Dyslipidemia lecture
- 1. DYSLIPIDEMIA PROF DR FARHAT BASHIR
- 2. 28 year old female referred for FH/O premature cardiac death. Her 21 year old brother died suddenly after a race. Autopsy revealed a completely occluded left coronary artery. Non- smoke, no H/O hypertension and diabetes mellitus. Height 5’8”, weight 166lb, pulse 72 beats/ min, BP 120/75 mmHg, Thickened Achilles tendon, corneal arcus FBG 80 mg/dl, AST and ALT N, BUN 10 mg/dl, Cr 0.8 mg/dl, TC 440mg/dl, LDL 385, TG 100, HDL 55
- 3. LIPIDS AND CARDIOVASCULAR DISEASE Dyslipidemia(abnormal plasma lipoproteins are a major modifiable risk factor for cardiovascular disease. They contribute to the development of atherosclerosis Elevated total cholesterol Elevated LDL Elevated TG Low HDL
- 5. LIPIDS AND ATHEROSCLEROSIS Atherogenic LDL, IDL lipoprotein(a) and possibly chylomicron remnants contribut to development of atherosclerosis Increased plasma concentration and reduced diameter favor sub-endothelial accumulation of these lipoproteins. Following oxidation these lipoproteins are no longer cleared by normal mechanism.
- 6. The LDL molecules enter the sub-endothelial space. Trigger a self-perpetuating inflammatory response to form foam cells, hallmark of atherosclerosis HDL removes cholesterol from the tissues to liver where it is metabolized and excreted in bile. Low HDL levels are often associated with TG elevation which also predisposes to atherosclerosis
- 9. HIGH LDL LEVELS ARE A LEADING CAUSE OF CORONARY HEART DISEASE SHOULD BE THE MAIN TARGET OF ANT CHOLESTEROL LOWERING REGIMEN
- 10. ETIOLOGY PRIMARY Single/multiple gene mutation Resulting in disturbance of LDL, HDL and TG, production orclearance. Suspected in patients with- premature heart disease, family history of atherosclerosis, serum cholesterol>240mg/dl, physical signs of hyperlipidemia. SECONDARY Sedentary lifestyle Diet Hypothyroidism Pregnancy Cholestatic liver disease Drugs ART Thiazide diuretic Beta blocker Hormones Nephrotic syndrome Anorexia Porphyria hyper[parathyroidism
- 11. SPECIFIC DYSLIPIDEMIA HIGH LDL>190mg/dl Genetic disorder Monogenic familial hypercholesterolemia Familial defective apolipoproteinB-100 (Apo B) Polygenic hypercholesterolemia Family testing to detect affected relatives
- 12. HIGH TRIGLYCERIDES Overweight and obesity Physical inactivity Cigerrete smoking Alcohol High carbohydrate diet Disease-type 2 Diabetes mellitus, CKD, nephrotic syndrome. Drugs-steroids, estrogens, retinoids, beta blockers.
- 13. LOW HDL<40mg/dl Elevated TG Overweight and obesity Physical inactivity Type 2 diabetes Cigerette smoking High carbohydrate intake Drugs-beta blockers, anabolic steroids, progestational agents.
- 14. COMPLICATIONS Atherosclerosis Hypertension Ischemic heart disease Stroke Retinopathy Nephropathy Fatty liver, NASH
- 22. INDICATION FOR FLP Total lipid profile/ fasting lipid profile Screening for primary / secondary prevention of cardiovascular disease Investigations of patients with clinical features of lipid disorder Testing relatives with single gene defects causing dyslipidemia
- 27. MANAGEMENT OF HYPERLIPIDEMIA IN CVD PATIENTS lipid profile in all patients should be established lipid-lowering therapy before discharge Lifestyle modifications daily physical activity weight management dietary therapy
- 28. • Reduce intake of saturated and trans-unsaturated fat to less than 710%of total energy • Reduce intake of cholesterol to <250mg/day. • Replace source of saturated Fat and cholesterol with lean meat,low fat dairy products and low glycemic index carbohydrates. • Reduce energy dense food e.g fat and soft drinks whilst increasing activity and exercise. • Increase consumption of cardioprotective and nutrient dense food such as vegetables, unrefined carbohydates such as vegetabes ,un refined carbohydrates,fish, pulses, nuts, legumes, fruit etc . • Adjust alcohol consumption ,reduce intake if excessive or if associated with hypertension , hypertriglyceridemia or central obesity . • Add supplementary food containing nutrients, such as omega-3 fatty acids , dietry fibers, plants sterols
- 29. • statin should be used that reduces LDL-C to 100 mg/dL AND achieves at least a 30% lowering of LDL-C. • triglycerides 200 mg/dL should be treated with statins to lower non– HDL-C to 130 mg/dL. • triglycerides 500 mg/dL should be started on fibrate therapy in addition to statin
- 30. HIGH RISK PATIENTS • intensification of LDL-C–lowering drug therapy with a bile acid sequestrant • to treat very high-risk patients with statin therapy to lower LDL-C to 70 mg/dL • very high risk* and who have triglycerides 200 mg/dL, a non–HDL-C goal of 100 mg/dL is reasonable • ezetimibe -for patients who do not tolerate or achieve target LDL-C with statins, bile acid sequestrants,‡ and/or niacin. • For all patients, it may be reasonable to recommend omega-3 fatty acids from fish or fish oil capsules (1 g/d) for cardiovascular disease risk reduction
- 31. PRIMARY PREVENTION WITH LIPID-LOWERING THERAPY • The clinical approach to primary prevention is founded on the public health approach that calls for lifestyle changes, including: 1) reduced intakes of saturated fat and cholesterol, 2) increased physical activity, and 3) weight control • trials show that Lipid-lowering drugs reduce risk for major coronary events and coronary death even in the short term.
- 32. SECONDARY PREVENTION WITH LIPID- LOWERING THERAPY • Lipid-lowering therapy reduces total mortality, coronary mortality, major coronary events, coronary artery procedures, and stroke in persons with established CHD • lipid measures should be taken on admission or within 24 hours. • Adjustment of therapy may be needed after 12 weeks.