BR 08-3 MANAGEMENT OF DYSLIPIDEMIA IN HYPERTENSION

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Abstract

Cardiovascular disease burden is increasing all over the world. The diagnosis of hypertension is considered when a person has persistently elevated BP (Systolic BP more than 140 mmHg and/or Diastolic BP more than 90 mmHg). Dyslipidemia denotes abnormal levels of lipids in the blood (Total Cholesterol >200 mg%, Low density lipoprotein (LDL) >100 mg%, Triglycerides (TGL) >150 mg% and High density lipoprotein (HDL) <40 mg in men and < 50 mg in women. Hypertension and Dyslipidemia constitute the important components of metabolic syndrome as per the definition of NCEP Guidelines-Adult Treatment Panel III (ATP III). The prevalence of the co-existence of hypertension and dyslipidemia is in the range of 15–31%. The co-existence of these two risk factors has more than the additive effect for endothelial dysfunction resulting in enhanced atherosclerosis leading to CVD. The term dyslipidemic hypertension (DH) was used in the context of familial DH. Non-familial forms of DH are more common than familial form. Some authors name this combination as Lipitension for easy understanding. Framingham Heart study shows that the majority of hypertension population have more than one risk factor predominantly atherogenic in nature. Dyslipidemia causes endothelial damage and loss of vasomotor activity. The damage may manifest as elevated BP. MRFIT study reveals that mild to moderate elevation of BP and Dyslipidemia can lead to multiplicative adverse impact on CVD. Framingham study results also reveal that moderately elevated BP and cholesterol had a similar risk.

RAAS promotes atherogenesis. Angiotensin II promotes atherogenesis through stimulation AT1 receptor, which increases lipid uptake in cells, vasoconstriction and free radical production to foster both hypertension and atherosclerosis. Hypertension damages vascular endothelium through altered shear stress and oxidative stress resulting in increased synthesis of collagen and fibronectin, reduced nitric oxide-dependent vascular relaxation and increased permeability to lipoproteins. Hypertension is also associated with up regulation of lipid oxidation enzymes. Hypertension is clearly associated with vascular endothelium (prothrombotic and pro inflammatory). Oxidative stress and vascular inflammation are increased in the pathogenesis of atherosclerosis. Reduction of both results in the reversal of vascular inflammation.

LDL is a major cause of endothelial dysfunction. Microalbuminuria is identified in hypertensive patients and it is also associated with lipid abnormalities including high levels of LDL and TGL, low levels of HDL and elevated levels of LP(a). Today CVD prevention is focussed on treating hypertension with the lowering LDL (<100 mg%),increasing HDL (>40 mg in men) and lowering TGL(<150 mg%). In ALLHAT trial, 10,000 patients were given pravastatin 40 mg daily. At the end of 5 years, only 16.7% reduction in LDL was noted. In ASCOT-LLA trial, intensive therapy lipid lowering was recommended along with Antihypertensive therapy. ACEIs, ARBs, Aldosterone antagonists and Nebivolol improve endothelial function and reduce BP. Statin treatment happens to be as a first line drug therapy in the management of dyslipidemia. Fibrates are generally reserved for Hypertriglyceridemia. Bile sequestrants, Nicotinic acid and drug like Ezetimibe locally acting at the intestine level are also used for dyslipidemia. Single pill combination like Atorvastatin with RASS blocker/Amlodipine may be considered the coexisting hypertension and dyslipidemia.

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