What is Hypercholesterolemia?

Hypercholesterolemia is not a disease, but a risk factor for the development of atherosclerosis. This term refers to high cholesterol in the blood.

The prevalence of hypercholesterolemia in various countries: in Japan – 7%, Italy – 13%, Greece – 14%, the Netherlands – 32%, the USA – 39%, Finland – 56%, Ukraine – 25%.

Causes of Hypercholesterolemia

Etiology of primary hypercholesterolemia unknown

Etiology of secondary hypercholesterolemia

  • Hypothyroidism.
  • Diabetes.
  • Nephrotic syndrome.
  • Obstructive liver disease.
  • Taking drugs (progestins, anabolic steroids, diuretics [except for indapamide], beta-blockers [except for those with internal sympathomimetic activity], some immunosuppressants).

Genetic aspects

  • Inherited hypercholesterolemia (* 143890, 19p13.2-p13.1, gene LDLR, FHC, R): PA hyperlipoproteinemia, xanthomas, IHD.

Risk factors

  • Heredity.
  • Obesity.
  • Lack of exercise.
  • Stress.

Pathogenesis during Hypercholesterolemia

Hypercholesterolemia is one of the main risk factors for the development of atherosclerosis and its complications. This risk increases in proportion to the increase in LDL cholesterol. To determine the nature and intensity of lipid-lowering therapy, the determination of the level of cholesterol, to which during treatment it is necessary to lower the indicator of a particular patient, is of primary importance.

The target cholesterol level is primarily associated with the prognosis of the disease, i.e. at risk of developing heart disease. For this purpose, for each patient, according to a special technique, the corresponding category of coronary risk and the target level of LDL cholesterol with a number of other risk factors are calculated.

Symptoms of Hypercholesterolemia

Diseases developing with atherosclerosis:

  1. Diseases of the peripheral arteries: mainly an obliterating atherosclerosis of the vessels of the lower extremities. It occurs when the normal blood supply to tissues is disturbed during the deposition of atherosclerotic plaques on the inner walls of the arteries. If you do not treat this disease, this leads to impaired blood circulation in the tissues of the lower extremities, to necrosis and ulcers. Ultimately, the need arises for amputation.
  2. Diseases of the carotid arteries: these include a violation of cerebral circulation. Carotid arteries supply blood to the brain. With atherosclerosis, plaques form on their inner wall. This leads to a narrowing of their lumen, resulting in a violation of cerebral circulation. It is manifested by impaired memory, some functions of the brain, and functions of the cerebellum. With a sudden violation of blood circulation, a stroke occurs.
  3. Aortic aneurysm: the aorta is the most important vessel in our body. From him, blood from the heart goes to all other organs and tissues. When atheromatous plaques are deposited on the aortic wall, it becomes thin and loses its elasticity. A constant flow of blood at a high speed in this situation leads to stretching of the aortic wall, the aorta becomes balloon-shaped. This expansion may rupture, resulting in massive internal bleeding, from which death occurs. In addition to this severe and dangerous complication, there is a risk of stratification of the aortic wall, this leads to a violation of the blood supply to tissues and organs.

Diagnosis of Hypercholesterolemia

Laboratory research

  1. Determination of LDL, HDL, and fasting triglycerides
  2. Cholesterol level exceeds 200 mg% (5.18 mmol / L)
  3. Determination of thyroxine and TSH in the initial stage to exclude hypothyroidism
  4. Caffeine can increase serum cholesterol

