Atherosclerosis . Important pathological process in which lipids are deposited in the intimate layers of the arteries.


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  • 1 General
  • 2 Epidemiology and frequency
  • 3 Etiopathogenesis
    • 1 Theory of reaction against aggression
    • 2 Monoclonal theory
    • 3 Theory of focal clonal senescence
    • 4 Lysosomal theory
  • 4 Aetiological factors
    • 1 Hyperlipidemia
    • 2 High blood pressure
    • 3 Smoking
    • 4 Genetic factors
    • 5 Physical inactivity
    • 6 Obesity
    • 7 Diabetes mellitus
    • 8 Trace elements
    • 9 Enzymes
  • 5 Pathological anatomy
    • 1 Early injuries
    • 2 Intermediate injuries
    • 3 Complicated injuries
    • 4 Location
  • 6 Clinical picture
    • 1 Cardiac manifestations
    • 2 Neurological manifestations
    • 3 Renal manifestations
    • 4 Abdominal manifestations
    • 5 Peripheral manifestations
  • 7 Diagnosis
    • 1 Chest X-ray
    • 2 Electrocardiogram
  • 8 Treatment
    • 1 Prophylactic treatment
    • 2 Treatment of the disease
    • 3 Invasive procedures
  • 9 Localized calcification or Mönckeberg sclerosis
  • 10 Sources


Atherosclerosis results from the action of various factors such as the metabolism of lipids , elements clotting blood , cytokines, hemodynamics and risk factors. The lesion is characterized by an infiltration of immunocompetent cells , such as macrophages and T lymphocytes , proliferation of the intima of the arterial wall and accumulation of lipids.

Epidemiology and frequency

The highest frequency is found in individuals over 50 years, however, other investigations have shown that the formation of the atherosclerotic lesion precursor to atheroma (fatty streak), can start from lactation , which denies the concept. that this disease is a process of senile evolution. It occurs in both sexes, although more frequently in men; It is pointed out that the woman of reproductive age is protected by the action of estrogens , since the frequency increases in this sex during menopause .

No direct relationship of atherosclerosis with race has been specified , however, some studies indicate that Europeans and Anglo-Saxons are affected more frequently than Japanese, Hindus and Africans, which seems to be more related to dietary and social habit, than with the racial factor.


There are several theories that try to explain the pathogenesis of atherosclerosis, among which are the following:

Theory of reaction against aggression

It is the most widely accepted and indicates that the endothelial cells of the intima are subject to repeated injuries that cause a loss of the normal function of these cells, which act as a barrier to permeability.

By decreasing functioning cells, exposure of subendothelial tissue to high concentrations of plasma constituents occurs, triggering monocyte and platelet adhesion; then monocytes migrate into the intima to become macrophages, which together with platelet aggregation cause the formation of microthrombi and release of secretory products of platelets and macrophages, these stimulate the proliferation of smooth muscle cells and cause a matrix deposit conjunctiva and lipid accumulation .

Monoclonal theory

This indicates that the proliferative lesions of the intima are a consequence of the multiplication of the individual smooth muscle cells .

Focal clonal senescence theory

This hypothesis states that the process of arteriosclerosis contributes to the intrinsic development of aging .

Lysosomal theory

It suggests that alterations in lysosome function aid atherogenesis by increasing lipid deposition in smooth muscle cells , which may be related to a relative deficit in cholesterol ester hydrolase activity in lysosomes .

Etiological factors

There are certain circumstances and habits that occur more frequently in individuals who develop atherosclerosis, compared to the general population; These are known as risk factors. Most people with atherosclerosis have one or more risk factors, in addition to aging.

These factors are classified as reversible and irreversible. Among the former are hypercholesterolemia, high blood pressure, and smoking , and irreversible are age, sex, and genetic factors.


Hypercholesterolemia and hypertriglyceridemia are important factors, as cholesterol and triglyceride levels rise as age increases .

For example, at birth, the cholesterol level is 1.5 mmol / L (60 mg / dl), at one month, the average is 3 mmol / L (120 mg / dl) and after one year it is 4.3 mmol / L (175 mg / dl). In the third decade there is another increase, and this continues until the age of 50 in men and until somewhat later in women.

The increase in cholesterol is associated with the elevation of low-density lipo proteins (LDL), and that of triglycerides, with very low-density lipoproteins (VLDL) and with the remnants of their catabolism (intermediate-density lipoproteins).

HDL (high-density lipoprotein) carries 20% of total cholesterol, and those with high HDL-cholesterol have a lower risk of developing ischemic heart disease. HDL levels are higher in women than in men.

There are factors that increase the HDL level, such as: estrogens , regular active exercise and moderate alcohol consumption ; their levels decrease, androgens and tobacco .

Arterial hypertension

It affects men and women equally, and diastolic hypertension is the most important. Changes in pressure caused by hemodynamic forces (forces generated by blood flow), determine a multiplication of the [cells] of the intima.

