ΕΥΧΑΡΙΣΤΙΕΣ H Οργανωτική Επιτροπή εκφράζει ιδιαίτερες ευχαριστίες στις εταιρίες που βοήθησαν με την ευγενή συμμετοχή τους στην επιτυχία της ημερίδας.
09:00-09:20 Έναρξη της ημερίδας Γενοβέφα Κολοβο Γεώργιος Γκουμάς Δημήτριος Σταμάτης Αθανάσιος Μιχαλ πουλος 09:20 10:40 Κυτταρικοί και χημικοί παράγοντες του αγγειακο τοιχώματος και αθηροσκλήρωση Πρόεδροι: Δέσποινα Περρέα, Δ. Σταμάτης Αγγειακό τοίχωμα: δημιουργία, φυσιολογική λειτουργία, παθολογία Μ. Δασκαλ πουλος Δυσλειτουργία του ενδοθηλίου Βασιλική Γιαννακοπο λου Χημικοί παράγοντες και αθηροσκλήρωση Γ. Σταματάκης Ασταθής πλάκα Αδαμαντία Ζηζή 10:40-11:00 Διάλειμμα-καφές 11:00-12:30 Εξελίξεις στην Προληπτική Καρδιολογία Πρόεδροι: Μαρία-Νανά Αναστασίου, Κ. Δημ πουλος Δυσλιπιδαιμίες νεότερα δεδομένα, οδηγίες Ελένη Μπιλιανο Θεραπεία της ανθεκτικής αρτηριακής υπέρτασης το 2011 Π. Καλογερ πουλος Εξελίξεις στην αντιμετώπιση του σακχαρώδους διαβήτη Στέλλα Ηρακλειανο Κάπνισμα: ο πιο σημαντικός παράγοντας κινδύνου; Γ. Γκουμάς 12:30-13:30 Διάλεξη Πρόεδροι: Σωτηρία Λυμπέρη, Ι. Χουρσαλάς Στατίνες και μή καρδιακή αγγειακή νόσος Δ. Μιχαηλίδης Personalized nutrition in cardiometabolic diseases: surfing the tsunami Pablo Perez -Martinez 13:30-14:15 Διάλειμμα-ελαφρύ γεύμα 14:15-16:15 Σ για και Υγεία Πρόεδρος: Α. Μιχαλ πουλος Η θέση της σόγιας στη σύγχρονη διατροφή Γ. Πανοτ πουλος Σόγια και Υγεία της Γυναίκας Ε. Δεληγεώρογλου Δράση της σόγιας στο μεταβολισμό των λιπιδίων Γενοβέφα Κολοβο Ο αντιφλεγμονώδης ρόλος των πρωτεϊνών της σόγιας και η σημασία του για τη λειτουργία του λιπώδους ιστού Γ. Πολίτης 16:15-17:15 Παρουσίαση περιστατικών Πρόεδροι: Δ. Μιχαηλίδης, Ε. Γανωτάκης Σο λα Παντσιώτη Ε. Πέτρου Μαρία Ζαφείρη Οι βεβαιώσεις παρουσίας θα αποσταλούν ΟΡΓΑΝΩΤΙΚΗ ΕΠΙΤΡΟΠΗ Γενοβέφα Κολοβο Γεώργιος Γκουμάς Δημήτριος Σταμάτης Αθανάσιος Μιχαλ πουλος ΓΡΑΜΜΑΤΕΙΑ Φαίδρα Κωνσταντινίδου Τηλ.: 210-9493341, Fax: 210-9493336 e-mail: akard@ocsc.gr
36 Ε Α ΔΕ Ε Α «Δ Α Η Η Α Η» 2012 Ω
Ά 21 ω : μ υ υπ π α μία υπ φα μα υ α ω α LDL αφαί (2004). 04/08/2004: ω υπ α ω α μ μ ωμα Heamashield dacron (Ω ) 25/08/2011: CAA LM, LAD, LCX Χ, RCA μ α ω 30-40%. αφ α: χω μα α, AR 3+. α φ α ω ί ω : α α μ υ αμ μα φυ ω α ω α ω ί α. 09/2011: α ω α μ 06/10/2011: α α α α α ί α (ATS #16), CABG x 1 ( SVG RCA)
Τ π ω (2004) Δ γ ω η Δ αφο ο γ ω η Φα α υ αγωγ Guidelines 2004 LDL αφα η.
