Prof. Ramzy H. El Mawardy. Cairo Egypt 2009
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1 Prof. Ramzy H. El Mawardy Ain Shams University Cairo Egypt 2009
2 Burden of HRN is increasing worldwide = 7 billion individuals. BP control is still poor = 60.70%. Global risk assessment is essential in HRN subjects (i.e. check for presence of associated conditions): Obesity (BMI). Metabolic syndrome. DM. Smoking. CAD. Renal disease / failure. Renal transplantation. Dyslipidaemia. Hypothyroidism. Drug intake. Hypertension ± LVH are important risk factors for CAD.
3 Prevalence of dyslipidaemia in HRN = 40%. This combination of risk factors will increase vasolopathy in different vascular beds. Cerebral. Coronary. Peripheral. A complete lipid id profile is essential before and during prescribing hypotensive agents / or in patients with other medical conditions, which may affect different lipids (TC, TG, LDL, HDL).
4 Questions: 1. Which drugs, what atdoses of hypotensive agents induce dyslipidaemia? 2. Do these agents affect S cholesterol, /S. triglyerides/ id HDL, LDL, VLDL etc? 3. Does hypotensive drug induced dyslipidaemia have any bad repercussions on future CV events? 4. What is the solution? What preferable agent to give in which clinical situation?
5 TG HDL T. Chol. LDL Diuretics, thiazides Beta Bt Blockers ± Ace inhibitors ARB s Ca C blockers α adrenergic B Aldosterone antagonists Central sympatholitics Metabolically neutral. Commonly used hypotensive agents induce dyslipidaemia. Those metabolically neutral are safe+ effective in HRN with dyslipidaemia or DM.
6 1 Drugs: Thiazides, diuretics. Beta blockers. Steroids. Cyclosporine. Oral contraceptives. Bile acid resins (mild TG).
7 2 Diseases: Alcohol abuse. DM. Hypothyriodism. h i Chronic renal failure. Nephrotic syndrome. Obesity. Renal transplantation.
8 Hydrochlorothiazed h TG 15%, HDL, 10%. Chlorthalidone TG 15%, HDL, 10%. In doses 25mg/50mg. Not in doses 6.25mg or / 12.5mg. Safe in combination Rx in 6.25 mg/12.5mg doses. Check for other metabolic disturbances with prolonged thiazide Rx: Uric acid ppt gout. Glucose ppt glucose intolerance. Potassium hypokalaemia VPB, VT.
9 Commonly used beta blockers induce dyslipidaemia TG 10 50%, HDL 7 20%. Non selective BBs without vasodilatory properties induce dyslipidaemia?? (e.g. propranolol, pindolol, nadolol). l) Selective BBs: have minimal effects on lipid profile.(e.g. atenolol, metoprolol and bisoprolol, acebutalol). Non selective BB's with vasodilatory properties have no or insignificant effects on dyslipidaemia eg e.g. carvedilol, nebivilol C bi i f hi id di i ( ) b Combination of thiazide diuretics (25mg)+ beta blockers synergistic detrimental affect on lipids.
10 1 Non dihydropyridines verapamil. 2 Dihydropuridines: Nifedeprine. Amlodipine. Felodipine. i Nicardipine. 3 Benzothiazepines. Diltiazem. Metabolically neutral: lipids. UA. Glucose. K. Na+. K. Na+. Indicated in HRN, + angina, + SVT, migrane (verapamil), old age, black race, renal dysfunction (3 rd line).
11 Methyldopa (aldomet). Clonidine. Metabolically neutral. Given in HRN + DM. Given in HRN + abnormal lipid profile. Given in HRN + renal dysfunction. Given in HRN + pregnancy.
12 Our aim is to minimize i i risks ik to HRN population. Life style modification is important in reducing: TG. HDL. Insulin sensitivity. LDL chol. (10%). Diet control ( Saturated fats 7 10% ( Diet control ( Saturated fats 7 10% ( polyunsaturated oils), omega fats will help in modifying lipid profile.
13 Use proper hypotensive agents in the suitable situations HRN + angina : BB + which BB? Carvedilol, nebivolol, bisoprolol. HRN + dyslipidaemia originally: No thiazide diuretics. Nor BB's non selective, non VD. Give ACEI, ARB's, Ca CB, aldosterone antagonists. HRN + DMII: ACEI, ARB' s + Small dose thiaz., Ca CB, aldosterone antagonists. HRN + renal dysfunction: (ACEI, ARB's, loop diuretics, Ca CB, central sympatholytic, no thiazides (GFR<30mm). HRN + renal transplantation: Ca CB, loop diuretics, statin.
7/7/ CHD/MI LVH and LV dysfunction Dysrrhythmias Stroke PVD Renal insufficiency and failure Retinopathy. Normal <120 Prehypertension
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