ ΣΥΝΕΔΡΙΟΥ: Σ. ΠΑΠΑΔΕΔΕ

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ΓΕΝΙΚΕΣ ΠΛΗΡΟΦΟΡΙΕΣ

ΣΥΝΕΔΡΙΟΓΛΑΥΚΩΜΑΤΟΣ

Υπό την αιγίδατης Ευρωπαϊκής Εταιρείας Γλαυκώματος

23ο

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ΔΙΟΙΚΗΤΙΚΟ ΣΥΜΒΟΥΛΙΟΕΛΛΗΝΙΚΗΣ ΕΤΑΙΡΕΙΑΣ ΓΛΑΥΚΩΜΑΤΟΣ

Πρόεδρος: Γ. Μαγκουρίτσας

Αντιπρόεδρος: Α.-Γ. Κώνστας

Γεν. Γραμματέας: Φ. Τοπούζης

Ταμίας: Α. Διαγουρτάς

Ειδ. Γραμματέας: Ε. Καρμίρης

Μέλη: Δ. Παπακωνσταντίνου

Ι. Χαλκιαδάκης

Ε Λ Λ Η Ν Ι Κ Η Ε Τ Α Ι Ρ Ε Ι Α Γ Λ Α Υ Κ Ω Μ Α Τ Ο Σ

Π.Γ.Ν.Α. «Γ. Γεννηματάς», Παν/κή Οφθ/κή Κλινική, Τμήμα ΓλαυκώματοςΛεωφ. Μεσογείων 154, 115 27 Αθήνα - Τηλ. 210-7791808 website: www.greekglaucomasociety.org

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Αγαπητοί σύνεδροι,

με ιδιαίτερη χαρά σας καλωσορίζουμε στο 23ο Συνέδριο Γλαυκώματος, που τελεί υπό την αιγίδα της Ευρωπαϊκής Εταιρείας Γλαυκώματος.

Το γλαύκωμα παραμένει η πρώτη αιτία μη αναστρέψιμης τύφλωσης παγκοσμίως με του-λάχιστον 60 εκατομμύρια πάσχοντες ανά την υφήλιο, εκ των οποίων τουλάχιστον 6.5 εκα-τομμύρια είναι πλήρως ή μερικώς τυφλοί. Παρά τις σημαντικές εξελίξεις στην αντιμετώπιση του, το ποσοστό των ασθενών με σοβαρή απώλεια όρασης στον πληθυσμό άνω των 50 ετών παραμένει αμείωτο κατά τις δύο παρελθούσες δεκαετίες.

Αναμφίβολα λοιπόν το γλαύκωμα είναι μία ιδιαίτερη νόσος με κοινωνικές και οικονομικές επιπτώσεις, αλλά και πολλά αναπάντητα ερωτήματα, που επιβάλλουν τη συνεχή έρευνα, τη συνεχιζόμενη εκπαίδευση και την τακτική ενημέρωση των οφθαλμιάτρων.

Η Ελληνική Εταιρεία Γλαυκώματος οργανώνει με ζήλο το ετήσιο αυτό Συνέδριο, προκειμένου να πληροφορηθείτε έγκυρα οτιδήποτε νεότερο αφορά στο γλαύκωμα. Το επιστημονικό κύρος της εκδήλωσης διασφαλίζεται από τη συμμετοχή πολλών διακεκριμένων ξένων και Ελλήνων ομιλητών. Θα συζητηθούν επίκαιρα θέματα, που αφορούν στην γενετική, στην παθογένεια της βλάβης, στις δυνατότητες των απεικονιστικών μεθόδων του οπτικού νεύρου, στη σημα-σία της σταδιοποίησης και του προσδιορισμού εξέλιξης του γλαυκώματος, στις συνέπειες της ανεπαρκούς συμμόρφωσης στην αγωγή, καθώς και στη χειρουργική προσέγγιση της νόσου.

Παρά τα οικονομικά δεδομένα της εποχής και την επιβολή χαμηλών προϋπολογισμών από

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φορείς έγκρισης των συνεδρίων, προσπαθούμε με σύνεση να διατηρούμε τις καθιερωμένες κοινωνικές εκδηλώσεις με το χαμηλότερο δυνατό κόστος συμμετοχής.

Φέτος θα απονείμουμε το Μετάλλιο Τιμής και Αξίας «Αναγνωστάκη -Τράντα» στον διεθνούς εμβέλειας καθηγητή Claude Francis Burgoyne, γνωστό για το ερευνητικό του έργο στον τομέα των βιο-μηχανικών ιδιοτήτων του οφθαλμού και της παθογένειας της γλαυκωματικής βλά-βης. Ειδική τιμητική διάκριση θα λάβει επίσης ο πρόεδρος της World Glaucoma Association, διακεκριμένος καθηγητής Tin Aung για την προσφορά του στον τομέα της γενετικής.

Το 23ο Συνέδριο σηματοδοτεί το τέλος εποχής της τετραετούς θητείας του νυν Προέδρου και Διοικητικού Συμβουλίου της Ελληνικής Εταιρείας Γλαυκώματος. Θεωρούμε ότι η αποτίμηση των εκδηλώσεων των τριών τελευταίων ετών ήταν θετική, λαμβάνοντας υπόψη τόσο τον αυ-ξημένο αριθμό προσέλευσης, όσο και τα ευμενή σχόλια πολλών συνέδρων, ξένων προσκε-κλημένων και χορηγών. Με δεδομένη την εμπειρία μας στην άρτια οργάνωση, πιστεύουμε ότι η συμμετοχή σας, σε συνδυασμό με την παρουσία των διακεκριμένων ομιλητών, στους φιλόξενους χώρους της «Μεγάλης Βρετανίας», θα συμβάλλει και φέτος στην επιτυχή έκβαση του Συνεδρίου.