Terminology hyperlipopoteinemia hyperlipidemia dyslipidemia Hyperlipoproteinemia is a metabolic disorder characterized by abnormally elevated concentrations of specific lipoprotein particles in the plasma. Hyperlipidemia ( plasma cholesterol and/or triglyceride) is present in all hyperlipoproteinemias. Dyslipidemia - abnormal cholesterol (TC, LDL-C, or HDL-C) and/or TG concentrations.
Donald S. Fredrickson (1924 Ο 2002)
Classification: Fredrickson Ο WHO; OMIM, Bethesda HLP-Phenotypes (Fredrickson, WHO) ATS Lipoproteins Lipids Defect I Chylomicron TG LP lipase IIA LDL LDL-C LDL-receptor IIB LDL + VLDL LDL-C, TG HMG.CoA reductase III IDL TC, TG Apo-E deficiency IV VLDL TG VLDL overproduction V Chylomicron + VLDL TG Apo-C2 deficiency Classification (OMIM) Recommended Original Hyperlipoproteinemia Type I Hyperlipoproteinemia Type Ib Apolipoprotein C2 deficiency Hyperlipoproteinemia Type Ic Chylomicronemia Familial Hypercholesterolemia Type II Hyperlipoproteinemia Hyperlipoproteinemia Type II Familial Hyperbetalipoproteinemia Hyperlipoproteinemia Type III Apolipoprotein E Deficiency Hyperlipoproteinemia Type IV Hyperlipoproteinemia Type V
Joseph L. Goldstein (left) and Michael S. Brown on the day of announcement of their Nobel Prize in Physiology or Medicine on October 15, 1985.
LDL receptor
LDL receptor mutations There are 5 broad classes of mutation of the LDL receptor. Class 3 mutations stop the binding of LDL to the receptor. Class 4 mutations inhibit the internalisation of the receptor-ligand complex. Class 5 mutations give rise to receptors that cannot recycle properly. This leads to a relatively mild phenotype as receptors are still present on the cell surface (but all must be newly synthesized).
THE LDL RECEPTOR AND ATHEROSCLEROSIS: Familial Hypercholesterolemia 1:500 people are heterozygous for LDL receptor mutations. These mutations are dominant, These individuals have elevated plasma cholesterol concentrations. Consequently, heterozygotes have a moderately increased risk, And homozygotes have a dramatically increased risk of atherosclerosis, particularly coronary artery disease. Normal Mutated
13/04/2012 Ο 18/04/2012 α Γ υ μα (<38 C), π α π α α μ ωμ α χ πω απ 3 μ υ. ECHO: MR 3-4+/4+, MR prolapse, ω χ ω?? 18/10/2011 ECHO (Ω ): υ LVH, LVEF 50%, AV DP max 49mmHg, mean 29mmHg, AVA 1,3cm2, MV π παχυ μ μ α MR 2+, a Aorta : 18-19mm (μ α). μπ α μ α α ω α μ α ί α (Voncon, Garamycin, Rifadin). 2 μ α: υχ α υ VT/ VF (not documented) απ ί ω, α ω ω Θ. 3 μ α: α μ υ αμ α, απ απ ω ω. υ μ υμ α α (CPK 2457, CKMB 47, LDH 724, TNI > 10 pg/ml) Χ???
18/04/2012 : α μ Ω : μ υ αμ α α π, χω ί μ ία α υμπ μα α ίμω 19/04/2012: TEE AV DPmax 79mmHg, mean 45mmHg, AVA 0,6cm2, MR 3-4+ μ π π ω π ία ωχί α. Β απ ί α α ί χ, α, απ μα α. υμ π α. 20/04/2012: αφ Θ ία 20/04-26/04/2012: π Dopamine α α μα, ω, ω α ω : μ α α ω : Voncon 500mg x3 ( α π 27/04). Ήπ α α πυ ί.
