HYPERCHOLESTEROLEMIE ET PREVENTION PRIMAIRE

Présentation au sujet: "HYPERCHOLESTEROLEMIE ET PREVENTION PRIMAIRE"— Transcription de la présentation:

1 HYPERCHOLESTEROLEMIE ET PREVENTION PRIMAIRE
Dr GERARDY CHC Waremme NS 1089/03-09

2 PREVENTION PRIMAIRE TRAITER UNE POPULATION ASYMPTOMATIQUE SUR LA BASE DUN CHOLESTEROL ELEVE POUR DIMINUER LE RISQUE DE PREMIER ACCIDENT VASCULAIRE, CEREBRAL OU CORONARIEN

3 Athérothrombose, première cause de mortalité
Atherothrombosis is the underlying condition that results in events leading to myocardial infarction, ischemic stroke, and vascular death. As such, the leading cause of death of the estimated 55,694,000 people worldwide who died in 2000 was atherothrombosis, manifested as cardiovascular disease, ischemic heart disease and stroke (52% of deaths). Other main causes of death were: AIDS (5%) violent death (12%) pulmonary disease (14%) infectious diseases (19%) cancer (24%).1 Mortality (%) The World Health Report, 2000, WHO Geneva, 2000. Reference: 1. The World Health Report 2001, WHO Geneva, 2001.

4 ATHEROSCLEROSE L’athérosclérose sous-jacente:
Un processus silencieux qui évolue sur des dizaines d’années Souvent très avancée lorsque les premiers symptômes apparaissent Cellules spumeuses ‘Strie lipidique’ Lésion intermédiaire Plaque fibreuse Lésion complexe/rupture Athérome Maladie coronarienne Maladies cérébrovasculaires Maladie vasculaire périphérique Atherosclerosis is the main cause of CVD. However, because it is a progressive condition, it may remain asymptomatic for many years before actually presenting as disease By this time it is too late to take preventative action CHD = coronary heart disease CVD = cardiovascular disease Asymptomatique Avec ou sans symptômes Symptomatique Croissance principalement par accumulation de graisse Muscle lisse et collagène Thrombose, hématome A partir de la première décennie A partir de la troisième décennie A partir de la quatrième décennie 4

5 Une approche préventive des maladies CV est-elle importante en pratique clinique ?
INTERHEART : facteurs de risque influençables et risque d’IM1 patients et témoins dans 52 pays Facteurs en rapport avec le mode de vie Atherosclerosis is well recognised as the pathological cause of the majority of CVD and progression of atherosclerosis is related to increased risk for future cardiovascular events.1 Multiple risk factors for the development of atherosclerosis and subsequent CVD, have been identified: dyslipidemia, family history of CVD, arterial hypertension lack of physical exercise, a diet low on fruits/vegetables, abdominal obesity, smoking, diabetes and stressful psychological factors, and more recently also a raised inflammatory status (hs-CRP).40 The relationship between a raised plasma cholesterol and atherosclerotic vascular disease fulfils all of the criteria for causality. The evidence that reducing plasma cholesterol reduces risk is equally unequivocal. The higher the risk, the greater the benefit2. Some of the risk factors have been incorporated in the Belgian SCORE tables (Fourth Joint European Societies Task Force) 2 which allow for estimates of the 10 year risk of fatal CVD. A Belgian SCORE of  5 % of CV death in 10 years is currently considered as a cut off point for more aggressive CV risk reduction through necessary life style changes and drug therapy. Patients with established CVD or a “CHD equivalent” (Type 2 diabetes or Type 1 diabetes with micro-albuminuria) and patients with very high levels of individual risk factors are automatically also considered being at high risk, warranting treatment. Of all the conventional modifiable risk factors in patients with CHD, dyslipidemia is the most prevalent (Fig. 1.2.a.). 9 facteurs de risque influençables sont responsables de 90% des premiers IM1 La prise en charge de chaque facteur de risque individuel a une influence sur le risque total La dyslipidémie est un des principaux facteurs de risque . 5

6 Quelles sont les priorités pour la prévention CV en pratique clinique ?
Patients avec maladie CV athérosclérotique Sujets asymptomatiques à haut risque CV: Plusieurs facteurs de risque, menant à un risque de décès CV à 10 ans ≥ 5% selon SCORE Diabète de type 2 et diabète de type 1 avec microalbuminurie Facteurs de risque individuels fortement augmentés, surtout si accompagnés d’une lésion d’organes Proches parents de personnes avec maladies CV athéroscléreuses prématurées ou risque CV fortement augmenté European Society of Cardiology, September 2007.