The areas most affected by atherosclerosis are those of arterial bifurcation, since there are variations in blood flow pressure; In these areas what is known as decreased lateral pressure occurs, which acts as an initial stimulus.

Atherosclerosis is rare in the pulmonary circulation, where very low blood pressures predominate; they only appear in it when there is a disease that determines an increase in pulmonary pressure.


When this risk factor is eliminated or decreased, the possibility of developing the disease also decreases and reaches the same risk as in non-smokers after having quit for a year. Carbon monoxide , a component of the cigarette , is reported to cause hyperlipidemia.

Genetic factors

Premature atherosclerosis often appears to be familial; in some cases it is attributed to inheritance of risk factors, but in others they are not identified, so the presence of genetic determinants of protective factors, such as HDL, and other non-lipid factors, such as apoprotein B and lipoprotein (a).

Physical inactivity

It has been observed that the individual with a more active life is less prone to sudden death , and although the mechanism by which physical activity reduces the risk of atherosclerosis is not known, it is suggested that it increases HDL values.


Its effect is more evident before the age of 50 and a close relationship has been identified between the type of obesity (abdominal) and ischemic heart disease; in addition, this class of obesity is associated with other risk factors, such as hypertriglyceridemia, hypercholesterolemia, hyperglycemia, and HT; A fundamental role of obesity in the elevation of cholesterol and triglyceride levels, related to age, is also pointed out .

Mellitus diabetes

Atherosclerosis is accelerated in the diabetic patient by various factors: hyperglycemia, hyperlipemia, lipoprotein abnormalities associated with diabetes , increased hypertension, and hyperinsulinemia.

The lumen of the artery is covered by endothelial cells, which serve as a barrier between the substances that circulate in the plasma and the cells of the arterial walls. The main function of these cells is to maintain a balance between coagulation and anticoagulation, which occurs continuously in the vascular walls; But in diabetes, endothelial cells are damaged by hyperglycemia, hyperlipidemia, and hypertension. It has recently been pointed out that immunocomplexes cause an alteration of the balance in favor of intravascular coagulation, platelets adhere and aggregate and form the clot, and cholesterol is deposited on the arterial walls.

Trace elements

A possible relationship between the deficit of some trace elements ( manganese , chromium , zinc , cadmium ) and some qualities of water is assessed : hardness, reactivity due to the presence of cobalt , fluorine , with the development of atherosclerosis. These can influence the metabolism of lipids and in controlling blood pressure.


Enzymes that intervene in metabolic processes have been found , such as in the synthesis of cholesterol and its esters (cholesterol esterase, fatty acid transferase, etc.); enzymes related to the metabolism of triglycerides and phospholipids (lipoprotein lipase, phospholipase); enzymes that intervene in the metabolism of connective tissue (hyalurodinase, chondroitin-sulfatase), and basic enzymes that catalyze the metabolic processes inherent in any type of tissue (glucose-6-phosphate dehydrogenase).

Pathological anatomy

Atherosclerosis is a localized nodular form of arteriosclerosis, and the lesions can be classified as early, intermediate, and complicated.

Early injuries

There are two types of injuries: initial and fatty streaks. Early lesions are focal, small and unobtrusive, or chemically detectable with a microscope and observed that the cells endothelial pinocytotic vesicles containing charged lipids ; They are seen in children and are located in areas susceptible to atherosclerosis.

Fat streaks can be seen with the naked eye on the endothelial surface of the aorta and coronary arteries , are small and unobtrusive, and increase during puberty in the aorta. These lesions may or may not progress depending on hemodynamic forces and atherogenic lipoprotein levels; Initially, stretch marks contain two types of cells: foamy, consisting of lipid-filled macrophages, mainly in the form of cholesterol, and T lymphocytes, especially CD8 + with some CD4 +.

Intermediate injuries

They are made up of fibrous plaques and represent the most characteristic lesion of atherosclerosis; They first appear in the abdominal aorta , carotid and coronary arteries , and increase progressively with age.

Complicated injuries

They consist of a calcified fibrous plaque in which there are varying degrees of necrosis, thrombosis, and ulceration; As necrosis and debris accumulation increase, the arterial wall progressively weakens and ruptures with the formation of aneurysms and hemorrhages , and if plaque is mobilized, arterial emboli occur.


The greatest involvement develops in the abdominal portion of the aorta and more in the lower extremities than in the upper ones. It is also frequent in the coronary arteries and its main branches, a short distance from the coronary orifices, and in the cervical and cerebral arteries, whose distribution is in patches.

Clinical picture

There is no defined clinical picture, since the symptoms are the result of ischemia of the organ whose arteries have been affected.

Cardiac manifestations

Atherosclerosis of the coronary arteries causes myocardial infarction and angina pectoris . After a silent period, atherosclerosis can produce ectasia and develop an aneurysm with increased lumen size. This occurs frequently in the aorta and predisposes to rupture and dissection rather than stenosis.

Neurological manifestations

They are caused by the involvement of the arteries that supply the CNS and cause strokes of the brain.