Απερχόμαστε έχοντας ολοκληρώσει το έργο μας και ευχόμαστε εκ των προτέρων στο νέο Διοικητικό Συμβούλιο, που θα προκύψει από τις καθιερωμένες εκλογές κατά τη διάρκεια του επικείμενου Πανελληνίου Οφθαλμολογικού Συνεδρίου στη Ρόδο, εποικοδομητική θητεία.

Εκ μέρους του Δ.Σ. της Ελληνικής Εταιρείας Γλαυκώματος

ο πρόεδροςΓιώργος Μαγκουρίτσας

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TIMHΘΕΝΤΕΣ ΜΕ ΤΟ«ΜΕΤΑΛΛΙΟ ΤΙΜΗΣ & ΑΞΙΑΣ Α. ΑΝΑΓΝΩΣΤΑΚΗ – Α. ΤΡΑΝΤΑ»

Η Ελληνική Εταιρεία Γλαυκώματος, απονέμει κάθε χρόνο από το 1994,το «Μετάλλιο Τιμής και Αξίας Α. Αναγνωστάκη - Α. Τράντα»,

σε διαπρεπείς οφθαλμιάτρους, για την συνεισφορά τους στον τομέα του γλαυκώματος.

Οι βραβευθέντες είναι (με χρονολογική σειρά):

1994 Professor Erik L. Greve, The Netherlands

1995 Professor Wolfgang Leydhecker, Germany

1996 Professor Raymond Eti enne, France

1997 Professor Giuseppe Scuderi, Italy

1998 Professor Robert Ritch, USA

1999 Professor Guenter K. Krieglstein, Germany

2000 Professor George L. Spaeth, USA

2001 Professor Bruno Boles Carenini, Italy

2002 Professor Thom Zimmerman, USA

2003 Professor Roger Hitchings, UK

2004 Professor Shlomo Melamed, Israel

2005 Professor Clive Migdal, UK

2006 Professor Paul L. Lichter, USA

2008 Professor Anders Heijl, Sweden

2009 Professor Anne Coleman, USA

2010 Professor Jeff rey Liebman, USA

2011 Professor George Baerveld, USA

2012 Professor Keith Barton, UK

2013 Professor Franz Grehn, Germany

2014 Professor Norbert Pfeiff er, Germany

2015 Professor Gábor Holló, Hungary

2016 Professor Murat Irkec Turkey

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ΙΣΤΟΡΙΚΗ ΑΝΑΔΡΟΜΗΑΝΔΡΕΑΣ ΑΝΑΓΝΩΣΤΑΚΗΣ (1826-1897)Ο Ανδρέας Αναγνωστάκης υπήρξε ο πρώτος Καθηγητής Οφθαλμολογίας στην Ιατρική Σχολή του Εθνικού Πανεπιστημίου Αθηνών (1856) έως και 41 χρόνια αργότερα. Το 1854 δημοσίευσε ένα άρθρο στα γαλλικά (Essai sur l’ exploration de la rétine et des milieux de l’ oeil sur le vivant, au moyen d’ un nouvel ophthalmoscope), στο οποίο περιέγραψε την εφεύρεση ενός απλουστευμένου οφθαλμοσκόπιου, που χρησιμοποιούσε μόνο ένα διάτρητο κοίλο κάτοπτρο. Αυτή ήταν η πρώτη εργασία στα γαλλικά για το οφθαλμοσκόπιο και είχε μεγάλη απή-

χηση στον οφθαλμολογικό κόσμο εάν λάβουμε υπόψη μας ότι το δικό του οφθαλμοσκόπιο πουλήθηκε σε 800 οφθαλμιάτρους μέσα σε λίγους μήνες. Οι αριθμοί αυτοί είναι εξαιρετικά μεγάλοι για την εποχή εκείνη, ιδίως λόγω του γεγονότος ότι το πρώτο οφθαλμοσκόπιο είχε εισαχθεί μόλις τρία χρόνια πριν από την τροποποίηση του Αναγνωστάκη από τον Hermann von Helmholtz.

ΑΛΕΞΙΟΣ ΤΡΑΝΤΑΣ (1867-1961)Το 1899 ο οφθαλμίατρος Αλέξιος Τράντας κατάφερε να παρατηρήσει in vivo τη γωνία του προσθίου θαλάμου σε ένα μάτι με μεγακερατοειδή, χρησιμοποιώντας άμεση οφθαλμοσκόπηση σε συνδυασμό με δακτυλική πίεση στο σκληροκερατοει-δές όριο. Ήταν ο πρώτος που χρησιμοποίησε τον όρο «γωνιοσκοπία» και το 1900 περιέγραψε την εικόνα της γωνίας φυσιολογικής και μη, σημειώνοντας περιπτώ-σεις πυκνής χρώσης του διηθητικού ηθμού, ιριδικών προβολών και κυκλοδιάλυ-σης. Σχεδόν επί δύο δεκαετίες, ο Τράντας κατέγραφε πολύτιμες κλινικές παρατη-

ρήσεις σχετικά με την εμφάνιση της γωνίας σε διάφορες παθήσεις, με αποτέλεσμα να αναγνωρισθεί το 1948 από την Βελγική Οφθαλμολογική Εταιρεία ως «πατέρας της γωνιοσκοπίας». Επίσης περιέγραψε τις υποκίτρινες εναποθέσεις του επιπεφυκότα πέριξ του σκληροκερατοειδούς ορίου ως παθογνωμονικές της εαρινής αλλεργικής επιπεφυκίτιδας, γνωστές μέχρι και σήμερα ως κηλίδες του Τράντα.