7 SCORE Belgique: Risque de décès CV à 10 ans
Femmes Hommes Non-fumeuses Fumeuses Age Non-fumeurs Fumeurs ≥170 ≥150 ≥130 <130 8 10 13 16 6 7 9 11 4 5 3 16 20 24 30 12 14 18 22 8 10 13 15 6 7 9 11 15 18 22 27 10 13 16 20 7 9 11 14 5 6 8 28 34 41 48 20 25 30 36 15 18 22 27 10 13 16 19 SCORE Belgique ©2003 ESC ≥68 a Risque de décès CV à 10 ans ≥170 ≥150 ≥130 <130 5 6 8 9 3 4 7 2 10 12 15 18 7 8 13 5 6 9 3 4 10 12 15 18 7 8 11 13 5 6 9 3 4 19 23 28 34 13 17 20 25 9 12 15 18 7 8 10 ≥10% ≥63 a 5-9% 2-4% ≥170 ≥150 ≥130 <130 3 4 5 2 1 6 7 9 11 4 5 8 3 2 6 8 10 12 4 5 7 3 2 12 15 19 23 9 11 13 17 6 8 4 5 7 <2% ≥58 a Pression systolique (mmHg) ≥170 ≥150 ≥130 <130 2 3 1 3 4 5 7 2 1 4 5 6 8 3 2 1 8 10 12 15 6 7 9 11 4 5 3 ≥53 a ≥170 ≥150 ≥130 <130 1 2 2 3 4 1 2 3 4 5 1 5 6 8 10 3 4 7 2 ≥48 a ≥170 ≥150 ≥130 <130 1 1 1 2 2 3 4 1 <45 a <175 ≥275 ≥225 ≥175 <175 ≥275 ≥225 ≥175 <175 ≥275 ≥225 ≥175 <175 ≥275 ≥225 ≥175 Cholestérol total (mg/dl) 1. European Journal of Cardiovascular Prevention and Rehabilitation 2007;4(Suppl.2):S1-S Journal of Hypertension 2007;25: 7

8 Une approche préventive des maladies CV est-elle importante en pratique clinique ?
EUROASPIRE III: patients en prévention primaire qui atteignent la valeur cible pour le LDL-C < 100 mg/dl1 Tous les patients: 27,8% Hommes: 31,4% Femmes: 36,6% In patients with a Belgian SCORE risk  5%, total cholesterol (TC) levels should be lowered below 175 mg/dL and low-density lipoprotein cholesterol (LDL-c) below 100 mg/dL, or even <80mg/dL (if feasible)3. The NCEP’s latest upgraded recommendations (2007) set the target level for LDL-c even lower, at <70mg/dL, in patients with a Framingham Risc Score of >20% (CV event) in 10 year.15 However according to EURASPIRE III in Belgium 6 out of 10 patients do not reach the target value of LDL-c < 100 mg/dL in primary prevention.5 In the CEPHEUS study in which Belgian centres have participated it was also observed that 4 out of 10 patients did not reach the target of LDL-c < 100 mg/dL in secondary prevention17 (Fig c.).Additionally, CEPHEUS showed that 7 out of 10 diabetics with CHD do not reach the target value of LDL-c  70 mg/dL.17 The results of EUROASPIRE III survey show that despite the existence and wide dissemination of clear, evidence-based guidelines, their integration into routine clinical care is still disappointing. Although implementation of clinical guidance is improving over time, there is still a large proportion of coronary patients who are not reaching the lifestyle, risk factor and therapeutic targets for CVD prevention. There is still considerable potential throughout Europe to raise standards of preventive care in order to reduce the risk of recurrent disease and death in patients with CHD. 1. Kotseva K, Wood D, De Backer G et al. Lancet 2009;373: 8

