ΕΚΤΙΜΗΣΗ ΚΑΡΔΙΑΓΓΕΙΑΚΟΥ ΚΙΝΔΥΝΟΥ-ΔΥΣΛΙΠΙΔΑΙΜΙΕΣ

Παρουσίαση με θέμα: "ΕΚΤΙΜΗΣΗ ΚΑΡΔΙΑΓΓΕΙΑΚΟΥ ΚΙΝΔΥΝΟΥ-ΔΥΣΛΙΠΙΔΑΙΜΙΕΣ"— Μεταγράφημα παρουσίασης:

1 ΕΚΤΙΜΗΣΗ ΚΑΡΔΙΑΓΓΕΙΑΚΟΥ ΚΙΝΔΥΝΟΥ-ΔΥΣΛΙΠΙΔΑΙΜΙΕΣ
Ευάγγελος Λυμπερόπουλος Λέκτορας Παθολογίας Ιατρικής Σχολής Παν/μίου Ιωαννίνων

2 ΠΑΡΑΓΟΝΤΕΣ ΚΙΝΔΥΝΟΥ: Ι. Εισαγωγή
ΙΙ. Συζήτηση επιμέρους παραγόντων κινδύνου ΙΙΙ. Υπολογισμός του κινδύνου

3 ΠΑΡΑΓΟΝΤΕΣ ΚΙΝΔΥΝΟΥ: Ι. Εισαγωγή
ΙΙ. Συζήτηση επιμέρους παραγόντων κινδύνου ΙΙΙ. Υπολογισμός του κινδύνου

4 Cardiovascular Disease is the Leading Cause of Death Worldwide1
HIV/AIDS 5 Pulmonary disease 7 Injuries 9 Cancer 13 Infectious and parasitic diseases 19 Cardiovascular disease* 29 5 10 15 20 25 30 Percentage of total deaths in 2002 *Ischemic heart disease, cerebrovascular disease, hypertensive heart disease, inflammatory heart disease and rheumatic heart disease 1. The World Health Report WHO Geneva, 2004. Available at: Accessed January 2006.

5 Επίπτωση της στεφανιαίας νόσου στην Ελλάδα (1981-2004)
Μεταβολή (%): Α: 74% Γ: 214%

6 Development of Atherosclerotic Plaques
Fatty streak Normal Lipid-rich plaque Foam cells Fibrous cap During the initiation of atherosclerosis, LDL cholesterol accumulates in the subendothelial extracellular space within the arterial wall. Local vascular cells mildly oxidize LDL to a form known as minimally modified LDL, which is able to stimulate recruitment of monocytes and eventual deposition of macrophages.1 These further oxidize LDL to a form that can be scavenged and internalized, resulting in so-called foam cells.1 Such cells form the earliest visible lesion of atherosclerosis, the fatty streak.2 The aggregation of LDL-rich foam cells, derived from macrophages and T lymphocytes within the intima, progresses to development of an atherosclerotic plaque.2 This results from the death and rupture of the lipid-laden foam cells in the fatty streak. A crucial component of the maturing atherosclerotic plaque is the formation of a fibrous cap that separates the highly thrombogenic lipid-rich core from circulating platelets and other coagulation factors.3 Stable atherosclerotic plaques are characterized by the necrotic lipid core covered by a thicker, almost protective vascular smooth muscle cell-rich fibrous cap.3 Such a cap can be better strengthened and maintained by reducing LDL cholesterol.3 References Diaz MN, Frei B, Vita JA, Keaney JF. Antioxidants and atherosclerotic heart disease. New Engl J Med. 1997;337(6): Ross R. The pathogenesis of atherosclerosis: A perspective for the 1990s. Nature. 1993;362: Weissberg PL. Atherosclerosis involves more than just lipids: Plaque dynamics. Eur Heart J. 1999;1(suppl T):T13-T18. Lipid core Thrombus