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ΓΕΝΙΚΕΣ ΠΛΗΡΟΦΟΡΙΕΣ

ΕΙΔΙΚΕΥΜΕΝΟΙ 150 € ΜΗ ΕΙΔΙΚΕΥΜΕΝΟΙ 70 €

Κατά την τιμολόγηση το παραπάνω κόστος εγγραφής επιβαρύνεται με 24% ΦΠΑ.

Η συμμετοχή στο Συνέδριο περιλαμβάνει δυνατότητα παρακολούθησης του επιστημονικού προγράμματος, παραλαβή συνεδριακού υλικού, είσοδο στην έκθεση, συμμετοχή στις κοινωνικές εκδηλώσεις του Συνεδρίου και παραλαβή του πιστοποιητικού συμμετοχής, βάσει των ωρών παρακο-λούθησης, που έχει θεσπίσει η UEMS.

Για νοσηλευτές και φοιτητές η συμμετοχή στο Συνέδριο είναι δωρεάν και περιλαμβάνει δυνατότητα παρακολούθησης του επιστημονικού προγράμματος, είσοδο στην έκθεση, παραλαβή του έντυπου προγράμματος και απλή βεβαίωση συμμετοχής. Η ιδιότητα τους θα πρέπει να πιστοποιείται με βε-βαίωση από τους επίσημους φορείς τους.

Καθ’ όλη τη διάρκεια του Συνεδρίου θα υπάρχει μετάφραση των ομιλιών, καθώς και σύστημα ηλε-κτρονικής καταμέτρησης των ωρών παρακολούθησης από τους συνέδρους, ακολουθώντας τα πρότυ-πα της UEMS. Το Συνέδριο μοριοδοτείται με 14 μόρια συνεχιζόμενης εκπαίδευσης, και η παραλαβή του πιστοποιητικού προϋποθέτει τη συμπλήρωση του ανώνυμου εντύπου αξιολόγησης.

Για εγγραφές και πληροφορίες διαμονής μπορείτε να απευθύνεστε στη Γραμματεία του Συνεδρί-ου, η οποία θα λειτουργεί μεταξύ 08.00 – 20.00 στο Ξενοδοχείο Μεγάλη Βρετανία.

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ΕΠΙΣΤΗΜΟΝΙΚΟ ΠΡΟΓΡΑΜΜΑ

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23ο

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ΠΕΜΠΤΗ 6 ΑΠΡΙΛΙΟΥ


14.30 - 15.15 ΕΓΓΡΑΦΕΣ (Ξενοδοχείο «King George»)

15.15 - 16.30 ΚΛΙΝΙΚΟ ΦΡΟΝΤΙΣΤΗΡΙΟ

«Ενδοφθάλμια πίεση και τονομετρία»

Συντονίστρια: Χ. Τερζίδου

Συμμετέχοντες: Σ. Κανδαράκης, Α. Μάνδαλος, Β. Τζίμης

16.30 - 17.45 ΚΛΙΝΙΚΟ ΦΡΟΝΤΙΣΤΗΡΙΟ

«Προσδιορισμός ρυθμού εξέλιξης στο γλαύκωμα»

Συντονιστής: Α. Διαγουρτάς

Συμμετέχοντες: Κ. Ανδρεάνος, Α. Καρύδης, Κ. Παπαδόπουλος, Γ. Τομαής

Διάλειμμα

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ΠΕΜΠΤΗ 6 ΑΠΡΙΛΙΟΥ

18.00 - 19.30 ΣΤΡΟΓΓΥΛΟ ΤΡΑΠΕΖΙ

«Δευτεροπαθή γλαυκώματα»

Συντονιστής: Γ. Κίτσος

Συμμετέχοντες: Ο. Μακρή, Ε. Μπαγκλή, Π. Παπαπάνος, Χ. Παππά,

Σ. Χαϊδούλης

19.30 - 20.30 ΔΟΡΥΦΟΡΙΚΟ ΣΥΜΠΟΣΙΟ ALLERGAN

«ΧΕΝ: το μέλλον στη χειρουργική του γλαυκώματος;»

Συντονιστής: Δ. Παπακωνσταντίνου

Συμμετέχοντες: Ε. Αναστασόπουλος, Σ. Κανδαράκης, Θ. Φιλιππόπουλος

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ΠΑΡΑΣΚΕΥΗ 7 ΑΠΡΙΛΙΟΥ

09.30 - 10.00 ΕΓΓΡΑΦΕΣ (Ξενοδοχείο «Grande Bretagne»)

10.00 - 10.30 ΕΠIΣΗΜΗ EΝΑΡΞΗ

Χαιρετισμός Προέδρου ΕΕΓ - Προσφωνήσεις


«Γλαυκωματικοί γρίφοι»

Συντονιστής: Β. Κοζομπόλης

Συμμετέχοντες: Ε. Αναστασόπουλος, Γ. Δαλιάνης, Γ. Κοψίνης,

A. Κωνσταντινίδης, Π. Παπαπάνος

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11.30 - 12.45 ΔΙΑΛΕΞΕΙΣ

«Update on pathogenesis»

Προεδρείο: Α. Κώνστας, Α. Πολυχρονάκος

E. Tamm Update on aqueous humor outflow and resistance

mechanisms

K. Martin Neural damage and neuroprotection in glaucoma

C. F. Burgoyne The site of damage in glaucoma

T. Aung Risk factors for angle closure and predictors of angle

widening after laser iridotomy

Διάλειμμα

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13.00 - 14.00 ΔΙΑΛΕΞΕΙΣ

«Update on detection and monitoring»