9 Effet comparatif des statines sur la baisse du LDL-C
LDL-C: LS mean change from baseline at week 6 10 20 40 80 Change from Baseline (%) Dose, mg (log scale) –60 –50 –40 –30 –20 –10 rosuvastatin atorvastatin simvastatin pravastatin X X X Presented: Poster / Oral at the 52nd Scientific Sessions of the American College of Cardiology (ACC), Chicago, March 28th to April 2nd 2003. Citation: J Am Coll Cardiol 2003 (suppl):315A-316A. Abstract 876-2 Am J Cardiol 2003 (In press) Background: The CURVES study1 was the first study to show the effects of various statins across their respective dose ranges, on LDL-C, HDL-C and TG. Study Design: Aim: Dose-comparison study to evaluate the safety and efficacy of Rosuvastatin (RSV) versus Atorvastatin (ATV), Pravastatin (PRA), and Simvastatin (SIM) in subjects with hypercholesterolemia Population: Numbers: 8350 subjects entered the dietary lead-in. At the end of a 6-week dietary lead-in, patients were randomised to either:- RSV10mg (n=158), 20mg (n=164), 40mg (n=158), 80mg (n=163) ATV10mg (n=158), 20mg (n=156), 40mg (n=160), 80mg (n=167) PRA10mg (n=162), 20mg (n=166), 40mg (n=164) SIM10mg (n=167), 20mg (n=164), 40mg (n=159), 80mg (n=165) Methodology: 6-week, open-label, dose-comparison study to evaluate the safety and efficacy of RSV (10-80mg) versus ATV (10-80mg), PRA (10-40mg), and SIM (10-80mg)in subjects with hypercholesterolemia. Key Results: (Rosuvastatin 80mg data are not shown as doses are unlicensed in the EU) RSV 10mg produced greater reductions in LDL-C than ATV 10mg, SIM 10-40mg and PRA 10-40mg. Conclusions: Across doses, RSV was more effective in lowering LDL-C than ATV, SIM, and PRA. RSV consistently raised high-density lipoprotein-cholesterol at all doses (Not shown here). References 1. Jones P, et al. Am J Cardiol 1998; 81: 582–587 X X *** ^ *** † *** ‡ Adapted from Jones et al., Am J Cardiol 2003; 92:

10 Le plus bas est-il le mieux? Relation entre LDL-C et évènements CV
Event rate % 30.00 4S - Pl 25.00 20.00 4S - Rx Primary Prevention Secondary Prevention LIPID - Pl 15.00 LIPID - Rx CARE - Pl PROSPER - Pl CARE - Rx This slide shows the relationship between LDL-C levels and CV event rate in a number of large statin clinical trials and demonstrates that the lower the level of LDL-C observed, the lower the CV event rate. This observation supports the NCEP recommendations to treat to a target LDL-C concentration. However, although substantial reductions in LDL-C were obtained with statins (by 23-37%) they do not entirely eliminate events, suggesting that lipid parameters besides LDL-C, such as HDL-C, triglyceride, lipoprotein (a), and LDL particle size and susceptibility to oxidation as well as other risk factors and pleiotropic effects of these drugs, influence CHD risk. The results from on-going trials should answer questions of whether further reductions in LDL-C will provide additional benefit.1 Reference 1. Adapted from Ballantyne CM. Am J Cardiol 1998;82:3Q-12Q. HPS - Pl 10.00 PROSPER - Rx HPS - Rx WOSCOPS - Pl ALLHAT - Pl ALLHAT - Rx 5.00 WOSCOPS - Rx AFCAPS / TexCAPS - Pl ASCOT - Rx AFCAPS / TexCAPS - Rx ASCOT - Pl 0.00 70(1.8) 90(2.3) 110(2.8) 130(3.4) 150(3.9) 170(4.4) 190(5.0) 210(5.4) LDL-C achieved mg/dL (mmol/L) Adapted from Ballantyne et al. Am J Cardiol 1998;82:3Q–12Q.

11 WOSCOPS (west of scotland coronary prevention study)

12 WOSCOPS Etude écossaise publiée dans le NEJM en Pravastatine versus placébo Hommes de 45 à 64 ans Cholestérol moyen 2.72 g/l Le risque CV absolu était élevé (14% atcd vasculaires, 44% de fumeurs, BMI élevé) Follow up de 5 ans

13 WOSCOPS Pour sauver 20 vies, il a fallu traiter 3302 pts en bonne santé pdt 5 ans Le risque de décès est passé de 1,8 à 1,2% soit une réduction du risque de 0.6% Si on traite 1000 sujets pendant 5 ans, on évite 24 IM, 8 revascularisations cardiaques, 9 morts (toutes causes)