7 Clinical Manifestations of Atherothrombosis
Cerebral Ischemic stroke Transient ischemic attack Cardiac Myocardial infarction Angina pectoris (stable, unstable) Peripheral Arterial Disease Critical limb ischemia, claudication Vascular disease is the result of a generalized process that may affect any of several vascular beds involving the cerebral, coronary, and peripheral arteries1. Cerebrovascular disease in cerebral arteries may precipitate a transient ischemic attack (TIA) or an ischemic stroke. A TIA, by definition, lasts for fewer than 24 hours. The majority clear within 1 hour. A TIA may be a warning of an impending stroke, with the risk for a stroke being 4% to 8% during the first month following a TIA and 24% to 29% during the next 5 years.1 Coronary vascular disease produces a spectrum of ischemic coronary syndromes that include stable angina, unstable angina, non–ST-segment elevation myocardial infarction (NSTEMI; also known as non–Q-wave MI), and ST-segment elevation (STEMI; also known as Q-wave MI).2 Peripheral arterial disease (PAD) produces a variety of symptoms ranging from intermittent claudication to pain at rest.3 Patients with the most serious form of PAD develop a critical limb ischemia that produces pain at rest and threatens the viability of the limb by increasing the risk for gangrene and necrosis.3 PAD is a strong marker for cardiovascular disease. References 1 Feinberg WM, Albers GW, Barnett HJ, et al. Guidelines for the management of transient ischemic attacks. Circulation. 1994;89: 2 American Heart Association. Heart Disease and Stroke Statistics–2003 Update. Available at: 3 Weitz JI, Byrne J, Clagett GP, et al. Diagnosis and treatment of chronic arterial insufficiency of the lower extremities: a critical review. Circulation. 1996;94:

8 Risk Factors for CHD Modifiable Nonmodifiable Dyslipidemia Smoking
Raised LDL Low HDL Raised TGs Smoking Hypertension Diabetes mellitus and IGT-MetSyn Obesity Dietary factors Thrombogenic factors Sedentary lifestyle Psychosocial factors Nonmodifiable Age Sex Family history of premature CHD Personal history of atherosclerosis Ethnic origin Outlined here are some of the modifiable risk factors that predispose an individual to the development or progression of CHD. Evidence has shown that lifestyles associated with a “Western culture,” such as a diet rich in saturated fats and high in calories, smoking, and physical inactivity, are some of the modifiable risk factors leading to an increase in the prevalence of CHD.1 Smoking is responsible for 50% of all avoidable deaths, half of which are due to CVD. Dyslipidemia—in particular, raised low-density lipoprotein (LDL) cholesterol and triglyceride (TG) levels, and low high-density lipoprotein (HDL) cholesterol—is associated with increased risk of CHD. However, raised LDL cholesterol has been shown to be most strongly associated with the development of atherosclerosis and the risk of CHD.1 Physicians must also be aware of the nonmodifiable risk factors for CHD such as age, sex, and family history. An in-depth family history of CHD and other atherosclerotic diseases should be an integral part of risk assessment. CHD risk is greater in males, in the elderly, and in individuals with a closely related family member with CHD. Also, the impact of any risk factor is intensified with increasing age.1 Reference Wood D, DeBacker G, Faergeman O, et al. Prevention of coronary heart disease in clinical practice: Recommendations of the Second Joint Task Force of European and Other Societies on Coronary Prevention. Atherosclerosis. 1998;140: Wood D, et al. Atherosclerosis. 1998;140:

9 Multiple Risk Factors: Additive Risk
The total severity of multiple low-level risk factors often exceeds that of a single severely elevated risk factor. Mean Absolute Risk (%) 27% 19% 13% 8% Multiple risk factors: additive risk Multiple relatively mild risk factors can greatly increase the risk of developing CHD. This slide is useful in supporting both the concept of the metabolic syndrome and the concept of global risk. Reference: Grundy SM, Pasternak R, Greenland P, Smith S Jr, Fuster V. AHA/ACC scientific statement: Assessment of cardiovascular risk by use of multiple-risk-factor assessment equations: a statement for healthcare professionals from the American Heart Association and the American College of Cardiology. J Am Coll Cardiol 1999;34: BP 165/95 mm Hg BP 165/95 mm Hg Age 56 years BP 165/95 mm Hg Age 56 years LDL-C 155 mg/dL BP 165/95 mm Hg Age 56 years LDL-C 155 mg/dL Smoker Grundy SM et al. J Am Coll Cardiol 1999;34:

10 ΔΕΥΤΕΡΟΓΕΝΗΣ ΠΡΟΛΗΨΗ

11 ΠΡΩΤΟΓΕΝΗΣ ΠΡΟΛΗΨΗ

12 ΠΑΡΑΓΟΝΤΕΣ ΚΙΝΔΥΝΟΥ: Ι. Εισαγωγή
ΙΙ. Συζήτηση επιμέρους παραγόντων κινδύνου ΙΙΙ. Υπολογισμός του κινδύνου

13 CAD Prevalence by Age and Gender in the US
Age and gender have historically been linked to CAD incidence. In this slide, CAD prevalence is examined in the US for At age 55 and older, a significant increase in CAD prevalence is observed in both men and women. At age 75+, CAD prevalence by population percentage is 18.6% for men and 16.1% for women. In addition to the steady increase in CAD risk with advancing age, this slide illustrates the significantly greater risk associated with male gender from the time, in the mid-forties, when the age-associated increase in risk becomes clinically significant. It can be seen as well that this gap narrows in the oldest, highest-risk age group. American Heart Association. Heart Disease and Stroke Statistics – 2004 Update. Dallas, Tex: American Heart Association; 2003.

14 Οικογενειακό ιστορικό
Am Heart J 1990;120:963-9

15 Ατομικό αναμνηστικό Αθηρωμάτωση καρωτίδων, αορτής, περιφερική αρτηριοπάθεια και ιστορικό αγγειακού εγκεφαλικού συχνά συνυπάρχουν με ΣΝ και προβλέπουν μελλοντικά στεφανιαία επεισόδια Προκλινική αθηρωμάτωση (IVUS, MRI ή CT) όπως πάχυνση ΙΜ, Ca στα στεφανιαία ή την αορτή, σχετίζονται με αυξημένο κίνδυνο ΕΜ ή θάνατο Εικόνα με EBCT

16 ROLE OF LDL IN CAUSING ATHEROSCLEROSIS
Monocyte LDL Adhesion Molecule MCP-1 LDL Cytokines Oxidised LDL Foam Cell Macrophage

17 Epidemiologic data have long demonstrated a strong causal link between elevated cholesterol and CHD. The Multiple Risk Factor Intervention Trial (MRFIT) examined the relationship between cholesterol levels and CHD mortality in 361,662 men at high risk for coronary artery disease. As shown in the graph on the left, MRFIT showed a positive association between total cholesterol (TC) level and the 6-year CHD death rate.1,2 The graph on the right shows the rate of new cases of CHD in men in the Framingham study. From the sixth year of follow-up there was a strong positive correlation between TC and incidence of CHD.2 References: 1. Martin MJ, Hulley SB, Browner WS, et al. Serum cholesterol, blood pressure, and mortality: implications from a cohort of men. Lancet. 1986;2: 2. Castelli WP. Epidemiology of coronary heart disease: the Framingham study. Am J Med. 1984;76:4-12. 17

