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Diagnostic Approach in Dyslipidemid رويكرد تشخيصي ديس ليپيدمي

Diagnostic Approach in Dyslipidemid رويكرد تشخيصي ديس ليپيدمي. Dr.Toba kazemi Associate Professor of Cardiology BUMS-BCRC 17 Esfand 1390. تعريف :.

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Diagnostic Approach in Dyslipidemid رويكرد تشخيصي ديس ليپيدمي

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  1. Diagnostic Approach in Dyslipidemid رويكرد تشخيصي ديس ليپيدمي Dr.Toba kazemi Associate Professor of Cardiology BUMS-BCRC 17 Esfand 1390

  2. تعريف : • به اختلال سطح چربیهای سرم که منجر به افزایش ریسک بیماریهای قلبی عروقی می شود، گفته می شود که شامل هیپرکلسترولمی، هیپرتریگلیسریدمی، LDLبالا و HDLپايين می باشد.

  3. اهميت ديس ليپيدمي

  4. 3.7 2.9 Relative Risk for Coronary Heart Disease (Log Scale) 2.2 1.7 1.3 1.0 40 70 100 130 160 190 LDL-Cholesterol, mg/dL Log-linear Relationship Between LDL-C Levels and Relative Risk for CHD • This relationship is consistent with a large body of epidemiological data and with data available from clinical trials of LDL-lowering therapy • These data suggest that for every 30-mg/dL change in LDL-C, the relative risk for CHD is changed in proportion by about 30%. The relative risk is set at 1.0 for LDL-C 40 mg/dL. Grundy S, et al. Circulation. 2004;110:227-239

  5. N = 5127 patients with no history of CHD 3 2.5 2 Relative CHD Risk 1.5 1 0.5 0 50 100 150 200 250 300 350 400 TG Level, mg/dL Risk of CHD by TG LevelThe Framingham Heart Study (30-Year Follow-Up) Men Women Univariate analysis of data from the Framingham Heart Study, including 5127 patients aged 30 to 60 years without CHD, to determine the relationship between TGs and CHD. Reprinted from Castelli WP. Am J Cardiol. 1992;70:3H-9H, with permission from Elsevier.

  6. تقسيم بندي

  7. عللايجاد • اوليه(ژنتيك) • ثانويه (تغييرات شيوه زندگي/بيماريها و.....)

  8. اوليه(ژنتيك) • Primary causes : single or multiple gene mutations that result in either overproduction or defective clearance of TG and LDL cholesterol, or in underproduction or excessive clearance of HDL • Primary disorders, the most common cause of dyslipidemia in children, do not cause a large percentage of cases in adults.

  9. Secondary causes • Secondary causes contribute to most cases of dyslipidemia in adults. • The most important secondary cause in developed countries is a sedentary lifestyle with excessive dietary intake of saturated fat, cholesterol, and trans fats. • Other :DM, alcohol overuse, chronic kidney disease, hypothyroidism, primary biliary cirrhosis and liver diseases • Drugs: Thiazides, β-blockers, retinoids, highly active antiretroviral agents, estrogen , progestins,

  10. هيپركلسترولمي فاميليال(FH) • FH is an AD disorder characterized : • elevated LDL-C + normal TG , tendon xanthomas, premature CAD • FH is caused by a large number (>1000) mutations in the LDL receptor gene. • The elevated levels of LDL-C in FH are due to an increase in the production of LDL from IDL (since a portion of IDL is normally cleared by LDL receptor-mediated endocytosis) and a delayed removal of LDL from the blood. • FH homozygotes: 2mutated LDL receptor • FH heterozygotes: 1 mutant allele • Individuals with FH homozygotes have higher LDL-C levels than those FH heterozygotes

  11. LDL receptor A mutated LDL receptor A normal LDL receptor

  12. HomozygousFH • 1 in 1 million persons worldwide. • The disease has >90% penetrance so both parents of FH homozygotes usually have hypercholesterolemia. • Clinical manifestation: • cutaneous xanthomas on the hands, wrists, elbows, knees, heels, or buttocks present in childhood • CHOL are usually >500 mg/dL and can be higher than 1000 mgldL. • Important complication of is accelerated atherosclerosis, which can result in disability and death in childhood. • Atherosclerosis often develops first in the aortic root, where it can cause aortic valvular or supravalvular stenosis, and typically extends into the coronary ostia, which become stenotic.

  13. HomozygousFH • Exams and Tests: • A physical examination may reveal xanthomas and corneal arcus. • A strong familyhistory of familial hypercholesterolemia or early heart attacks • High levels of LDL in either or both parents. • Individuals from families with a strong history of early heart attacks should have blood tests done to determine lipid levels.