Hypercholesterolemia Treatment

According to the results of completed clinical studies, the residual cardiovascular risk in the treatment with statins is 60-70%. Therefore, it is necessary to search for new approaches aimed at further reducing mortality in the pharmacotherapy of atherosclerosis. The scientific sessions of the American Cardiology Association (Chicago, November 2006) and the meetings of the American College of Cardiology (New Orleans, March 2007) actively discussed the reduction of target lipid levels for very high-risk patients and strategies for increasing HDL cholesterol.
Of particular interest was the report on the main results of the randomized METEOR study (Measuring Effects on Intima Media Thickness: an Evaluation Of Rosuvastatin). This classic regression study was conducted on a population of patients with hypercholesterolemia with a low risk of atherosclerosis complications. The rationale for its implementation was the following: determined by the ultrasound method, TIM is a reliable marker of atherosclerotic vascular lesions related to cardiovascular risk factors and predictors of cardiovascular events; the effect of statins on TIM progression was studied as part of secondary prevention in high-risk patients with elevated LDL cholesterol; further studies are needed to evaluate the effectiveness of statin use in low-risk patients with subclinical atherosclerosis.

According to the design of the METEOR study, 702 patients took rosuvastatin at 40 mg / day, 282 took a placebo. After 2 years of follow-up, the study was completed by 530 and 208 patients, respectively. The primary endpoint of the study was the change in maximum TIM in 12 segments of the carotid arteries. The average age of patients (60% of men) was 57 years old, 16-22% of patients smoked, hypertension was detected in 20% of the study participants. The average baseline LDL cholesterol level is 155 mg / dL (3.96 mmol / L). The average decrease in LDL cholesterol for 2 years of therapy in the rosuvastatin group was 49%, the increase in HDL cholesterol was 8%, and the decrease in TG was 15.7%. While taking rosuvastatin, a fairly low average level of LDL cholesterol was achieved – 78 mg / dl (2.01 mmol / l). The maximum TIM score in the rosuvastatin group decreased by 0.0014 mm, and in the placebo group it increased by 0.0131 mm (p <0.001). Rosuvastatin treatment was well tolerated; the incidence of serious and non-serious adverse reactions in the placebo and rosuvastatin groups did not differ. Thus, in middle-aged patients with a low risk of coronary heart disease (<10% on the Framingham 10-year risk scale) and proven subclinical atherosclerosis, rosuvastatin therapy for 2 years prevented an increase in TIM. With placebo, there was a statistically significant progression of atherosclerosis. In the group of patients receiving rosuvastatin, the progression of atherosclerosis was absent and, on the contrary, there was a tendency to regress it (statistically unreliable); statistically significant regression was observed only in relation to the maximum TIM of segments of the common carotid artery.

The great interest of specialists was caused by the results of a secondary analysis of the data of the ASTEROID study, which evaluated lipid-lowering therapy in 1455 patients. According to intracoronary ultrasound data, the chances of regression of coronary atherosclerosis have been shown to increase significantly if LDL cholesterol during statin therapy is reduced by at least 37% over a 2-year period with a simultaneous increase in HDL cholesterol by 7-8%. Most often, the reverse development of atherosclerosis was observed in patients who managed to achieve (and maintain!) A LDL cholesterol content of not more than 87 mg / dl (<2.3 mmol / l). The average lipid profile in patients with significant regression of coronary atherosclerosis (n = 370) was as follows: total cholesterol – 4.02 mmol / l, TG – 1.46 mmol / l, HDL cholesterol – 1.15 mmol / l, LDL cholesterol – 2.08 mmol / L.
The data of modern regression studies (ASTEROID, REVERSAL, METEOR) suggest the possibility of an effective and safe “course” treatment with statins. They also suggest that the lower the level of LDL cholesterol, the better it is, at least for people with documented coronary atherosclerosis and a high risk of its complications. This academic season, for the first time, emphasis has been placed on the fact that when choosing statins, one should take into account not only the level of LDL cholesterol, but also the effect of such treatment on the state of reverse cholesterol transport (increasing the level of HDL cholesterol).

Hypercholesterolemia Prevention

To prevent hypercholesterolemia, it is necessary to reduce the consumption of animal fats, limit the intake of carbohydrates, it is enough to consume proteins and vitamins. Vitamins C and P contained in vegetables and fruits and vitamin B6 found in bread products and yeast are especially useful.