Προεδρείο: Β. Κοζομπόλης, Σ. Χαϊδούλης

S. Miglior Pearls and pitfalls using OCT for glaucoma diagnosis

B. Chauhan Role of staging damage in glaucoma

F. Meier-Gibbons How should we manage subjects at risk?

14.00 - 15.30 Γεύμα

15.30 - 16.30 ΔΟΡΥΦΟΡΙΚΟ ΣΥΜΠΟΣΙΟ BIANEΞ

«Βελτιώνοντας τη φαρμακευτική αντιμετώπιση του γλαυκώματος»

Συντονιστής: Α. Κώνστας

Συμμετέχοντες: L. Quaranta, Γ. Λαμπίρης, Κ. Μπομπορίδης

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16.30 - 17.45 ΔΙΑΛΕΞΕΙΣ

«Perspectives in management»

Προεδρείο: Α. Κανδαράκης, Γ. Λαμπίρης

A. Labbe Is preservative-free treatment really worth it?

L. Quaranta Looking for quality of life in real life

K. Martin Long-term outcomes of trabeculectomy

N. Pfeiff er Minimally Invasive Glaucoma Surgery: The opti ons

Διάλειμμα


«Αντιπαραθέσεις σε επίκαιρα θέματα γλαυκώματος»

Συντονιστής: Ι. Χαλκιαδάκης

Συμμετέχοντες: Ε. Δετοράκης, Ν. Ματθαίου, Θ. Παππάς, Χ. Τερζίδου,

Θ. Φιλιππόπουλος

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19.00 - 20.00 ΔΟΡΥΦΟΡΙΚΟ ΣΥΜΠΟΣΙΟ NOVARTIS

«Προσδιορίζοντας και επιτυγχάνοντας τον θεραπευτικό στόχο»

Συντονιστής: Φ. Τοπούζης

Συμμετέχοντες: Ε. Καρμίρης, Α. Κατσάνος, Β. Κοζομπόλης

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ΣΑΒΒΑΤΟ 8 ΑΠΡΙΛΙΟΥ


«Η σύγχρονη χειρουργική προσέγγιση του γλαυκώματος:

MIGS, tubes, and… the trab»

Συντονιστής: Δ. Παπακωνσταντίνου

Συμμετέχοντες: Α. Διαγουρτάς, Κ. Καραμπάτσας, Ν. Μυλόπουλος

10.30 - 11.30 ΔΙΑΛΕΞΕΙΣ

«Perspectives in diagnosis»

Προεδρείο: Ε. Καρμίρης, Ι. Χαλκιαδάκης

J. G. Feijoo New tonometers: toys or tools?

D. Garway-Heath New developments in visual function testing

B. Chauhan OCT: recent advancements, next steps and expectations

Διάλειμμα

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11.45 - 13.00 ΔΙΑΛΕΞΕΙΣ

«The future…»

Προεδρείο: Γ. Μαγκουρίτσας, Φ. Τοπούζης

D. Garway-Heath The future of imaging: structure to complement or

to substitute function?

T. Aung Glaucoma genetics: recent advances and future directions

«Anagnostakis - Trantas» lecture

C. F. Burgoyne The biomechanics of the glaucomatous eye

Απονομή βραβείου «Μετάλλιο Αναγνωστάκη - Τράντα»

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13.00 - 14.00 ΔΟΡΥΦΟΡΙΚΟ ΣΥΜΠΟΣΙΟ THEA

«Τρία “κλειδιά” για την επιτυχία της φαρμακευτικής αγωγής στο γλαύκωμα»

Συντονιστής: Φ. Τοπούζης

Συμμετέχοντες: A. Labbe, N. Pfeiffer, Α. Κώνστας

14.00 - 15.30 Γεύμα

15.30 - 16.30 ΔΟΡΥΦΟΡΙΚΟ ΣΥΜΠΟΣΙΟ RAFARM

«Η συμμόρφωση ως καθοριστικός παράγοντας στην αντιμετώπιση του

γλαυκώματος. Διαδραστική παρουσίαση περιστατικών»

Συντονίστρια: Χ. Τερζίδου

Συμμετέχοντες: Γ. Δαλιάνης, Π. Παπαπάνος, Ι. Χαλκιαδάκης

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16.30 - 17.45 ΔΙΑΛΕΞΕΙΣ

«Update on treatment»

Προεδρείο: Α. Διαγουρτάς, Γ. Κοψίνης

S. Miglior Under- and overtreatment

A. Azuara-Blanco Management of angle closure

G. Sunaric-Μégevand When not to decide trabeculectomy as primary procedure

N. Pfeiffer New medications and delivery systems

Διάλειμμα

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18.00 - 19.00 ΔΙΑΛΕΞΕΙΣ

«Hot topics in glaucoma»

Προεδρείο: Κ. Καραμπάτσας, Ν. Μυλόπουλος

A. Azuara-Blanco Telemedicine in glaucoma

L. Quaranta Normal tension glaucoma: should we treat differently?

G. Sunaric-Mégevand SLT in the glaucoma treatment algorithm


«Γλαύκωμα: oι εξελίξεις τρέχουν, η απώλεια όρασης καλά κρατεί»

Συντονιστής: Γ. Μαγκουρίτσας

Συμμετέχοντες: Α. Κώνστας, Δ. Παπακωνσταντίνου, Φ. Τοπούζης

ΛΗΞΗ ΣΥΝΕΔΡΙΟΥ

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ΠΕΡΙΛΗΨΕΙΣ ΔΙΑΛΕΞΕΩΝ



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Tin Aung, FRCS(Ed), FRCOphth, PhDProfessor of Ophthalmology Singapore National Eye Centre; Singapore Eye Research Institute; National University of Singapore

Risk factors for angle closure and predictors for angle widening after laser iridotomy

Angle closure glaucoma (ACG) is major cause of blindness. Recent advances in imaging have led to the identification of novel risk factors for ACG such as iris thickness, anterior chamber width and volume and lens vault. Studies have shown subtypes of ACG based on anterior segment par-

amenters. These new risk factors for ACG have improved our understanding of ACG risk and population screening. Several novel genes for ACG have also been recently identified, which may lead to new insights on possible mechanisms explain-ing the pathogenesis of ACG. Recent studies on laser iridotomy have investigated response to iridotomy and predictors of angle widening after iridotomy in patients with ACG. This talk will provide an overview of the current management of ACG.