  14. Dysbetalipoproteinemia • Dysbetalipoproteinemia,, is a rare lipid disorder characterized by high levels of blood cholesterol & TG. • CHOL range from 300-600 mg/dL. TG are usually >400 mg/dL and may exceed 1000 mg/dL. • Moderately elevated total cholesterol and triglyceride levels accompanied by the presence of palmar crease xanthomasconfirm the diagnosis dysbetalipoproteinemia

  15. Clinicalfindings • Patients may have no physical findings or may have skin lesions called xanthomas, particularly in more severe presentations. • Xanthomastriatapalmaris • Tuberoeruptive and tuberous xanthomas • Corneal arcus , • Xanthelasmas • Obesity or signs of hypothyroidism may be noted.

  16. علايم باليني • علامتي كه مشخصا مربوط به ديس ليپيدمي فندارد • ممكنست فرد با علايم مثل بيماري كرونر يا عروق محيطي • High levels of TGs (> 1000 mg/dL) can cause acute pancreatitis. • خطر بيماري كرونر زودرس • طبيعي شدن ليپيد مانع ايجاد يا پيشرفت عوارض(pancreatitis/premature CAD).

  17. يافته هاي باليني • High levels of LDL :eyelid xanthelasmas; arcuscorneae; tendinousxanthomas . • familial hypercholesterolemia :the above findings plus planar or cutaneousxanthomas • severe elevations of TGs can have eruptivexanthomas • Patients with dysbetalipoproteinemia can have palmar and tuberous xanthomas • Severe hypertriglyceridemia (> 2000 mg/dL) can give retinal arteries and veins a creamy white appearance (lipemiaretinalis). • Extremely high lipid levels also give a lactescent (milky) appearance to blood plasma.

  18. Diagnosis • Lipid profile measurement • Testing should be postponed until after resolution of acute illness, because TGs increase and cholesterol levels decrease in inflammatory states. Lipid profiles can vary for about 30 days after an acute MI; however, results obtained within 24 h after MI are usually reliable enough to guide initial lipid-lowering therapy. • TC, TGs, and HDL cholesterol are measured directly. • LDL cholesterol = TC − [HDL cholesterol + (TGs ÷ 5)] (Friedewald formula). • This calculation is valid only when TGs are < 400 mg/dL and patients are fasting

  19. Screening: A fasting TC, TGs, HDL cholesterol, and calculated LDL cholesterol should be obtained in all adults ≥ 20 yr and should be repeated every 5 yr. • screening patients < 20 yr: atherosclerotic risk factors, such as diabetes, hypertension, cigarette smoking, and obesity; premature CAD in a parent, grandparent, or sibling; or a cholesterol level > 240 mg/dL or known dyslipidemia in a parent. • 12 hours fasting

  20. Other tests • 1- Lp(a) measurement : • Patients with premature atherosclerotic cardiovascular disease • cardiovascular disease with normal or near-normal lipid levels • high LDL levels refractory to drug • Patients with an extensive family history of heart disease • 2-C-reactive protein and homocysteinemeasurement may be considered in the same populations. • 3-Tests for secondary causes

  21. 3-Tests for secondary causes : • FBS, • liver enzymes, • Creatinin • TSH • urinary protein • For who? (newly diagnosed dyslipidemia , when a component of the lipid profile has changed for the worse. • A definite age after which no require screening ?? • into their 80s, especially in the presence of atherosclerotic cardiovascular disease.

  22. US Hypertriglyceridemia (HTG) Prevalence US Adult Population Total = 217 million TG ≥500 mg/dL ~2.5% 5-6 M patients TG 200-499 mg/dL* ~13% ~28 M patients

  23. HIGH TG • INDEPENDENT RISK FACTOR FOR HEART ATTACK • INDEPENDENT RISK FACTOR FORSTROKE • ASSOCIATED WITH LOW HDL • ASSOCIATED WITH INCREASED CLOTTING VIA HIGH PLASMINOGEN ACTIVATOR INHIBITOR ACTIVITY, HYPOFIBRINOLYSIS (CAN’T CHOP UP BLOOD CLOTS EASILY) • A FUNDAMENTAL PART OF METABOLIC SYNDROME, HIGH CHD RISK

  24. اغلب ثانويه به عوامل ديگراستروژنهاي اگزوژن,OCPالكل زيادديابت خوب كنترل نشدهمصرف كورتن سيستميكنارسايي كليه

  25. Familial hypertriglyceridemia • Familial hypertriglyceridemia is a common disorder passed down through families in which the level of TG are higher than normal. • The condition is not associated with a significant increase in cholesterol levels. • An autosomal dominant fashion • Familial hypertriglyceridemia does not usually become noticeable until puberty or early adulthood. • Obesity, hyperglycemia (high blood glucose levels), and high levels of insulin are often also present and may cause even higher triglyceride levels. • about 1 in 500 individuals in the United States. • Risk factors are a family history of hypertriglyceridemia or a family history of heart disease before the age of 50.