18 Effect of Lowering LDL-C on CHD Events
PROVE-IT P40 POSCH-PL 4S-PL Primary prevention trials 25 Secondary prevention trials POSCH-Rx 20 CARE-PL 4S-Rx PROVE-IT A80 15 LIPID-PL % Pateints with CHD Event CARE-Rx HPS-PL 10 LIPID-Rx WOSCOPS-PL WOSCOPS-Rx HPS-Rx LRC-PL Populations with low cholesterol levels (150 mg/dL) and low LDL-C levels (70 mg/dL) have a low incidence of coronary artery disease. Epidemiological studies show that lowering plasma cholesterol levels results in a progressive decrease in cardiovascular events.1-4 Combined data from the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) and West of Scotland Coronary Prevention Study (WOSCOPS) trials suggest that reducing cholesterol levels from 285 mg/dL to 190 mg/dL decreases the incidence of CHD events from 170/1,000 patients in 10 years to 70/1,000 patients in 10 years.3,4 Physicians today are under increasing pressure to attain LDL-C goals below 100 mg/dL,5 and these targets could be reduced still further in the light of findings from ongoing clinical trials. Statins can achieve LDL-C reductions of up to 50–60% when used in high doses,6 however, statins in monotherapy are unable to reduce LDL-C levels beyond this level, leaving many hypercholesterolaemic patients at significant risk of coronary events. Strategies that combine lipid modifying agents with complementary mechanisms of action may further enhance the benefits of statin therapy.7 References 1. Castelli WP. Epidemiology of coronary heart disease: the Framingham study. Am J Med 1984; 76: 4–12. 2. Sacks FM, Pfeffer MA, Moye LA et al., for the Cholesterol and Recurrent Events Trial Investigators. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med 1996; 335: 1001–9. 3. Shepherd J, Cobbe SM, Ford I et al., for the West of Scotland Coronary Prevention Study Group. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med 1995; 333: 1301–7. 4. Downs JR, Clearfield M, Weis S et al., for the AFCAPS/TexCAPS Research Group. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TexCAPS. JAMA 1998; 279: 1615–22. 5. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001; 285: 2486–97. 6. Grundy SM. Statin trials and goals of cholesterol-lowering therapy. Circulation 1998; 97: 1436–9. 7. Izzat NN, Deshazer ME, Loose-Mitchell DS. New molecular targets for cholesterol-lowering therapy. J Pharmacol Exp Ther 2000; 293: 315–20. 5 ASCOT-PL LRC-Rx ASCOT-Rx AFCAPS-PL AFCAPS-Rx 40 50 70 90 110 130 150 170 190 210 (mg/dl) (mmol/l) LDL cholesterol 18

19 PROCAM Study CHD risk according to LDL-C and TG increased TG confers raised CHD risk at all levels of LDL-C Figure 51 The PROCAM study also showed that increased TG levels confer increased risk at all levels of LDL-cholesterol.

20 Size and apolipoprotein composition are the main factors determining atherogenicity of triglyceride-rich particles Figure 45 Atherogenicity of TG-rich particles is a function of size and apolipoprotein content. Chylomicrons and large VLDL are too large to penetrate the intima, while small VLDL and LDL can penetrate the intima and are therefore atherogenic.

21 INITIATION OF ATHEROSCLEROSIS BY REMNANTS
Monocyte Vessel Lumen Remnant Adhesion Molecule Endothelium MCP-1 Remnant Cytokines Modified remnant Intima Foam Cell Macrophage

22 HDL-C Levels in the Context of Global Risk Factors for CAD: PROCAM
It is evident that low levels of HDL-C are associated with increased risk for CAD and that reductions in risk for CAD are accompanied by increases in levels of HDL-C. HDL-C level as a risk marker for CAD is commonly accepted and clinically useful. Whether this relationship is causal is not too clear. In part, the interweaving of lipid risk factors makes it difficult to isolate any one element beyond that of LDL-C (and even that is being compartmentalized into numerous risk subdivisions). In addition, all of the lipid risk factors are responsive to additional elements of global CAD risk. In this slide, which presents the estimated risk for coronary events in men aged 35 to 65 years in the Prospective Cardiovascular Münster Heart (PROCAM) study by baseline HDL-C, there is a clear, graded, inverse relationship between low levels of circulating HDL-C and the risk for CAD. However, the strength of this relationship is evidently responsive to a complex of other risk factors. Thus, if the population of middle-aged men in PROCAM is stratified into deciles of risk according to the PROCAM algorithm, men in the lowest decile are at low risk for a coronary event, even at lower levels of HDL-C. Among men in the highest decile of risk, however, those with HDL-C of 25 mg/dL had a risk for coronary events more than twice that of men with an HDL-C of 55 mg/dL. International Task Force for Prevention of Coronary Heart Disease. PROCAM (Prospective Cardiovascular Münster Heart Study): HDL cholesterol and myocardial infarction [slide kit]. Available at: Accessed November 15, 2004.

