GBUZ “Center for Speech Pathology and Neurorehabilitation”, Moscow
The mechanisms of development of osteoporosis and atherosclerosis, which bring these diseases closer together, are considered. Data are presented indicating that osteoporosis, calcification of the aorta and heart valves, as well as atherosclerotic vascular damage are interrelated pathological processes. It is emphasized that statins can have a beneficial effect on bone metabolism, while bisphosphonates, on the contrary, have a positive effect on the lipid spectrum. New approaches to the prevention and treatment of osteoporosis based on the use of combination drugs are discussed. Such a drug, combining powerful antiresorptive and anabolic aspects of osteoporosis therapy, is Fosavance, containing the original alendronate at a dose of 70 mg and vitamin D3 at a dose of 2800 IU.
Osteoporosis and atherosclerosis, the clinically significant consequences of which are, respectively, skeletal bone fractures and cardiovascular accidents, are the most common causes of decreased quality of life and increased mortality, especially in people over 50 years of age [1, 2]. In this age group, the risk of osteoporotic fractures of the spine and/or femur and vascular complications associated with atherosclerosis simultaneously increases sharply. The changes leading to such disorders begin several decades before their manifestation and are initially not clinically manifested, although they ultimately lead to the development of serious diseases, disability and death.
The condition of bone tissue in adults changes over time from maximum density at a young age to its progressive decrease, especially in postmenopausal women [3]. It is important to emphasize that osteoporosis is asymptomatic until a low-energy fracture occurs. The evolution of atherosclerosis also includes a number of preclinical stages - from fatty spots to fibrous plaques, but the first symptoms and even more severe damage to cardiac tissue or the brain develop only with rapid progression or rupture of unstable plaques.
The clinical relationship between vascular calcification and decreased bone density is becoming increasingly clear, especially in women. Convincing data have been obtained indicating that osteoporosis, calcification of the aorta and heart valves, as well as atherosclerotic vascular damage are interrelated pathological processes [4, 5].
In women with osteoporotic fractures, there was an increase in the incidence of aortic calcification, the severity of which correlates with a decrease in bone mineral density (BMD) [5–7]. A relationship has been identified between a decrease in BMD of the spine and proximal femur and an increase in calcium content in the coronary arteries according to electron beam computed tomography [8]. It is known that atherosclerotic vascular damage is often complicated by calcification of the atherosclerotic plaque, which increases the risk of vascular complications - myocardial infarction, cerebral stroke, and worsens the outcomes of vascular surgery [9].
In addition to increasing the number of fractures, osteoporosis also increases overall mortality from all causes [10]. Low BMD is an independent risk factor for cardiovascular mortality in older men and women, more important than blood pressure and blood cholesterol levels [11]. According to an epidemiological study that included 9704 women over 65 years of age, each decrease in BMD of the proximal radius by one standard deviation from normal increased the risk of premature death (not associated with osteoporotic fractures) over the next 2 years by 40, and especially death from stroke [12 , 13]. Other studies have also found that patients with decreased BMD are more likely to experience increased lipid levels, develop more severe coronary atherosclerosis, and have a significantly increased risk of stroke and myocardial infarction [14, 15]. In their study, R. Van der Recke et al. showed that in the early postmenopausal period, a decrease in BMD by one standard deviation from peak bone mass is associated in women with a 43% increased risk of overall mortality and premature death from cardiovascular pathology [15]. In a study of postmenopausal women, low-density lipoprotein (LDL) cholesterol levels were inversely and significantly correlated with BMD, suggesting that lipids and bone tissue share common factors linking osteoporosis and atherosclerosis [16].
