ΠΡΟΣΕΧΩ ΤΗΝ ΚΑΡΔΙΑ ΜΟΥ. ΠΟΣΟ ΕΥΚΟΛΟ ΕΙΝΑΙ; Δημήτριος Ρίχτερ, MD, FESC, FAHA - Διευθυντής Καρδιολογικής Κλινικής Ευρωκλινικής Αθηνών - Μέλος ΔΣ ΕΛΙΚΑΡ Γενικός Γραμματέας Ελληνικής Εταιρείας Λιπιδιολογίας Αντιπρόεδρος Κολεγίου Μεταβολικών Νόσων Γενικός Γραμματέας Ινστιτούτου Θρόμβωσης Κύριοι πρόεδροι, αγαπητοί συνάδελφοι, θα ήθελα να ευχαριστήσω την Καρδιολογική Εταιρεία και την Ομάδα Πρόληψης για την τιμητική τους πρόσκληση στο βήμα αυτό όπου θα συζητήσουμε για τη δευτερογενή πρόληψη της ισχαιμικής καρδιοπάθειας.

Introduction 1948 Beginning of epidemiology approximately 25 years after CAD reached the awareness of US Physicians in 1923 CAD was considered not preventable Opinions on the need to treat asymptomatic abnormalities (hypertension-cholesterol) differed

Human organism can tolerate high amount of lipids in his diet. Humans can receive all the energy requested daily exclusively through lipid ingestion. During the last years various studies correlate fat with atherosclerosis. At the moment there is no clear scientific evidence of such correlation.

1950 Diseases of the Heart- Friedberg: ‘A relationship of tobacco to arteriosclerotic heart disease appears extremely unlikely’

INTER-HEART: Population-attributable risk of acute MI in the overall population Risk factor PAR adjusted for age, sex, smoking PAR adjusted for all (99% CI) ApoB/ApoA-1 (fifth quintile compared with first) 54.1 (49.6-58.6) 49.2 (43.8-54.5) Current smoking 36.4 (33.9-39.0) 35.7 (32.5-39.1) Diabetes 12.3 (11.2-13.5) 9.9 (8.5-11.5) Hypertension 23.4 (21.7-25.1) 17.9 (15.7-20.4) Abdominal obesity 33.7 (30.2-37.4) 20.1 (15.3-26.0) Psychosocial 28.8 (22.6-35.8) 32.5 (25.1-40.8) Vegetable and fruits daily 12.9 (10.0-16.6) 13.7 (9.9-18.6) Exercise 25.5 (20.1-31.8) 12.2 (5.5-25.1) Alcohol intake 13.9 (9.3-20.2) 6.7 (2.0-20.2) All combined 90.4 (88.1-92.4) PAR=population-attributable risk

Οι κυριότερες αιτίες θανάτου του Ελληνικού πληθυσμού 1988- 98. 1. Καρδιακές παθήσεις 2. Νεοπλάσματα 3. Αγγειακά εγκεφαλικά 4. Νόσοι αναπνευστικού συστήματος 5. Ατυχήματα 6. Νόσοι πεπτικού συστήματος 7. Νόσοι ουροποιητικού συστήματος 8. Άλλες νόσοι κυκλοφορικού συστ.. 9. Νόσοι Κεντρικού ΝΣ 10. Ενδοκρινοπάθειες Χειμώνας Η. et al. Καρδιά και Αγγεία 2003

CVD: 38600 θάνατοι/έτος ΣΝ: 19500 θάνατοι/έτος Στα φετινά στατιστικά στοιχεία που εξέδωσε η ΑΗΑ η Ελλάδα παρουσιάζει μια ενδιάμεση ως χαμηλή θέση όσον αφορά την καρδιαγγειακή θνησιμότητα μεταξύ των Δυτικών χωρών. Το ανθρώπινο κόστος της στεφανιαίας νόσου με βάση τα στοιχεία αυτά υπολογίζεται σε 19500 θανάτους ετησίως ενώ συνολικά περισσότεροι από 38000 θάνατοι ετησίως οφείλονται σε νοσήματα του καρδιαγγειακού συστήματος. Και στη χώρα μας οι αριθμοί αυτοί είναι μεγαλύτεροι από το άθροισμα των θανάτων που οφείλονται στις 6 επόμενες αιτίες θανάτου.