23 INHIBITION OF ATHEROSCLEROSIS BY HDL
Monocyte LDL/remnant Adhesion Molecule MCP-1 LDL/remnant Cytokines Oxidised LDL/remnant Foam Cell Macrophage HDL PROMOTE CHOLESTEROL EFFLUX

24 INHIBITION OF ATHEROSCLEROSIS BY HDL
Monocyte LDL/remnant Adhesion Molecule MCP-1 LDL/remnant HDL INHIBIT OXIDATION OF LDL Cytokines Oxidised LDL/remnant Foam Cell Macrophage HDL PROMOTE CHOLESTEROL EFFLUX

25 INHIBITION OF ATHEROSCLEROSIS BY HDL
Monocyte HDL INHIBIT ADHESION MOLECULE EXPRESSION LDL/remnant Adhesion Molecule MCP-1 LDL/remnant HDL INHIBIT OXIDATION OF LDL Cytokines Oxidised LDL/remnant Foam Cell Macrophage HDL PROMOTE CHOLESTEROL EFFLUX

26

27 LDL-C/HDL-C Ratio as Risk Indicator for Total and CAD Mortality: PROCAM
This slide presents age-standardized total and CAD death rates, segregated for smokers and nonsmokers, for all male subjects aged 35 to 65 years in PROCAM according to LDL-C/HDL-C ratio.1 It is evident that the higher levels of HDL-C shown by lower LDL-C/HDL-C ratios exert a protective effect, even in the presence of another major risk factor such as smoking. 1. Cullen P, Schulte H, Assmann G. The Münster Heart Study (PROCAM): Total mortality in middle-aged men is increased at low total and LDL cholesterol concentrations in smokers but not in nonsmokers. Circulation. 1997;96:

28 Emerging Risk Marker: Lp (a)
This prospective population study was designed to assess the role of elevated Lp (a) as a coronary risk factor. Serum Lp (a) levels were evaluated in 788 male participants aged 35 to 65 years in the Münster Heart Study (PROCAM) who were followed up for 10 years. Incidence of coronary events per 1000 per 10 years was evaluated. In men with high coronary risk, it was determined that Lp (a) levels >20 mg/dL were associated with increased coronary event incidence in comparison with levels <20 mg/dL. von Eckardstein A, Schulte H, Cullen P, Assmann G. Lipoprotein(a) further increases the risk of coronary events in men with high global cardiovascular risk. J Am Coll Cardiol. 2001;37:

29 Επιπολασμός της Υπέρτασης σε σχέση με την Ηλικία και το Φύλο
Επιπολασμός της Υπέρτασης (%) This slide shows the results of an analysis of worldwide data (from published literature dated 1980 to 2002) on the prevalence of hypertension (age- and gender-specific).1 Hypertension was defined as systolic BP ≥140 mmHg, or diastolic BP ≥ 90 mmHg or the use of antihypertensive medication. Only data for the established market economies (i.e. US, Canada, Spain, England, Germany, Greece, Italy, Sweden, Australia, Japan) are given on this slide. Other data (not shown) are available for former socialist economies (Slovakia), India, Latin America and the Caribbean, Middle East, Asia, and sub-Saharan Africa. As illustrated, the prevalence of hypertension increases with advancing age. At young ages, the prevalence was higher in males than in females; from age 60, however, the trend was reversed, with prevalence higher in women than in men. The reasons for gender differences in BP are not known, although it has been suggested (but not proven) that estrogen may be responsible for lower BP in younger women.2 References Kearney PM, et al. Global burden of hypertension: analysis of worldwide data. Lancet 2005;365:21723. August P, et al. Hypertension in women. J Clin Endocrinol Metab 1999;84:1862–6. 2029 3039 4049 5059 6069 70 Ηλικία (έτη) Data for established market economies (US, Canada, Spain, England, Germany, Greece, Italy, Sweden, Australia, Japan) Kearney et al. Lancet 2005;365:21723