  26. Familialhypertriglyceridemia- • Exams and Tests • People with a family history of this condition should have blood tests to check very low density lipoprotein (VLDL) and triglyceride levels. Blood tests usually show a mild to moderate increase in triglycerides (about 200 to 500 mg/dL)

  27. رويكرد تشخيصي تريگليسريد بالا • رد علل ثانويه • بررسي ميزان تريگليسريد • بيش از 500درمان بر اساس تري گليسريد • در صورتی که تری گلیسرید خون بین dL/mg500 -200 باشد ابتدا بایدChOL–HDL- Non را محاسبه کنیم و سپس تصمیم بگیریم • .(Non-HDL chol=Total Chol-HDL) • Target Non-HDL =LDL+30))

  28. LOW HDL علل: • اغلب همراه با مقاومت به انسولين است ( تري گليسريد بالا ، چاقي . اضافه وزن ، فعاليت فيزيكي كم ، ديابت تيپ 2 ) • سيگار • رژيم با كربو هيدرات خيلي زياد • داروها (بتابلوكرها ، استروئيدهاي آنابوليك ، پروژستين ها )

  29. درمان LOW HDL

  30. Ddiagnostic approach-summary 1-Measure fasting lipoproteins 2-primary/secondary 3- Identify CAD or CAD equivalents & CAD risk factors Slide 32 4- If ≥ 2 major risk factors without CAD or CAD equivalent, assess 10-yr risk of MI or CAD death using Framingham risk tables 5-refer to NCEP ATP III Guidelines for Treatment of Hyperlipidemia

  31. سطح چربیهای سرمی در افراد بالغ (mg/dl)

  32. Rule out secondary causes(FBS,U/A,CR,TSH,LFT) • Sedentarylifestyle, obesity, and smoking are all associated with low HDL-C levels, and patients should be counseled about these issues. • Patients with hyperlipidemia, especially hypertriglyceridemia, who drink alcoholshould be encouraged to decrease their intake. • Drugs • Attempts should be made to diagnose the primary lipid disorder

  33. CAD equivalents: • Peripheral arterial disease • Abdominal aortic aneurysm • Symptomatic carotid artery disease • Diabetes mellitus • Major CAD risk factors in dyslipidemia: • Cigarette smoking • Hypertension (BP ≥ 140/90 or on antihypertensive drug) • Low HDL (≤ 40 mg/dL [1.03 mmol/L]) • Family history of premature CAD (CAD in a male 1st-degree relative < 55 or in a female 1st-degree relative < 65) • Age (men ≥ 45, women ≥ 55)

  34. Framingham Ten Year Risk Men Women

  35. Framingham Ten Year Risk 0

  36. Framingham Ten Year Risk 0 3 Non-Smoker 0

  37. Framingham Ten Year Risk 0 3 HDL = 43 0 1

  38. Framingham Ten Year Risk 0 3 0 SBP = 119, untreated 1 0 4

  39. Framingham Ten Year Risk 0 3 0 1 0 4

  40. سطح ايده الLDLوNon HDL در افراد مختلف

  41. TREATMENT

  42. Ddiagnostic approach-summary 1-Measure fasting lipoproteins 2-primary/secondary 3- Identify CAD or CAD equivalents & CAD risk factors 4- If ≥ 2 major risk factors without CAD or CAD equivalent, assess 10-yr risk of MI or CAD death using Framingham risk 5-refer to NCEP ATP III Guidelines for Treatment of Hyperlipidemia

  43. معرفی بیمار شماره 1: • خانم 54 ساله ای به کلینیک پیشگیری از بیماریهای غیرواگیر جهت بررسی وضعیت سلامت خود مراجعه می کند .وي هیچگونه علامتی ندارد و تاکنون کاملاً سالم بوده است. سابقه دیابت، هیپرتانسیون و بیماری قلبی عروقی را در خانواده ذکر نمی کند. در معاینه نکته غیرطبیعی مشاهده نشد. • آزمایشات خون بیمار بعد از 12 ساعت ناشتایی به شرح زیر است: • FBS=85 Chol = 220 TG= 332 HDL=42 LDL=111

  44. بیمار خانم 54 ساله ای است که به جز سن بالا ریسک فاکتور دیگرقلبي عروقي ندارد. فشارخون و قند خون بیمار در حد طبیعی است. کلسترول توتال، LDL و HDL تقریباً در حد قابل قبولي است، اما تری گلیسرید بیمار بالاست • Non HDL- ChOL = 220-42=178

  45. باتشكر از همه شركت كنندگان www.bums.ac.ir/heart

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