Εκρηκτική αύξηση του επιπολασμού της παχυσαρκίας στις αναπτυγμένες χώρες CMAJ 2004;171:240-2

Overweight (%) children 7-11 years 10 17 18 31 36 22 19 12 27 15 16 33 35 34 26 32 Overweight (%) children 7-11 years Equivalent to BMI>25 © IOTF 2004. IOTF-Cole et al definition of overweight 32

Lyon Diet Heart Study: Cumulative Survival without Cardiac Death and Nonfatal MI Experimental Canola oil– based margarine, fiber, low cholesterol, low saturated fat, fruits, vegetables Control % Without Event Lyon Diet Heart Study: cumulative survival without cardiac death and nonfatal MI In the Lyon Diet Heart Study, patients with previous myocardial infarction were randomized to either a Western-type diet or a Mediterranean-type diet that included high monounsaturated fat. Patients in the intervention group were instructed to consume fruit every day; more bread, fish, and root and green vegetables; and less meat (beef, lamb, and pork were to be replaced with poultry); butter and cream were replaced with margarine (supplied to patients) that was similar in composition to olive oil, and olive and canola oils were recommended for salads and food preparation. At extended follow-up of a mean of 46 months, significant reductions in composite endpoints that included combinations of cardiac death, nonfatal myocardial infarction, unstable angina, stroke, heart failure, pulmonary or peripheral embolism, and minor events requiring hospitalization were demonstrated in patients on the Mediterranean-type diet compared with patients on the Western-type diet. Presented here is the combined primary endpoint of recurrent nonfatal myocardial infarction or cardiac death, for which the risk ratio (based on time to first event) was 0.28 (95% confidence interval 0.15–0.53; p=0.0001). The group randomized to Mediterranean-type diet had 14 events compared with 44 in the group randomized to Western-type diet. References: de Lorgeril M, Renaud S, Mamelle N, et al. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet 1994;343:1454-1459. de Lorgeril M, Salen P, Martin J-L, Mamelle N, Monjaud I, Delaye J, Mamelle N. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation 1999;99:779-785. P = 0.0001 1 2 3 4 5 Year de Lorgeril M et al. Circulation 1999;99:779-785. 1999 Lippincott Williams & Wilkins. www.lww.com

Promoting the Mediterranean Diet in Greece

Twenty-five year follow-up data from the Seven Countries study1 shows that serum total cholesterol levels are linearly related to CHD mortality across cultures. The relative increase in CHD mortality rates with a given increase in cholesterol are similar. However, the large between country difference in CHD mortality rates at a given cholesterol level indicates that other factors, such as diet, also play a role in the development of CHD.The link between high cholesterol levels and increased incidence of CHD has also been shown in the prospective part of the Multiple Risk Intervention study.2 In epidemiological studies measurements of serum cholesterol have been routinely used. The relationship between cholesterol levels and the incidence of CHD is almost entirely dependent on low-density lipoprotein (LDL) cholesterol, the main carrier of cholesterol and a major atherogenic lipoprotein.3 Results from the Framingham study 4 during 26 years of observation show that men have twice the incidence of CHD mortality and morbidity compared with women. This difference tends to diminish during the later years, after the menopause. Other factors that influence susceptibility to CHD include ethnic background and social class. 5-7 References 1. Verschuren WM et al. J Am Med Assoc 1995;274(2):131–6. 2. Martin MJ et al. Lancet 1986;ii:933–6. 3. Kannel WB et al. In Proceeding of Golden Jubilee International Congress, Minnesota, 1980. Eds Loan MS, Holman RT. Oxford, Pergamon Press 1982:339–48. 4. Lerner DJ, Kannel WB. Am Heart J 1986;11(2):383–90. 5. Rosamond WD et al. N Engl J Med 1998;339:861–7. 6. Goff DC et al. Circulation 1997;95:1433–40. 7. Poulter N. In Cardiovascular Disease: Risk Factors and Intervention. Eds: Poulter N, Sever P, Thom S. Radcliffe Medical Press, Oxford, 1993.  

Akira Endo HO O Compactin H3C H CH3 The purpose of this presentation is to provide a broad overview of the efficacy and safety of rosuvastatin (CRESTOR), an HMG-CoA reductase inhibitor (statin) manufactured and marketed by AstraZeneca.

Effects of lipid-lowering therapy on CHD events in statin trials Secondary 25 4S - P Prevention Primary 20 Prevention 4S - S Simvastatin LIPID - P Patients with CHD event (%) 15 CARE - P Pravastatin HPS - P Lovastatin 10 LIPID - S WOSCOPS - P Atorvastatin CARE - S The introduction of statins has had a dramatic impact on the treatment of atherosclerosis and the prevention of cardiovascular events. Data from many placebo-controlled trials show a clear association between the degree of LDL-C reduction and the degree of clinical benefit.1 By lowering lipid levels and reducing the risk of CHD, statins are among the most effective agents to reduce morbidity and mortality available to clinical practice. Kastelein JJP. The future of best practice. Atherosclerosis. 1999;143 (Suppl 1):S17-S21. WOSCOPS - S HPS - S ASCOT - P * S=statin treated 5 ASCOT - S * P=placebo treated AFCAPS - P AFCAPS - S *Extrapolated to 5 years 90 110 130 150 170 190 210 LDL-C (mg/dL) Modified from Kastelein JJP. Atherosclerosis. 1999;143(Suppl 1): S17-S21.