30

31 Συστολική ΑΠ/Διαστολική BP (mmHg)
Κίνδυνος Καρδιαγγειακής Θνησιμότητας 8 8X 6 4 4X For individuals aged 4069 years, each increment in systolic BP of 20 mmHg or diastolic BP of 10 mmHg doubles the risk of cardiovascular disease (stroke, ischemic heart disease, other vascular diseases) across the entire BP range. Benefits are therefore to be gained from lowering BP in terms of reduced risk of cardiovascular mortality. Reference Lewington S, et al. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet 2002;360:1903–13. 2 2X 1X 115/75 135/85 155/95 175/105 Συστολική ΑΠ/Διαστολική BP (mmHg) *Άτομα ηλικίας 40–69 ετών Lewington et al. Lancet 2002;360:1903–13

32 2 mmHg μείωση της μέσης ΣΑΠ
Μετα-ανάλυση 61 προοπτικών μελετών παρατήρησης 1 εκατομμύριο ενήλικες 12.7 εκατομμύρια ανθρωπο-έτη 7% μείωση της θνητότητας από Ισχαιμική Καρδιοπάθεια 2 mmHg μείωση της μέσης ΣΑΠ Trials have shown that BP lowering can produce rapid reductions in cardiovascular disease risk. In fact, even a 2 mmHg decrease in systolic BP would result in approximately 7% lower mortality risk from ischemic heart disease and a 10% lower mortality risk from stroke. Reference Lewington S, et al. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet 2002;360:1903–13. 10% μείωση της θνητότητας από ΑΕΕ Lewington et al. Lancet 2002;360:1903–13

33 Αιτίες Θανάτου Διαβητικών
2/3 των διαβητικών πεθαίνουν από καρδιαγγειακή νόσο CHD, stroke, and peripheral vascular disease Other 67% Επιπλοκές μακροαγγειοπάθειας (στεφανιαία νόσος, ΑΕΕ, και περιφερική αγγειακή νόσος, αποτελούν την κύρια αιτία νοσηρότητας και θνητότητας. Adapted from Alexander CM, Antonello S Pract Diabet 2002;21:21-28.

34 Framingham Study: Diabetes Mellitus and CHD Mortality
18 Annual CHD Deaths per Persons 16 17 17 17 17 DM Non-DM 14 12 10 8 8 8 6 Framingham Study: DM and CHD Mortality: 20-Year Follow-up In this 20-year follow-up from the Framingham Heart Study, coronary heart disease (CHD) death is increased twofold in diabetic men relative to nondiabetic men. Among women, there is an even greater excess in CHD death, fourfold higher in diabetic women compared with nondiabetic women, which may in part be due to more adverse cardiovascular risk factors, particularly low high-density lipoprotein (HDL) cholesterol, in diabetic women. In addition, this slide shows that the absolute CHD death rate in diabetic women is the same as in diabetic men, suggesting that diabetes leads to the abolishment of the female protection against CHD. However, most studies show a diminution but not complete abolishment of the sex difference between diabetic women and diabetic men. Reference: Kannel WB, McGee DL. Diabetes and cardiovascular disease: the Framingham study. JAMA 1979;241: 4 4 4 2 Men Women Kannel WB, McGee DL. JAMA 1979;241:

35 NCEP ATP III Guidelines
ΣΑΚΧΑΡΩΔΗΣ ΔΙΑΒΗΤΗΣ ΣΤΕΦΑΝΙΑΙΑ ΝΟΣΟΣ NCEP ATP III Guidelines

36 Smoking Cigarette smoking is a well-established risk factor for CAD. The relationship between smoking and CAD risk is dose-dependent. Smoking cessation is associated with CAD risk reduction, and the reduction in risk begins within months after a smoker quits. Coronary plaque development is facilitated by smoking. Smoking prevention and smoking cessation should be emphasized in clinical strategies for CAD reduction. Smoking has an important part in the risk-assessment component of the NCEP ATP III guidelines because of both the magnitude of the CAD risk associated with it and the substantial benefit to be derived from smoking cessation. In addition, smokers can benefit at least as much as nonsmokers from LDL-C–lowering therapy. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002;106:

37 PROCAM (Münster Heart Study): Age Standardized Death Rates in Men According to Cigarette Smoking
Deaths per 1,000 10,856 men aged years; Number of deaths: total: 473; coronary deaths: 138; cancer: 195

38 INTERHEART STUDY: Smoking and the risk of MI
Lancet 2004; 364:

39 ΚΡΙΤΗΡΙΑ ΓΙΑ ΤΗ ΔΙΑΓΝΩΣΗ ΤΟΥ ΜΕΤΑΒΟΛΙΚΟΥ ΣΥΝΔΡΟΜΟΥ (3≥5)
Κοιλιακή παχυσαρκία Περίμετρος μέσης (cm) Άνδρες >102 Γυναίκες >88 Τριγλυκερίδια ≥150 mg/dL HDL χοληστερόλη Άνδρες <40 mg/dL Γυναίκες <50 mg/dL Αρτηριακή πίεση ≥130/85 mm Hg Γλυκόζη ορού ≥100 mg/dL

40 Prevalence of the metabolic syndrome among
8,348 Greek adults aged >18 years, by age and gender. WATCH METS

41 Metabolic Syndrome Increases Risk for CHD and Type 2 Diabetes
High LDL-C Metabolic Syndrome Type 2 Diabetes Metabolic syndrome increases risk for CHD and type 2 diabetes The National Cholesterol Education Program (NCEP) has traditionally focused on high low-density lipoprotein cholesterol (LDL-C) as a risk factor for coronary heart disease (CHD). In the NCEP Adult Treatment Panel III (ATP III) recommendations published in JAMA in 2001, the NCEP suggested that the metabolic syndrome might independently predict the development of both type 2 diabetes and CHD. Reference: Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001;285: Coronary Heart Disease Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA 2001;285:

42 C-reactive protein (CRP)
CRP is a marker of inflammation CRP levels predict vascular risk

43 hsCRP predicts risk of MI and stroke in apparently healthy men
3.5 2.0 * *** 3.0 1.5 2.5 Relative risk of MI Relative risk of ischaemic stroke 2.0 1.0 1.5 1.0 0.5 0.5 In the epidemiological Physicians’ Health Study in 543 healthy middle-aged men, the relative risk of future MI increased significantly (p<0.001) with increasing levels of CRP. Increasing levels of CRP were also associated with significantly increased risk (p=0.02) of future thromboembolic stroke. Reference Ridker PM et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997; 336: 973–979. Abbreviations CRP=C-reactive protein; MI=myocardial infarction 1 2 3 4 1 2 3 4 Quartile of CRP Quartile of CRP CRP=C-reactive protein; MI=myocardial infarction *p=0.02 versus quartile 1; ***p<0.001 versus quartile 1 Ridker PM et al. N Engl J Med 1997; 336: 973–979

44 Risk ratio as function of renal clearance and treatment
2.0 1.8 1.6 1.4 Risk Ratio 1.2 1.0 0.8 0.6 0.4 0.2 20 40 60 80 100 120 140 Renal Clearance [ml/min]

45 Mortality from All Causes According to Quintile of Measures of Renal Function
Figure 1. Mortality from All Causes According to Quintile of Measures of Renal Function. For cystatin C, creatinine, and estimated glomerular filtration rate (GFR), the fifth quintile was subdivided into three roughly equal groups, labeled 5a, 5b, and 5c. Shlipak, M. G. et al. N Engl J Med 2005;352:

46 INTERHEART STUDY 90-94% of the population attritutable risk for a MI worldwide Lancet 2004; 364:

47 ΠΑΡΑΓΟΝΤΕΣ ΚΙΝΔΥΝΟΥ: Ι. Εισαγωγή
ΙΙ. Συζήτηση επιμέρους παραγόντων κινδύνου ΙΙΙ. Υπολογισμός του κινδύνου

48 ΑΤΟΜΑ ΠΟΛΥ ΥΨΗΛΟΥ ΚΙΝΔΥΝΟΥ:
Στεφανιαία νόσος (ΣΝ) Καταστάσεις ισοδύναμου κινδύνου με τη ΣΝ ΑΤΟΜΑ ΥΨΗΛΟΥ ΚΙΝΔΥΝΟΥ:  2 ΠΑΡΑΓΟΝΤΕΣ ΚΙΝΔΥΝΟΥ ΑΤΟΜΑ ΧΑΜΗΛΟΥ ΚΙΝΔΥΝΟΥ 0-1 ΠΑΡΑΓΟΝΤΕΣ ΚΙΝΔΥΝΟΥ

49 ΚΑΤΑΣΤΑΣΕΙΣ ΙΣΟΔΥΝΑΜΟΥ ΚΙΝΔΥΝΟΥ
ΜΕ ΤΗ ΣΤΕΦΑΝΙΑΙΑ ΝΟΣΟ Σακχαρώδης διαβήτης Άλλη αγγειακή νόσος: Αθηρωματική νόσος των καρωτίδων Περιφερική αγγειοπάθεια Ανεύρυσμα κοιλιακής αορτής

50 ΑΤΟΜΑ ΠΟΛΥ ΥΨΗΛΟΥ ΚΙΝΔΥΝΟΥ:
Στεφανιαία νόσος (ΣΝ) Καταστάσεις ισοδύναμου κινδύνου με τη ΣΝ ΑΤΟΜΑ ΥΨΗΛΟΥ ΚΙΝΔΥΝΟΥ:  2 ΠΑΡΑΓΟΝΤΕΣ ΚΙΝΔΥΝΟΥ ΑΤΟΜΑ ΧΑΜΗΛΟΥ ΚΙΝΔΥΝΟΥ 0-1 ΠΑΡΑΓΟΝΤΕΣ ΚΙΝΔΥΝΟΥ

51 ΠΟΥ ΤΡΟΠΟΠΟΙΟΥΝ ΤΟ ΣΤΟΧΟ ΤΗΣ ΥΠΟΛΙΠΙΔΑΙΜΙΚΗΣ ΑΓΩΓΗΣ
ΠΑΡΑΓΟΝΤΕΣ ΚΙΝΔΥΝΟΥ ΠΟΥ ΤΡΟΠΟΠΟΙΟΥΝ ΤΟ ΣΤΟΧΟ ΤΗΣ ΥΠΟΛΙΠΙΔΑΙΜΙΚΗΣ ΑΓΩΓΗΣ ΚΑΠΝΙΣΜΑ ΥΠΕΡΤΑΣΗ (ΑΠ>140/90mmHg ή χορήγηση αντιυπερτασικών φαρμάκων) HDL CHOL<40mg/dl ΗΛΙΚΙΑ (άνδρες >45 έτη /γυναίκες>55 έτη) ΘΕΤΙΚΟ ΟΙΚΟΓΕΝΕΙΑΚΟ ΙΣΤΟΡΙΚΟ (μείζον αγγειακό σύμβαμα σε 1ου βαθμού συγγενή ηλικίας <55/65 ετών για άνδρες και γυναίκες)

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53 Figure 2. The new European Risk Chart based on SCORE data. For low CVD risk regions based on total cholesterol. Conroy et al, Eur Heart J, 2003, 24: The low risk chart should be used in Belgium, France, Greece, Italy, Luxembourg, Spain, Switzerland and Portugal; the high risk chart should be used in all other countries of Europe

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