26/04/2012 : μ αφ φ ωμ, απ, α μ υ αμ α υ ίω α α μ π υ ία α ω α υ μ / α α α αχ α ω ωμ α χ πω ( ) 02/05/2012: CORO CT: ω SVG α α μω μ α. VRT (volume rendering technique): ω α χ φα αία α ία, χ απ α απ ω χ ί ATS ( υμπί / μμα??). Β α α α ω α ί α α α ί χα μ π ία π φ α ( μ ωμα??). 04/05/2012: π ICD 10/05/2012: CA LM >50% μ ( ω π ί α 1-2mm), π ί, μ ωμ backflow, SVG RCA 70% μ ( π ί, no backflow), RCA (native) 70% μ ( π ί ).
CORO CT
CORO CT
CAA-LM
CAA LM
CAA SVG
CAA RCA
CAA LM
CAA SVG
CAA SVG 2
ΩΔΗ Ε Δ Α Δ ΔΑ Η Α DUKE (Circulation 2005;111;394-434) 1. Θ α μ α π μ ω υπ μ α μ (Sreptococcus viridans, S. bovis, HACEK group, S. aureus, community acquired Enterococci) πίμ α α μ α : απ μ ω μ α μ υμ α μ ω απ υ α αίμα, π υ φ α μ αφ 12 ω απ α μ α π φ ω απ π α μ α α χ υ φ ί >4 (μ π α υ αία α χ υ φ ί μ μα μία α ). α μ α μ α α α Coxiella Burnetti πυ Q.
ΩΔΗ Ε Δ Α Δ ΔΑ Η Α DUKE (Circulation 2005;111;394-434) 2. ί π μυ α ί υ Θ ECHO : α ω μ α α μ α, υμ α μ χω ί α υπ χ α α α α μ πα υ ία απ μα α μ αφυ πί π α ί α. μφ α π α α ί α π υ π ΰπ χ ( πί α α α π ΰπ χ α φυ μα α πα ί).
ΩΔΗ Ε Δ Α Δ ΔΑ Η Α DUKE (Circulation 2005;111;394-434) 1. ρ ΰπ ρχ υ α αρ α β βη χρ η φ β ω ώ υ ώ 2. υ 38 C 3. α φα μ α: α α μ α, π π υμ μφ α α, μυ ω α υ μα, α α α μ α ία, α μ α ία π π φυ α, Janeway 4. φα μ α: π αμα φ ί α, ί α Osler, Roth, RF 5. ί : α μ α ( αφ απ μα α απ ί α ω μ ί ω ίω ), α ία ίμω μ μ α μ π υ ί α υμ α μ ω.
ΩΔΗ Ε Δ Α Δ ΔΑ Δ ΑΓ Ω Η (Circulation 2005;111;394-434) Β Γ Ω : 2 Ή Ή Θ Β Γ Ω : Ή
AHA/ACC/ESC 2008 GUIDELINES FOR DEVICE BASED THERAPY JACC Vol. 51, No. 21, 2008 May 27, 2008:e1 62 CLASS I 1. ICD therapy is indicated in patients who are survivors of cardiac arrest due to VF or hemodynamically unstable sustained VT after evaluation to define the cause of the event and to exclude any completely reversible causes. (Level of Evidence: A) (16,319Ο324) 2. ICD therapy is indicated in patients with structural heart disease and spontaneous sustained VT, whether hemodynamically stable or unstable. (Level of Evidence: B) (16,319Ο324) 3. ICD therapy is indicated in patients with syncope of undetermined origin with clinically relevant, hemodynamically signifi- cant sustained VT or VF induced at electrophysiological study. (Level of Evidence: B) (16,322) 4. ICD therapy is indicated in patients with LVEF less than or equal to 35% due to prior MI who are at least 40 days post-mi and are in NYHA functional Class II or III. (Level of Evidence: A) (16,333) 5. ICD therapy is indicated in patients with nonischemic DCM who have an LVEF less than or equal to 35% and who are in NYHA functional Class II or III. (Level of Evidence: B) (16,333,369,379) 6. ICD therapy is indicated in patients with LV dysfunction due to prior MI who are at least 40 days post-mi, have an LVEF less than or equal to 30%, and are in NYHA functional Class I. (Level of Evidence: A) (16,332) 7. ICD therapy is indicated in patients with nonsustained VT due to prior MI, LVEF less than or equal to 40%, and inducible VF or sustained VT at electrophysiological