Glaucoma Genetics: Recent advances and future directions

Recent genome wide association studies (GWAS) have led to the successful identification of genes and genetic risk factors for primary open angle glaucoma (POAG). Other GWAS studies have investigated the genes underlying quantitative traits that are important in POAG such as intraocular pressure, central corneal thickness and optic disc traits. In the past few years, several advances have been made in the genetics of primary angle closure glaucoma (PACG). In 2012, we reported a GWAS identifying three common genetic variants associated with PACG (Vithana EN et al, Nature Genetics 2012). We

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ΠΡΟΣΚΕΚΛΗΜΕΝΟΙ ΟΜΙΛΗΤΕΣ

recently expanded our GWAS of PACG to >10,000 ACG cases/20,000 controls and identified 5 more novel genes for ACG (Khor CC et al, Nature Genetics, 2016). In 2014, we also conducted a GWAS underlying anterior chamber depth, a major risk factor for PACG, and identified an association with ABCC5.In 2015, we conducted a GWAS on 1500 patients with exfoliation syndrome (XFS) matched to 1200 controls from Japan, and fol-lowed up the most significant findings on a further 6,500 patients and 19,000 controls from 17 countries across 6 continents. We discovered a significant association between a new locus on chromosome 19, CACNA1 and increased susceptibility to XFS (Aung T, et al, Nature Genetics, 2015). Further recent work has recently led to the identification of 5 more novel loci for XFS, providing new insights into the biology of the disease.In this talk, an overview of recent advances in glaucoma genetics will be presented and directions for future research will be discussed, in order for attendees to update their knowledge of this rapidly advancing field.

Augusto Azuara Blanco, MDProfessor of OphthalmologyCentre for Experimental Medicine Queen’s University Belfast Belfast, United Kingdom

Management of angle closure

Glaucoma is the leading cause of irreversible blindness according to the World Health Organisation. Approximately 4 million people are blinded by this condition, and the vast majority are in low-income

countries. Chronic primary angle-closure glaucoma is less common than open angle glaucoma but more severe, and causes

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approximately half of worldwide glaucoma blindness. The current prevalence of angle closure glaucoma is just over 20 million, and expected to rise to 34 million by 2040.3 It is most prevalent in women and among people of East Asian origin. In European populations it accounts for approximately 2 of 10 glaucomas.In this presentation we will review the evidence on different options to manage chronic primary angle-closure glaucoma. We will describe in some detail the results of the EAGLE trial that reported recently the superiority of clear-lens extraction in terms of patient, clinical and economic outcomes

Telemedicine in glaucoma Telemedicine is a term that describes different interventions, but the concept of telemedicine is providing medical services/consultations at a distance (i.e., where doctor and patient are at different geographical locations). In ophthalmology, mainly to provide care for people with retinal conditions but also for glaucoma, telemedicine has been successfully used. In this pres-entation we will review some successful models for remote glaucoma care and also describe some potential opportunities and challenges for implementation.

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Claude F. Burgoyne, MD Clinical Professor of OphthalmologyOregon Health and Sciences UniversityDirector, Opti c Nerve Head Research LaboratoryDevers Eye Insti tute, Legacy Research Insti tuteOregon, USA

Update on Pathogenesis - Site of Damage in Glaucoma

While glaucomatous damage to the visual system likely includes pathophysiologies within the reti nal photoreceptors, reti nal ganglion cell (RGC) soma, distal RGC axon, lateral geniculate/superior colliculus and visual cortex, extensive evidence from ourselves and others suggests that damage to the RGC axons within the lamina cribrosa (LC) of the opti c nerve head (ONH) is an early pathophysiology underlying glaucomatous neuronal loss in mice, rats, monkeys and humans. However, while RGC axonal insult within the ONH is central to glaucomatous vision loss and its manifestati ons are the source of all current forms of clinical staging (visual fi eld, reti nal nerve fi ber layer (RNFL) thickness, etc.), we propose that RGC axonal insult within the ONH is not the pathophysiology that defi nes the opti c neuropathy of glaucoma. In making this statement, we acknowledge the essenti al need to preserve RGC axons, soma and their peripheral connecti ons in all glaucoma pati ents, because preservati on of vision is the goal of all glaucoma therapy. However, we also emphasize that, to date, selecti vely killing RGC soma or axons alone, by whatever mechanism, has not been shown to create a glaucomatous opti c neuropathy. We propose that the defi ning pathophysiology of a glaucomatous opti c neuropathy is the deformati on, remodeling, and mechanical failure of the ONH connecti ve ti ssues. We view these phenomena as acti ve, interacti ve processes, driven by and driving astrocyte, microglial, fi broblast, and oligodendrocyte mechanobiology. These cells, and the neural and connecti ve ti ssue phenomena they propagate, have primary and secondary eff ects on RGC axon, laminar beam and retrolaminar capillary and myelin homeostasis that may

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initi ally be “protecti ve” but eventually lead to RGC axonal injury, repair and/or cell death.

