Abstract

Cardiovascular disease remains the largest contributor to non-communicable adverse disease outcomes. Treatment and prevention of cardiovascular disease have evolved at a dramatic pace in the last 40 years. Serum-cholesterol has emerged as the dominant risk factor for coronary artery disease and events. The link between serum-cholesterol and arterial atherosclerosis is well documented. The attainment of cholesterol goals has historically concentrated on low-density lipoprotein cholesterol (LDL-C) levels. Current evidence and guidelines have shifted to the attainment of non-HDL-C target levels which represent a more thorough inclusion of small dense atherogenic particles. Methods to reduce serum-cholesterol mainly centre around the use of the HMG CoA-reductase inhibitors also known as the statins. High intensity statins like atorvastatin (80 mg) and rosuvastatin (40 mg) are now the preferred starting therapies to lower cholesterol by at least 40–50% in patients with established cardiovascular disease as secondary prevention. In the event of failure of these medications, evidence suggests that the addition of ezetimibe may enhance the total serum-lowering levels to 50–60%. New therapies aimed at inhibiting PCSK9 revealed exciting new targets for LDL-C lowering, but the high cost of these antibodies could preclude access to this therapeutic intervention. Aggressive pursuit of lower LDL-C or non-high-density lipoprotein cholesterol (non-HDL-C) levels may reduce the incidence of secondary myocardial infarctions, strokes and death from cardiovascular disease.

Highlights

  • Measurement of Cholesterol – To Fast or Not to Fast?Patients with established cardiovascular disease (CVD) are at a higher risk for future CVD events.[1]

  • Prevention in high risk patients or very high risk groups is referred to as secondary prevention.[1,2,3]. These individuals who are at high risk include those patients with established atherosclerotic disease such as: previous myocardial infarctions (MIs), a current history of angina, recipients of coronary revascularisation, type 2 diabetes, type 1 diabetes with microalbuminuria, genetic dyslipidaemia, chronic kidney disease (GFR < 60 ml/min/1.73 m2), a previous stroke, a history of transient ischaemic attacks (TIA) and patients with peripheral artery disease (PAD)

  • Therapy with alirocumab and high intensity statins resulted in significant hazard reductions in nonfatal MI (HR 0.86, 95%CI 0.77-0.96, p = 0.006), ischaemic stroke (HR 0.73, 95%CI 0.57-0.93, p=0.01) and unstable angina (HR 0.61, 95%CI 0.41-0.92, p=0.02) at 4 years

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Summary

Introduction

Patients with established cardiovascular disease (CVD) are at a higher risk for future CVD events.[1]. Past dyslipidaemia guidelines have generally emphasised the need for fasting lipograms before starting therapy to ensure the accuracy in results.[2] There is recent evidence which has questioned the fasting requirement for lipograms.[4,5] From population-based studies, TC, high density lipoprotein cholesterol (HDL-C) and non-LDL-C only varied by 2% with population based studies.[4] Robust evidence supports the use of non-fasting blood draws for routine clinical practice and the role of the fasting lipograms has a much more limited use.[5] The limited role of the fasting lipograms should be utilised only in the setting of abnormally increased triglyceride (TG) levels and prior to starting treatment in patients with genetic forms of dyslipidaemia.[4,5] For the purposes of monitoring LDL-C, a fasting sample may still be required.[4] Both the South African Diabetes Guidelines and the current EDL, have moved away from the need for a fasting lipograms to initiate statin therapy as secondary prevention.[6,7] The authors of the diabetes guidelines, state at the first visit a patient with type 2 diabetes should have their total cholesterol and triglycerides measured If either of these is elevated only a ten-hour fast lipogram should be performed.[6] www.tandfonline.com/oemd 15 The page number in the footer is not for bibliographic referencing.

Consider increasing dose if started on less than atorvastatin
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