Calcification of the aorta and coronary arteries, called by many researchers “the skeletons in the closet of atherosclerosis” [17], is widespread among the elderly and may be the basis of cardiovascular morbidity and mortality [18, 19], while it is associated with bone resorption processes [20] and spinal fractures [6, 21]. Overall, all osteoporotic vertebral fractures were found to be an independent risk factor for cardiovascular disease-related mortality. These data suggest that the increase in the incidence of osteoporosis, ectopic calcification and atherosclerosis in the same patients cannot be explained only by nonspecific age-related factors that determine the independent accumulation of these pathological conditions in old age; they probably have a common pathogenetic basis. This assumption has been confirmed in experimental and clinical studies. It was found that bone and vascular tissue have a number of common morphological and molecular properties. Vascular calcification consists of the same components as bone tissue, such as calcium salts, phosphates associated with hydroxyapatite, osteopontin, bone morphogenic protein, matrix Gla protein, type I collagen, osteonectin, osteocalcin, etc. [22–25] . A certain similarity is assumed between the mechanisms of development of osteoporosis and atherosclerosis, since both processes are associated with the involvement of monocytic cells, which, in atherosclerosis, differentiate in the vascular wall into macrophage-like “foam” cells, and in osteoporosis, into osteoclasts. In addition, in the wall of an artery affected by atherosclerosis, there are precursors of osteoblasts, which have the ability to synthesize mineral components characteristic of bone tissue [26]. Of particular importance may be the fact that oxidized LDL, which is involved in the development of atherosclerotic vascular damage, stimulates mineralization mediated by both bone osteoblasts and osteoblast-like cells isolated from the vascular wall [26, 27]. In addition, oxidized LDL induces the expression of monocyte chemotactic factor and macrophage colony-stimulating factor by vascular endothelial cells, which in turn are an inducer of osteoclast differentiation. Thus, oxidized LDL can potentially stimulate osteoclast-mediated bone resorption and the development of osteoporosis [28]. According to other authors [29], transforming growth factor β and vitamin D, which are involved in bone tissue remodeling, have the ability to stimulate the activity of osteoblast-like cells in the vascular wall. In patients with chronic renal failure, an accelerated development of osteoporosis and atherosclerotic vascular damage is observed. It is believed that both processes are associated with impaired calcium metabolism and hyperproduction of parathyroid hormone [30, 31]. The latter suppresses the activity of enzymes that regulate lipoprotein synthesis, and active metabolites of vitamin D inhibit the expression of receptors on monocytes/macrophages involved in the uptake of LDL. It should also be emphasized that in the development of atherosclerotic vascular damage, an important role is played by the hyperproduction of pro-inflammatory cytokines – interleukin-6 and tumor necrosis factor α (TNF-α), which in turn induce bone tissue resorption [32, 33]. Animal studies have shown that mice lacking the osteoprotegerin gene (a member of the TNF-α receptor superfamily that inhibits the activity of the osteoprotegerin ligand that induces bone resorption) develop severe osteoporosis in combination with severe vascular calcification [34].
According to other authors, administration of TNF-α to mice causes ectopic calcification of the vascular wall [35]. There are probably other mechanisms that determine the relationship between osteoporosis and ectopic vascular calcification. For example, there is evidence that an increase in homocysteine levels, on the one hand, is a risk factor for atherosclerosis [36] and, on the other hand, is associated with a decrease in BMD [37]. Finally, one of the universal mechanisms of atherosclerotic vascular damage and osteoporosis in postmenopausal women is estrogen deficiency.
Numerous factors influence the biological mechanisms linking atherosclerosis and osteoporosis, including age, genetics, body type, comorbidities, lifestyle, and diet. Today, there are effective treatment methods that can increase BMD and slow down the progression of atherosclerosis. However, if there are mechanisms linking osteoporosis and atherosclerosis, there must also be treatments that can increase bone mass and reduce atherogenesis at the same time.
One such treatment method is the use of statins. These drugs are called “blockbuster drugs,” which is associated with the rapidly growing volumes of their consumption and proven beneficial effects on vascular atherosclerosis [9]. Statins inhibit the conversion of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG–CoA reductase) to mevalonate (the first step in cholesterol synthesis). Inhibition of cholesterol synthesis in hepatocytes increases the expression of LDL receptors, and therefore LDL and their precursors are removed from the bloodstream. In addition to reducing cholesterol synthesis, inhibition of HMG-CoA reductase by statins has a pronounced effect on other substances involved in the synthesis of mevalonate, which leads to quite diverse and widespread effects in different tissues and cells, including blood vessels and bones, which substantiates the possibility of a therapeutic relationship, because during the synthesis of mevalonate, the formation of isoprenoid compounds occurs, which are important for the post-translational modification of proteins [38]. According to experimental studies, administration of simvastatin to ovariectomized female rats at a dose of 1–10 mg/kg (comparable to the dose of the drug used in humans) for 35 days leads to increased bone tissue formation, an increase in the volume of trabecular bones (spine, femur) by 40–90% [39]. Other studies have also shown that statins inhibit the development of steroid-induced osteoporosis and osteonecrosis in laboratory animals [40, 41]. The work of G. Mundy et al. [39] has prompted a host of clinical studies to determine whether people receiving statins, in addition to beneficial cardiovascular effects, also increase BMD with a reduced risk of fractures. The results of such work turned out to be contradictory. According to some authors, taking statins is associated with a significant reduction in the risk of skeletal bone fractures, especially the most dangerous in terms of life prognosis, fractures of the proximal femur, while other authors did not find a connection between taking statins and the risk of fractures [42]. It should be noted that almost all studies (with the exception of one) were retrospective, which somewhat reduces the significance of the results obtained. The relationship between the duration of treatment, the dose of statins and the reduction in the incidence of skeletal bone fractures is unclear.