Anagnostakis - Trantas lecture: The biomechanics of the glaucomatous eye

In a series of previous publicati ons we have proposed a framework for conceptualizing the opti c nerve head (ONH) as a biomechanical structure. That framework proposes important roles for intraocular pressure (IOP), IOP-related stress and strain, cerebrospinal fl uid pressure (CSFp), systemic and ocular determinants of blood fl ow, as well as potenti al roles for infl ammati on, auto-immunity, geneti cs and other non-IOP related risk factors in the physiology of ONH aging and the pathophysiology of glaucomatous damage to the ONH. This biomechanical paradigm specifi cally proposes that IOP-related stress and strain: 1) are substanti al within the neural and connecti ve ti ssues of the ONH at all levels of IOP (i.e. even when it is low); 2) underlie ONH aging; and 3) underlie the two central pathophysiologies of glaucomatous damage to the ONH — deformati on, remodeling, and mechanical failure of the connecti ve ti ssues and axonal compromise within the lamina cribrosa (LC) by a variety of IOP-related and IOP-independent mechanisms. We have additi onally proposed that modeling the ONH as a biomechanical structure provides a logic for classifying the principal components of the suscepti bility of an individual ONH to a given level of IOP. While these concepts remain central to the discussion of ONH biomechanics in general, and the pathophysiology of glaucomatous damage to the ONH ti ssues specifi cally, a large group of investi gators have expanded our understanding of glaucoma through the applicati on of biomechanics and mechanobiology to the cornea, trabecular meshwork, sclera and ONH. In this talk I will try to summarize current knowledge on the biomechanical alterati ons to these ti ssues in aging and glaucoma.

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Balwantray C. Chauhan, PhDMathers Professor and Research DirectorDalhousie University, Halifax, Canada

OCT: Recent advancements, next steps and expectations

Optical coherence tomography (OCT) has revolutionized ophthalmology. With advances in hardware, image quality and speed, ophthalmologists are able to visualize the optic nerve head and retina with unprecedented resolution. Visualizing this anatomy has highlighted the need to better understand our clinical examination and the significant interindividual variability among eyes. This presentation

will review recent advances that are relevant to glaucoma and identify where there are needs for decision-making tools to help clinicians best exploit OCT advances.

Role of Staging Damage in glaucoma

Staging of glaucomatous damage aids clinicians in planning the management of patients. Most commonly, staging of damage has been made with single examinations on the basis of the visual field examination or optic disc examination. This presentation will review the applications and limitations of current staging systems. It will focus on staging glaucoma damage on the basis of serial examinations with perimetry and imaging to emphasize that glaucoma is a progressive disease and that staging should take into account the age, extent of damage and rate of change.

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Julian García Feijoo, MD Professor of Ophthalmology. Universidad Complutense. Head Glaucoma Deparment Hospital Clínico San Carlos, Madrid, Spain

Garway Heath, MDProfessor of Ophthalmology for Glaucoma and Allied StudiesUniversity College LondonUnited Kingdom

New developments in visual function testing

Standard automated perimetry, with a bowl perimeter, has become the gold standard vision function test for glaucoma. Various improvements have been made, mostly to the thresholding algorithm, but

the instrumentation is little changed for more than 30 years. Technological developments in display technology bring new pos-

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sibilities, such as scanning laser and head mounted devices. Better understanding of psychophysical alterations in glaucoma has motivated research into optimal perimetric stimuli and thresholding algorithms. The presentation will review current develop-ments and potential benefits to clinical practice.

The future of imaging: structure to complement or to substitute function?

Visual field test result variability makes the evaluation of glaucoma stability challenging. There has been much hope that imaging, with objective quantification of optic nerve structure, would provide more reliable measurements for monitoring glaucoma. The presentation will review the requirements for surrogate measurements to replace, or supplement, vision function testing and the current evidence to support the use of imaging. New approaches to combine structure and function will be introduced.

Antoine Labbé, MD, PhD, FEBOCentre Hospitalier National d’Ophtalmologie des Quinze-Vingts,Institut de la Vision, Paris France.Service d’Ophtalmologie, Hôpital Ambroise Paré (AP-HP), Paris, France

Is preservative free treatment really worth it?

There is a large body of evidence from experimental and clinical studies showing that the long-term use of antiglaucoma medications may induce ocular surface changes, causing ocular discomfort, tear film instability, conjunctival inflammation, subconjunctival fibrosis, epithelial apoptosis, corneal sur-


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face impairment, and the potential risk of failure for further glaucoma surgery. These undesirable effects may also lead to treat-ment discontinuation and reduced quality of life in patients with glaucoma. On the basis of all these experimental and clinical reports, it would be advisable to use preservative free solutions whenever possible, especially in patients with the greatest ex-posure to high doses or prolonged treatments, in those suffering from pre-existing or concomitant ocular surface diseases, and those experiencing side effects related to the ocular surface.

Keith Martin, MA, DM, MRCP, FRCOphth Professor of Ophthalmology Cambridge Univeristy United Kingdom

Neural damage and neuroprotection in glaucoma

Progressive visual loss despite effective lowering of intraocular pressure leads to visual disability and blindness in a minority of glaucoma patients, but as glaucoma is so common this still amounts to a large number of affected individuals. Thus, there remains a need for new treatments to slow visual

deterioration in glaucoma patients progressing despite our best efforts, and ultimately to restore visual function after it has been lost.Neuroprotection aims to augment the benefit provided by IOP lowering in order to slow the rate of RGC cell death and preserv-ing the remaining level of vision. Neuroregenerative approaches are a key target of the National Eye Institute Audacious Goals Initiative and therapies that stimulate regeneration of the optic nerve have recently been shown to restore some visual function in animal models of optic nerve injury. There is a compelling argument for a combined neuroprotective/neuroregenerative ap-

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proach when considering future treatment strategies for glaucoma.In this lecture, some of the techniques being explored to protect and regenerate the optic nerve using gene therapy, stem cells and other approaches will be considered. Particular attention will be paid to those strategies that are most likely to be useful clinically and how they might be assessed in cost-effective clinical trials within a realistic timeframe.

