Cardiovascular disease remains the leading cause of death in most industrialized countries. Most often, they result in the development of atherosclerosis under the influence of multiple factors especially dyslipidemia.
DIAGNOSIS:
Screening for lipid abnormality:
Screening is done when extravascular lipid deposits (see Chapter corneal Arc), in assessing the overall risk in a subject other cardiovascular risk factor and a fortiori when atheromatous disease. This screening should be as systematic in all individuals between 20 and 30 years. In particular, it must advise among first-degree relatives of an dyslipidemic subject and / or with history of cardiovascular disease (screening for children between 4 and 10 years). It does not seem useful to “track” after the age of 75 in primary prevention but conversely it should not interrupt a safe and effective treatment in a subject not having another pathology conditioning its life expectancy.
The lipid profile is achieved after 12 hours of fasting, distance (2-3 months) of any acute condition that can affect the results (infectious episode, surgery, stroke in particular myocardial infarction, birth).
In an asymptomatic subject, without associated risk factor, the balance sheet includes a measurement of total cholesterol (TC) and triglycerides (TG).
If both parameters are less than 2 g / L, no further assessment is required and it is not necessary to repeat the prior 5 years in men under 50 and premenopausal women before and 3 years on the other hand. If one of the two parameters is abnormal, it is justified to apply for an “exploration of a lipid abnormality” aspect of serum fasting TC, TG and HDL-cholesterol by precipitation.
These elements can be determined by calculation according to the Friedewald formula LDL cholesterol (applicable if the TG levels are less than 4 g / L): LDL-C = TC – HDL cholesterol – TG / 5 g / L.
The apolipoprotein measurements is of little use in current practice. To confirm and typing dyslipidemia, it is advisable to practice 2-3 doses a month apart in a stable metabolic period (unmodified free diet).
Eliminate secondary hyperlipidemia:
They are common, we must therefore consider hypothyroidism, cholestasis, nephrotic syndrome, renal failure, diabetes, lupus erythematosus, an iatrogenic therapy (estrogen orally, retinoids, steroids, thiazides, protease inhibitors). The assessment should include a TSH, alkaline phosphatase and / or ã-GT, creatinine, fasting glucose and research of proteinuria by dipstick. Usually there is no need to prescribe a treatment unless persistent abnormalities after treatment of the case.
TREATMENT:
Treatment of pure cholesterol by increasing the LDL cholestérol:
The therapeutic decision is based on LDL-cholesterol, the presence of other risk factors (smoking being, hypertension, diabetes, age over 45 years in men and 55 in women or postmenopausal, history Early atherosclerosis in a relative of the first degree [before age 55 for men and 65 for women], low HDL cholesterol <0.35 g / L) and the context of primary or secondary prevention of atherosclerotic disease. Or as an isolated elevation of triglycerides should be supported.
Dietary advice remains the basic treatment and there is rarely urgent to prescribe lipid-lowering. The diet should be acceptable, simple, with a minimum of prohibited indicating the patient’s priorities. In some cases they are enough to reduce lipid parameters in the objectives. Reduce saturated fat (cessation of preparations rich in butter, reduced cheese, cold cuts and meats) remains the primary goal as well to strengthen the consumption of fish, vegetable fat, fruit and vegetables.
Nutritional advice is justified in primary prevention in all patients whose LDL cholesterol is greater than 1.60 g / L or greater than 1.3 g / L in the presence of more than two associated risk factors and secondary prevention.
In case of insufficient results after 3 to 6 months of dietary management, drug therapy is indicated if the LDL cholesterol remains above 2.2 g / L in the absence of risk factor, 1.9 g / L if another risk factor is associated, 1.6 g / L if at least two other risk factors are associated.
The goal is a reduction of 25 to 30% in LDL-cholesterol.
The HMG-CoA reductase inhibitors or statins, which inhibit hepatic cholesterol synthesis, are currently the treatment of choice for hypercholesterolemia is a significant drop of LDLcholestérol 25 to 40%, HDL-cholesterol is slightly modified.
Fibrates, which remain the most effective agents for reducing hypertriglyceridemia and raise HDL cholesterol can be interesting in some mixed dyslipidemia.
Cholestyramine (Questran) can be of service in combination with statins in severe hypercholesterolemia (synergistic effect).
Ezetimibe, too inhibitor of intestinal cholesterol absorption, easier to use is an interesting alternative in combination with statins.
The treatment will be much daily and indefinitely continued safe.
If the recommendations of the 2000 AFSSAPS remain the reference in primary prevention, secondary prevention they are likely to be revised downwards. Indeed after demonstrating the interest of statin therapy for secondary prevention of atherosclerotic disease with a 25 to 38% of the morbidity and mortality recent studies show the benefit of treatment regardless of the baseline LDL-cholesterol even less than 1.3 g / L (current threshold).
Secondary prevention aims to achieve LDLcholestérol less than 1 g / L (and perhaps even lower). This is reinforced by the results of studies using high doses at once (40 mg pravastatin, simvastatin, atorvastatin, 80 mg fluvastatin) who report an additional benefit. The protective effects of statins by a mechanism other than lowering LDL cholesterol remains to be established. Only one study with fibrates showed a 22% decrease in cardiac morbidity and mortality.
For patients with type 2 even in primary prevention, the objectives are similar to those of secondary prevention because the risk is comparable due to the high frequency of risk factors (note that in diabetes and hypertriglyceridemia the presence of microalbuminuria are additional risk factors).
Control of lipid parameters:
Until reaching the target, the control of lipid parameters should be performed every two months. Once the objective “achieved and stabilized” there is no need to repeat the test more than once every six months. However, regular dosages remains essential to ensure adhesion of the patient and the effectiveness of treatment, major elements for these treatments continued indefinitely.
CONCLUSION:
The prevention of cardiovascular disease means taking early and effective management of risk factors, particularly lipid.
This prevention should help decrease the incidence and aggravation of these diseases and thus the financial cost they entail.
The arguments for treating dyslipidemia are now strong and must carry conviction doctors before that of their patients.