14 WOSCOPS Nombre de patients à traiter pour éviter:
Un evnt coronarien : 44 Un evnt coronarien majeur : 40 Une mort coronaire : 296 Une mort (globale) : 112 Un AVC : 642

15 WOSCOPS

16 AFCAPS/TEXCAPS (air force/texas coronary atherosclerosis prevention study)

17 AFCAPS/TEXCAPS Etude publiée dans le JAMA en Lovastatine versus placébo chez 6600 pts Hommes et femmes (15%) de 43 à 73 ans CT 2.21 g/l, LDL-C 1.51 g/l, HDL bas

18 AFCAPS/TEXCAPS Baisse de 25% du LDL-C et hausse de 6% du HDL-C
Diminution de l’incidence du 1er evnt coronarien majeur (IM, AI, MS) Pas de différence sur la mortalité globale Pas d’effet protecteur de la Lovastatine si l’hs-CRP est normale mais haut effet protecteur si l’hs-CRP est accrue

19 AFCAPS/TEXCAPS Si on traite 1000 sujets pendant 5 ans, on évite 12 IM, 17 revascularisations cardiaques Nombre de patients à traiter pour éviter: Un evnt coronarien : 87 Un evnt coronarien majeur : 50 Une mort coronaire : 823

20 ETUDE ASCOT (anglo-scandinavian cardiac outcome trial)
Etude publiée dans le Lancet en 2003 – Atorvastatine 10 mg versus placébo patients hypertendus de 40 à 79 ans Prédominance d’hommes CT < 2.5 g/l Follow up de 3 ans

21 ETUDE ASCOT (anglo-scandinavian cardiac outcome trial)
Diminution de 36% des accidents coronaires et de 27 % des AVC Diminution non significative (13%) de la mortalité toutes causes

22 JUPITER L’objectif primaire était de savoir si le traitement à long-terme avec la Rosuvastatine 20 mg diminuait la survenue du 1er évènement CV majeur comparé au placébo Patients avec un LDL-C normal ou bas mais avec une hs-CRP accrue The primary objective was to evaluate the effect of rosuvastatin on the rate of occurrence of the combined endpoint of cardiovascular death, stroke, myocardial infarction, unstable angina or arterial revascularisation Secondary objectives are to evaluate the effects of rosuvastatin on: total mortality noncardiovascular mortality incidence of diabetes mellitus venous thromboembolic events bone fractures adverse events. Reference Ridker PM. Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein: rationale and design of the JUPITER trial. Circulation 2003; 108: 2292–2297. Abbreviations JUPITER=Justification for the Use of statins in Primary prevention: an Intervention Trial Evaluating Rosuvastatin Ridker PM. Circulation 2003; 108: 2292–2297