Kidney manifestations

It can cause renal artery stenosis and thus contribute to the pathogenesis of arterial hypertension and manifestations of renal failure .

Abdominal manifestations

Occasional mesenteric ischemia causes intestinal infarction, causing abdominal pain crises.

Peripheral manifestations

Atherosclerosis of the branches of the aorta that supply the lower limbs (iliac, femoral, popliteal, etc.) causes intermittent pain in the calf, thigh and hip muscles, which exacerbates during walking and forces the patient to stop with frequency (intermittent claudication); Physical examination revealed weakness of the pulses and coldness of the affected limb with trophic changes in the skin, subcutaneous cellular tissue and muscles, and ulcerative lesions in the lower limbs.


The histological study is the only one that allows the diagnosis to be made with certainty, however, there are some tests that can help to discover the etiological factors, such as: glycemia, which reveals diabetes mellitus ; serology, to differentiate the atherosclerotic aneurysm from a syphilitic one; urea and creatinine, to determine if there is kidney damage, and the lipidogram, which constitutes the most useful laboratory examination, the figures of which are as follows:

  • Cholesterol … 3.87 to 6.50 mmol / L
  • Total lipids .4.5 to 10.0 g / L
  • LDL cholesterol .1.30 to 4.90 mmol / L
  • HDL cholesterol:

Male: less than 0.91 mmol / L Female: less than 1.16 mmol / L

  • Triglycerides ..0.34 to 1.70 mmol / L
  • ß-lipoproteins .3.6 to 6.4 g / L

The turbidity test will be altered.

Torax X ray

It reveals the presence of an aneurysm of the aorta and atherosclerotic plaques in the aortic arch. Through angiography, the deformations of the vascular lumen are observed; myocardial perfusion defects demonstrable with radioactive isotope imaging techniques. Digital exercise plethysmography, which shows atherosclerosis of the lower limbs.


It shows the characteristic alterations of the T wave and the ST segment in the course of ischemic heart disease.

Despite the aforementioned, detection of atherosclerosis is usually done when any clinical complication appears due to decreased blood flow in a vessel.

The most reliable indicator currently is ischemic heart disease, which is synonymous with coronary heart disease and atherosclerotic heart disease; cerebrovascular accident is a less reliable criterion.


Prophylactic treatment

It is aimed at suppressing risk or etiological factors, and includes the following measures:

  • Avoid obesity .
  • Avoid sedentary life.
  • Eliminate the factors that determine a constant tension.
  • Decrease cholesterol- rich foods .
  • Suppress the habit of smoking.
  • Control diabetes mellitus and high blood pressure .

Treatment of the disease

There is no specific medication, but treatment for hyperlipidemia is recommended:

  • Derivatives of fibric acid (lowers VLDL): clofibrate, 2g / d, and genfibrocil, 1.2g / d. and nicotinic acid (lowers VLDL and LDL): 2 to 4 g / d.
  • Bile acid binding resins (promote steroid excretion and increase LDL clearance): cholestyramine, 12 to 16 g / d, and colestipol, 15 to 20 g / d.
  • HMG-CoA reductase inhibitors (block cholesterol synthesis and increase receptor mediated LDL clearance): lovastatin, 10 to 80 mg / d; simvastatin, 10 to 40 mg / d, and provastatin, 10 to 40 mg / d.
  • Probucol: its mechanism is unknown and it acts on LDL; dose: 1g / d.
  • Estrogens : Premarin, 0.625 mg / d, and estradiol, 2 mg / d. Its mechanism is unknown.

Invasive procedures

  • Iliac bypass, with the purpose of interrupting the enterohepatic circulation of bile acids.
  • LDL apheresis, plasmapheresis and portocava shunt.

Currently it is pointed out that there are several nutrients ( lipids , carbohydrates , ethanol ) that play a fundamental role in the diet of patients with atherosclerosis, in particular lecithin of plant origin and more recently the phospholipid polyene (phospholipids with linoleic acid) , known as essential phospholipid (EPL), since it modifies the metabolism of lipids and lipoproteins, so the EV infusion of these products is suggested; the recommended dose is 4.5 to 30 g / d for PLA, and for lecithin, 18 g / d.

Localized calcification or Mönckeberg sclerosis

This type of arteriosclerosis is common in the lower extremities and in the arteries of the genital apparatus in both sexes, which are equally affected. It is rare in children under 50 years. The process involves degeneration of smooth muscle cells followed by calcium deposition . Upon palpation, the radial artery can be found as a rigid tube.

The diagnosis is made by means of X-rays , which demonstrate the presence of regular concentric calcifications in the cross sections and the appearance of train rails in the longitudinal sections. Changes in the mean are isolated and do not produce light stenosis, so they have little effect on circulation. However, in the lower extremities, calcification of the stocking is frequently associated with atherosclerosis and causes arterial occlusion. These variations, which can also cause aortic valve disease, are frequent in the elderly.


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