AHA/ACC/ESC 2008 GUIDELINES FOR DEVICE BASED THERAPY CLASS IIa 1. ICD implantation is reasonable for patients with unexplained syncope, significant LV dysfunction, and nonischemic DCM. (Level of Evidence: C) 2. ICD implantation is reasonable for patients with sustained VT and normal or nearnormal ventricular function. (Level of Evidence: C) 3. ICD implantation is reasonable for patients with HCM who have 1 or more major risk factors for SCD. (Level of Evidence: C) 4. ICD implantation is reasonable for the prevention of SCD in patients with ARVD/C who have 1 or more risk factors for SCD. (Level of Evidence: C) ICD implantation is reasonable to reduce SCD in patients with long-qt syndrome who are experiencing syncope and/or VT while receiving beta blockers. (Level of Evidence: B) (349Ο354) 6. ICD implantation is reasonable for non hospitalized patients awaiting transplantation. (Level of Evidence: C) 7. ICD implantation is reasonable for patients with Brugada syndrome who have had syncope. (Level of Evidence: C) 8. ICD implantation is reasonable for patients with Brugada syndrome who have documented VT that has not resulted in cardiac arrest. (Level of Evidence: C) 9. ICD implantation is reasonable for patients with catecholaminergic polymorphic VT who have syncope and/or documented sustained VT while receiving beta blockers. (Level of Evidence: C) 10. ICD implantation is reasonable for patients with cardiac sarcoidosis, giant cell myocarditis, or Chagas disease. (Level of Evidence: C)
AHA/ACC/ESC 2008 GUIDELINES FOR DEVICE BASED THERAPY CLASS IIb 1. ICD therapy may be considered in patients with nonischemic heart disease who have an LVEF of less than or equal to 35% and who are in NYHA functional Class I. (Level of Evidence: C) 2. ICD therapy may be considered for patients with long-qt syndrome and risk factors for SCD. (Level of Evidence: B) (16,349Ο354) 3. ICD therapy may be considered in patients with syncope and advanced structural heart disease in whom thorough invasive and noninvasive investigations have failed to define a cause. (Level of Evidence: C) 4. ICD therapy may be considered in patients with a familial cardiomyopathy associated with sudden death. (Level of Evidence: C) 5. ICD therapy may be considered in patients with LV noncompaction. (Level of Evidence: C)
AHA/ACC/ESC 2008 GUIDELINES FOR DEVICE BASED THERAPY CLASS III 1. ICD therapy is not indicated for patients who do not have a reasonable expectation of survival with an acceptable functional status for at least 1 year, even if they meet ICD implantation criteria specified in the Class I, IIa, and IIb recommendations above. (Level of Evidence: C) 2. ICD therapy is not indicated for patients with incessant VT or VF. (Level of Evidence: C) 3. ICD therapy is not indicated in patients with significant psychiatric illnesses that may be aggravated by device implantation or that may preclude systematic follow-up. (Level of Evidence: C) 4. ICD therapy is not indicated for NYHA Class IV patients with drugrefractory congestive heart failure who are not candidates for cardiac transplantation or CRT-D. (Level of Evidence: C) 5. ICD therapy is not indicated for syncope of undetermined cause in a patient without inducible ventricular tachyarrhythmias and without structural heart disease. (Level of Evidence: C) 6. ICD therapy is not indicated when VF or VT is amenable to surgical or catheter ablation (e.g., atrial arrhythmias associated with the Wolff- Parkinson-White syndrome, RV or LV outflow tract VT, idiopathic VT, or fascicular VT in the absence of structural heart disease). (Level of Evidence: C) 7. ICD therapy is not indicated for patients with ventricular tachyarrhythmias due to a completely reversible disorder in the absence of structural heart disease (e.g., electrolyte imbalance, drugs, or trauma). (Level of Evidence: B) (16)
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