Long-term outcomes of trabeculectomy

Despite an increasing number of alternative approaches available to the glaucoma surgeon, trabeculectomy remains arguably the ‘gold standard’ glaucoma operation to which others are compared. As trabeculectomy was developed in Cambridge, by John Cairns and Peter Watson, we have alarge number of trabeculectomy patients with very long follow up. We recently studied the performance of trabeculectomy surgery over a 20-year period and examine the associations between outcome and risk factors for trabeculectomy failure.A total of 234 patients (330 procedures) who had undergone trabeculectomy surgery at Addenbrooke’s Hospital, Cambridge, United Kingdom were identified where 20 year follow up was available. Surgical success was defined as “complete success” while intraocular pressure (IOP) remained <21 mm Hg with no additional medication and as “qualified success” if those requiring ad-ditional topical medication were included. Functional success was defined if patients did not progress to legal blindness (visual acuity <3/60 or visual field After 20 years, 57% were classified as complete success, 88% were classified as qualified success, and 15% had become blind. Those at risk of trabeculectomy failure were younger or had uveitic glaucoma. Those with pseudoexfoliation or aphakia were more likely to progress to blindness. Furthermore, those using 2 or more topical medications or with advanced visual field loss at the time of surgery were more at risk of both trabeculectomy failure and blindness.This study indicates that trabeculectomy survival at 20 years may be approximately 60% with no topical medication and approxi-

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mately 90% with additional topical medication. Patient age, preoperative topical medication use, glaucoma type, and glaucoma severity will independently influence this outcome. Trabeculectomy surgery therefore remains a successful long-term solution to IOP control.

Frances Meier-Gibbons, MDEye Center, Rapperswil, Zurich Switzerland

How should we manage subjects at risk?

Patients at risk for glaucoma can be divided into 2 groups: 1) Glaucoma suspects2) Patients with general, systemic, or local risk factorsGlaucoma suspects are defined as patients with a conspicuous optic nerve head or a nerve fiber layer

defect and/or visual field defects matching to glaucoma and/or an elevated intraocular pressure (>/= 21 mm Hg). Usually the diagnosis of primary open angle glaucoma is supported when 2 or more of these findings are present. The second group consists of patients with general risk factors such as higher age, black race, family history of glaucoma; sys-temic risk factors as associated diseases or local risk factors as high intraocular pressure level, thin corneas, suspicuous looking optic discs, pseudoexfoliation, or pigmentary dispersion.During the lecture we will discuss different ways of monitorings these patients to detect progression leading to the diagnosis of glaucoma.

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Stefano Miglior, MD Professor of Ophthalmology Hospital San Paolo University of Milano-Bicocca, Milano, Italy

Norbert Pfeiffer, MDProfessor of Ophthalmology, Mainz University, Mainz, Germany

New medications and delivery systems

Most glaucoma patients can be treated with topical medical therapy – but by no means all! Thus, new medications and new delivery systems are necessary. Nitric oxide reduces actinomyosin contractility and, thus, relaxes the trabecular meshwork. Latanoprostene bunod is such a drug. It is cleaved into

latanoprost and butanediol by esterases and reduces IOP more than latanoprost. Rho-Kinase inhibitors antagonize stiffness

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and contraction of the trabecular meshwork. IOP lowering efficacy is similar to that of latanoprost. Netarsudil can be combined with latanoprost for greater efficacy. Trabodenosone regulates metalloproteinase activity and reduces IOP. TGF-ß may increase trabecular meshwork fibrosis and increase IOP. Its antagonism may be therapeutically helpful.General trends to increase the benefits of medical therapy include medications without preservatives, fixed combinations and slow release medications.

Luciano Quaranta, MD PhD Associate Professor in Ophthalmology Univesity of Brescia, Brescia-Italy

Looking for quality of life in real life

The ultimate goal of glaucoma management is the preservation of patients’ visual function and quality of life (QoL). The disease itself as well as the medical or surgical treatment can have an enormous im-pact on a patient’s QoL. Even the mere diagnosis of a chronic, irreversible, potentially blinding disorder can adversely affect the patient’s sense of well-being and QoL by eliciting significant anxiety. Patients

with primary open-angle glaucoma rarely present with visual symptoms, at least early in the course of the disease. A betterunderstanding of patient-reported QoL can improve patient–physician interaction and enhance treatment adherence by custom-izing treatment options based on individual patient profile, thus optimizing long-term prognosis. These aspects are summarized and critically appraised in this presentation.

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Normal tension glaucoma; should we treat differently?

The precise pathogenesis of open-angle glaucoma remains to be elucidated, but elevated intraocular pressure (IOP) is considered the principal risk factor for the development and progression of glaucomatous neuropathy. Currently, meaningful lowering of IOP is the only available therapeutic strategy in glaucoma. Importantly, recent evidence suggests that 24-hour IOP characteristics may play an important role in the long-term prognosis of glaucoma. With the advent of large, well designed, population-based epidemiological studies it became apparent that a significant propor-tion of open-angle glaucoma cases presents with glaucomatous neuropathy and an IOP within the so called normal range (21 mm Hg or less, i.e. below the statistical upper limit of normal range). Most, but not all, clinicians consider normal tension glaucoma (NTG) a distinct clinical entity. It has been demonstrated that NTG patients are characterized by a pattern of visual field damage closer to the fixation as compared to high pressure glaucoma and that, within a NTG population, patients with IOP at, or below 15 mm Hg exhibit a significant higher risk for retinal nerve fibre layer defects closer to fixation. It is well documented that a proportion of treated open-angle glaucoma patients continue to deteriorate despite a statistically significant and clinically meaningful IOP reduction. It may be that in these cases other pressure-independent factors are con-tributory. Several clinical trials have demonstrated the role of vascular factors as part of the multifaceted pathogenesis of open-angle glaucoma. A parameter that has been strongly associated with glaucoma prevalence and progression is ocular perfusion pressure (OPP). More specifically, evidence has highlighted the role of reduced OPP in the incidence, prevalence, and progres-sion of glaucomatous neuropathy in several ethnic groups. Particularly in NTG, increased OPP fluctuation has been linked to the severity of disease at diagnosis and the subsequent risk of progression. These aspects are summarized and critically appraised in this presentation.