23 JUPITER: population et valeurs initiales1
hommes et femmes apparemment en bonne santé sans maladie coronarienne Hommes de ≥ 50 ans, femmes de ≥ 60 ans LDL-C < 130 mg/dl hs-CRP ≥ 2,0 mg/l CRESTOR® n = 8 901 Placebo n = 8 907 Âge (années) 66 Hommes (%) 61,5 62,1 IMC (kg/m²) 28,3 28,4 TAS : TAD (mmHg) 134/80 Fumeurs (%) 15,7 16,0 Antécédents familiaux de coronaropathie† (%) 11,2 11,8 Syndrome métabolique‡ (%) 41,0 41,8 Utilisation d’aspirine (%) 16,6 CT (mg/dl) 186 185 LDL-C (mg/dl) 108 HDL-C (mg/dl) 49 TG (mg/dl) 118 hs-CRP (mg/l) 4,2 4,3 Glucose (mg/dl) 94 HbA1c (%) 5,7 Patients in each group were similar at entry and had a median age of 66 years. The study population was diverse and included a large female population (38.2%) and a large proportion of black or hispanic individuals (25.2%). Patients had low to normal LDL-C at baseline (median 108 mg/dL). The treatment groups were well matched in terms of laboratory parameters at baseline. Reference Ridker P et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008; 359: Patients recruited into the JUPITER study would not usually be eligible for statin therapy according to current treatment guidelines. In order to be eligible for the study, men had to be  50 years of age and women had to be  60 years of age. As a result, all eligible study patients had age as a risk factor as defined by the NCEP ATP III treatment guidelines (NCEP ATP III definition: men  45, women  55 yrs)1. A substantial number of patients also had other cardiovascular risk factors including hypertension, low HDL-C, family history of premature CHD and smoking amongst others.2,3 Reference Grundy SM et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines. Circulation 2004; 110: Ridker P et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008; 359: Ridker PM et al. Baseline characteristics of participants in the JUPITER trial, a randomised placebo-controlled primary prevention trial of statin therapy among individuals with low low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein. Am J Cardiol 2007; 100: The mean LDL-C of participants enrolled in JUPITER (104 mg/dL) is substantially lower than in the two previous trials in patients without established coronary heart disease (192 mg/dL in WOSCOPS, 150 mg/dL in AFCAPS/TexCAPS). Moreover, the JUPITER trial included 6801 women compared with no women in WOSCOPS and 997 women in AFCAPS/TexCAPS. Data from the JUPITER study therefore provides unique data on lipid lowering in the absence of hyperlipidaemia, and provides an important database for statin prevention in women. Ridker PM, Fonseca FAH, Genest J, Gotto AM, Kastelein JJP, Khurmi NS, Koenig W, Libby P, Lorenzatti AJ, Nordestgaard BG, Shepherd J, Willerson JT, Glynn RJ on behalf of the JUPITER Trial Study Group. Baseline characteristics of participants in the JUPITER trial, a randomized placebo-controlled primary prevention trial of statin therapy among individuals with low low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein. Am J Cardiol 2007; 100: 1659–1664. Abbreviations WOSCOPS=West of Scotland Coronary Prevention Study; AFCAPS/TexCAPS=Air Force/Texas Coronary Atherosclerosis Prevention Study; CVD=cardiovascular disease; CHD=coronary heart disease; LDL-C=low-density lipoprotein cholesterol; HDL-C=high-density lipoprotein cholesterol; hsCRP=high sensitivity C-reactive protein †Antécédents familiaux de coronaropathie prématurée : parent au premier degré avec coronaropathie à un âge < 55 ans (homme), < 65 ans (femme). ‡ Syndrome métabolique selon les critères de l’AHA/NHLBI 1. Ridker P et al. N Eng J Med 2008;359: 23

24 Effets sur le LDL-C, le HDL-C, les TG et l’hs-CRP at 12 mois
10 LDL-C HDL-C TG hsCRP 4% p<0.001* -10 17% Percentage change from baseline (%) -20 p<0.001 -30 Results. Compared to placebo, treatment with rosuvastatin 20 mg resulted in a significant change from baseline at 12 months for LDL-C, HDL-C, TG and hsCRP and these effects were maintained over the study period:- LDL-C: At 12 months, LDL-C declined from 108 mg/dL (2.8 mmol/L) at baseline to 55 mg/dL (1.4 mmol/L) in the rosuvastatin group and to 110 mg/dL (2.8 mmol/L) in the placebo group. The difference between groups was statistically significant at 12, 24, 36 and 48 months (p< 0.001). HDL-C: At 12 months, HDL-C increased from 49 mg/dL (1.3 mmol/L) at baseline to 52 mg/dL (1.3 mmol/L) in the rosuvastatin group and to 50 mg/dL (1.3 mmol/L) in the placebo group. The difference between groups was statistically significant at 12 months (p< 0.001), 24 months (p< 0.001) and 36 months (p=0.003) but this statistical difference was not maintained at 48 months (p=0.34). TG: At 12 months, TG declined from 118 mg/dL (1.3 mmol/L) at baseline to 99 mg/dL (1.1 mmol/L) in the rosuvastatin group and to 119 mg/dL (1.3 mmol/L) in the placebo group. The difference between groups was statistically significant at 12, 24, 36 and 48 months (p< 0.001). hsCRP: At 12 months, hsCRP declined from 4.2 mg/L at baseline to 2.2 mg/L in the rosuvastatin group and in the placebo group from 4.3 mg/L at baseline to 3.5 mg/L. The difference between groups was statistically significant at 12, 24, 36 and 48 months (p< 0.001). Note: all values presented above are median. The mean LDL-C difference between groups at 12 months was 47 mg/dL (1.2 mmol/L). Reference Ridker P et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008; 359: 37% -40 p<0.001 50% -50 p<0.001 -60 *P-value at study completion (48 months) = 0.34 Ridker P et al. N Eng J Med 2008;359:

25 JUPITER - Primary Endpoint Tps de survenue du 1er épisode d’IM mortel ou non, du stroke mortel ou pas, du 1er épisode d’angor instable ou de revascularisation artérielle 0.08 Placebo Hazard Ratio 0.56 (95% CI ) P< 0.06 Cumulative Incidence Rosuvastatin 20 mg 0.04 NNT for 2y = 95 5y* = 25 Results: At the time of study termination (median follow-up 1.9 years, maximal follow up 5.0 years), 142 first major cardiovascular events had occurred in the rosuvastatin group and 251 in the placebo group which represented a 44% relative risk reduction (HR 0.56; 95% CI: 0.46 to 0.69; p< ). The rates of the primary endpoint were 0.77 and 1.36 per 100 person-years of follow-up in the rosuvastatin and placebo groups, respectively. The number of patients who would need to be treated with rosuvastatin for 2 years to prevent one primary endpoint event is 95, the number needed to treat (NNT) for 4 years is 31. If this figure is projected out to 5 years based on the model proposed by Altman and Andersen then the NNT is 25. Reference Ridker P et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008; 359: NOTE: COPYRIGHT PERMISSIONS REQUIRED FOR THIS SLIDE 0.02 0.00 1 2 3 4 Follow-up (years) Number at Risk Rosuvastatin 8,901 8,631 8,412 6,540 3,893 1,958 1,353 983 544 157 Placebo 8,901 8,621 8,353 6,508 3,872 1,963 1,333 955 534 174 *Extrapolated figure based on Altman and Andersen method Ridker P et al. N Eng J Med 2008;359:

26 JUPITER – Mortalité totale
0.06 Hazard Ratio 0.80 (95% CI ) p=0.02 Placebo 0.05 Rosuvastatin 20mg 0.04 Cumulative Incidence 0.03 0.02 Results: Looking now at total mortality, there were 198 deaths in the rosuvastatin group compared to 247 deaths in the placebo group – HR 0.80; 95% CI: 0.67 to 0.97; p=0.02. Significantly reducing the risk of death from any cause is a unique finding for statins in a patient population without established coronary heart disease. The rates of death from any cause were 1.00 and 1.25 per 100 person-years of follow-up in the rosuvastatin and placebo groups, respectively. Reference Ridker P et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008; 359: NOTE: COPYRIGHT PERMISSIONS REQUIRED FOR THIS SLIDE 0.01 0.00 1 2 3 4 Follow-up (years) Number at Risk Rosuvastatin 8,901 8,847 8,787 6,999 4,312 2,268 1,602 1,192 683 227 Placebo 8,901 8,852 8,775 6,987 4,319 2,295 1,614 1,196 684 246 Ridker P et al. N Eng J Med 2008;359:

27 CAS CLINIQUE Homme de 61 ans, retraité
Consulte pour asthénie et constipation FRCV: arrêt récent (3 mois) du tabagisme (a fumé 1 pq/j pdt 40 ans); pas de notion d’HTA bilan lipidique non connu pas de diabète l’hérédité est négative

28 EXAMEN CLINIQUE Taille 171 cm Poids 73 kg BMI: 25 Vitiligo
PA: 145/90 mmHg FC: 60/min Auscultation cardio-pulmonaire normale Pas de souffle vasculaire

29 EXAMENS COMPLEMENTAIRES
Analyse sanguine? Radiographie? Avis d’un spécialiste?

30 BIOLOGIE Augmentation de la TSH avec abaissement de la T3L. La T4L est à la limite inférieure de la normale. Les Ac sont positifs. CT 2.35, LDL-C 1.45, HDL 0.52 et TG 1.3 g/l

31 PRESCRIPTIONS Avis endocrinologique? Echographie thyroïdienne?
Scintigraphie thyroïdienne? Mise sous hormones thyroïdiennes? Mise sous statine? Mise sous hypotenseur? (PA 145/90 mmHg)

32 FOLLOW UP Mise sous L-Thyroxine (jusqu’à 1.6 µg/kg/j) avec contrôle de la TSH après 8 semaines Après 8 semaines, bilan thyroïdien normalisé mais CT 2.25 et LDL-C 1.35 g/l; PA: 145/85 mmHg

33 PRESCRIPTIONS Statine? Hypotenseur? Mesures hygiéno-diététiques?

34 ECHELLE SCORE Homme, 61 ans, tabagique pdt 40 ans, HTA systolique 145 mmHg, CT 2.25 g/l Score risk (risque de décéder d’un problème cardio-vasculaire dans les 10 ans) 9%

35