Prof. Ramzy H. El Mawardy Ain Shams University Cairo Egypt 2009
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.
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).
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?
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.
1 Drugs: Thiazides, diuretics. Beta blockers. Steroids. Cyclosporine. Oral contraceptives. Bile acid resins (mild TG).
2 Diseases: Alcohol abuse. DM. Hypothyriodism. h i Chronic renal failure. Nephrotic syndrome. Obesity. Renal transplantation.
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.
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.
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).
Methyldopa (aldomet). Clonidine. Metabolically neutral. Given in HRN + DM. Given in HRN + abnormal lipid profile. Given in HRN + renal dysfunction. Given in HRN + pregnancy.
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.
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.