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Gordana Sunaric-Mégevand MD, FMH, FEBO Clinical Research Centre A. de RothschildCentre Ophtalmologique de Florissant Geneva, Switzerland

When NOT to decide trabeculectomy as primary procedure?

Trabeculectomy, almost 50 years old, is still regarded as the gold standard procedure for glaucoma surgery because of its potent IOP lowering effect. Although modifications in the original technic have greatly improved its safety profile, there are still potential complications which may be avoided by

performing newer, less invasive glaucoma surgeries. This is particularly the case for younger patients, high myopia or patients with co-existing systemic diseases or medication (e.g., warfarin), which makes filtering surgery potentially dangerous. The grater offer of different newer technics allows today a more individualized surgical approach for each patient, age group and different type of glaucoma. This allows a balance in safety and efficacy for the best of the patients’ quality of vision and quality of life.

SLT in the glaucoma treatment algorithm

In the era of minimally invasive glaucoma surgery (MIGS), the interest of safe, easy and cost effective glaucoma treatment is growing. SLT has the potential to reduce antiglaucoma medication use, improving convenience, comfort and appearance, which may potentially improve patients’ quality of life. While there is an overlap of target patient population with the newer surgeries, trabeculoplasty has the advantage of being less invasive, is an extraocular procedure, does not need to be combined with lens extraction and is much less costly. Recently various studies have investigated the safety and efficacy of SLT in different subtypes

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of glaucoma, the optimal power settings and predictive factors for success. With regard to an increasing glaucoma prevalence and a more older population in western countries, SLT may achieve more importance in future.

Ernst R. Tamm, MDProfessor and Chairman,Institute of Human Anatomy & Embryology, University of RegensburgGermany

Update on aqueous humor outflow and resistance mechanisms

Several prospective randomized multicenter studies identified intraocular pressure (IOP) as the criti-cal risk factor for the onset and progression of glaucomatous optic nerve damage. IOP is generated

and maintained by the aqueous humor circulation system in the anterior eye. Aqueous humor passes the trabecular meshwork (TM) outflow pathways, which provide resistance to aqueous humor outflow and IOP builds up in response to this resistance. It is generally agreed upon that the bulk of outflow resistance in the normal eye is localized in the inner wall region of the TM outflow pathways, which comprises the juxtacanalicular connective tissue (JCT) and the inner wall endothelium of Schlemm’s canal. Outflow resistance in the inner wall region is lowered through the contraction of the ciliary muscle or the relaxation of contractile myofibroblasts in the posterior part of the TM and the adjacent scleral spur. Patients with primary open-angle glau-coma (POAG) typically suffer from an abnormally high outflow resistance in this region. There is increasing evidence that the increase in TM outflow resistance in POAG is the result of a characteristic change in the biological properties of the resident cells in the JCT, which acquire the phenotype of contractile myofibroblasts. In support of this concept are histopathological studies of

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human samples, cell and molecular biological experiments, and recent findings in genetically modified mouse models of POAG. This scenario strengthens simultaneously both their actin cytoskeleton and their directly associated extracellular matrix fibrils, leads to overall stiffening of the tissue, and is modulated by transforming growth factor-β (TGF-β)/connective tissue growth factor (CTGF) signaling. Essentially comparable changes appear to occur in SC endothelial cells in glaucoma. Causative therapy concepts targeting the aqueous outflow pathways in glaucoma should aim at interfering with this process either by attenuating TM or SC stiffness, and/or by modulating TGF-β/CTGF signaling.

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ΚΥΡΙΟΙ ΧΟΡΗΓΟΙ ΣΥΝΕΔΡΙΟΥ

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ΧΟΡΗΓΟΙ ΣΥΝΕΔΡΙΟΥ

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ΣΥΝΕΔΡΙΟΓΛΑΥΚΩΜΑΤΟΣΥπό την αιγίδατης ΕυρωπαϊκήςΕταιρείας Γλαυκώματος

23ο

6-8 ΑΠΡΙΛΙΟΥ 2017

ΔΙΟΙΚΗΤΙΚΟ ΣΥΜΒΟΥΛΙΟ

ΠΡΟΕΔΡΟΣΓ. ΜΑΓΚΟΥΡΙΤΣΑΣ

ΑΝΤΙΠΡΟΕΔΡΟΣΑ. ΚΩΝΣΤΑΣ

ΓΕΝ. ΓΡΑΜΜΑΤΕΑΣΦ. ΤΟΠΟΥΖΗΣ

ΤΑΜΙΑΣΑ. ΔΙΑΓΟΥΡΤΑΣ

ΕΙΔ. ΓΡΑΜΜΑΤΕΑΣΘ. ΚΑΡΜΙΡΗΣ

ΜΕΛΗΔ. ΠΑΠΑΚΩΝΣΤΑΝΤΙΝΟΥΙ. ΧΑΛΚΙΑΔΑΚΗΣ

ΑΘΗΝΑ, Ξενοδοχείο «Grande Bretagne»ΠΡΟΓΡΑΜΜΑ ΣΥΝΕΔΡΙΟΥΥΠΕΥΘΥΝΗ ΓΡΑΜΜΑΤΕΙΑΣ ΣΥΝΕΔΡΙΟΥ: Σ. ΠΑΠΑΔΕΔΕ

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