One of the problems associated with this issue, according to GR Mundy, CJ Edwards et al. is that when a person uses statins in standard doses, most of the drug substance ends up in the liver, and only a small amount reaches the bones [43, 44]. Nevertheless, an analysis of the results of all studies allows us to draw a preliminary conclusion that during treatment with statins there is still a decrease in the risk of hip fractures [45]. It is important that fibrates and other lipid-lowering drugs had no effect at all on the risk of skeletal bone fractures. Therefore, the decrease in the incidence of fractures during treatment with statins cannot be explained solely by the lipid-lowering effect of these drugs. Clearly, the question of whether statins have clinically significant antiosteoporotic activity requires further study. It should be especially emphasized that the molecular mechanisms of action of statins and the most powerful anti-osteoporotic drugs - aminobisphosphonates - have a certain similarity, since both groups of drugs affect different stages of cholesterol synthesis from acetyl coenzyme A [46]. Statins block the early stage associated with the conversion of HMG-CoA reductase to mevalonate, and bisphosphonates block the formation of geranyl and farnesyl pyrophosphate, which in turn leads to the suppression of phenylation of transpeptidases and apoptosis of osteoclasts. It should be noted that bisphosphonates themselves have the ability to reduce LDL levels and increase high-density lipoprotein levels [47].
Bisphosphonates are the most effective inhibitors of bone resorption and are widely used in the treatment and prevention of osteoporosis. Osteoclasts absorb bisphosphonates bound to bone tissue, which leads to disruption of several osteoclast functions. Potent nitrogen-containing bisphosphonates, such as alendronate and risedronate, are not metabolized and act at relatively later stages of mevlonate metabolism compared to statins, limiting the prenylation of proteins normally attached to the cell membrane, thereby interfering with the ability of osteoclasts to change the shape of their membrane and resorptive function in in general [48].
The mineral components of the bones to which the bisphosphonate binds accumulate the drug for its further absorption by osteoclasts. Another way to deliver significant amounts of bisphosphonate to tissue is to encapsulate it in liposomes, which particularly facilitates drug delivery to macrophages [49]. A similar approach was taken by HD Danenberg et al. who found that the use of liposomal alendronate led to a significant decrease in the number of monocytes and macrophages and inhibited neointimal hyperplasia in stents in rabbits with hypercholesterolemia [50]. These results indicate the possibility of using a similar method for treating patients undergoing cardiac catheterization or placement of stents. In animal studies, the bisphosphonates alendronate and ibandronate, at doses that effectively inhibited bone resorption, also reduced arterial calcification, and clinical studies of this effect in postmenopausal women were planned [51]. However, in older women, treatment with ibandronate did not affect the progression of aortic calcification [52].
Thus, deciphering the mechanisms that determine the relationship between the development of osteoporosis and atherosclerosis is essential for the development of new approaches to the study of risk factors for atherosclerotic vascular lesions, and the development of new methods for the prevention and treatment of these diseases. To date, a number of papers have been published on aging and vascular calcification, its relationship with diabetes, osteoporosis and menopause, as well as the mechanisms of vascular calcification in the context of bone biology and the correlation between arterial calcification and osteoporosis. The main conclusion that can be drawn is that vascular intimal calcification, especially fibrotic plaques, is closely associated with aging and the progression of atherosclerosis, being the “meeting point” of bone biology with chronic inflammation in atherosclerotic plaques. Calcification of extracellular substance is a complex and multifactorial process, limited by the influence of matrix proteins and regulated by inhibitors and activators of calcification and bone formation. The molecular mechanisms that link the propensity of arteries and bones to calcify and are part of a larger process associated with the expression of regulatory proteins in bone matter and atherosclerotic plaques are becoming increasingly understood [53].
Bone is an active tissue that not only performs a purely mechanical frame function: supporting the body, but is also an active metabolic organ with multiple hormonal, para- and autocrine cellular interactions. It has been shown that regulation of cellular differentiation of mesenchymal stem cells, activation of adipocytogenesis and increased activity of osteoclasts are associated with aging of bone tissue and increase the risk of fractures in elderly people simultaneously with the progression of atherosclerosis in blood vessels [53].
The choice of the optimal way to treat or prevent osteoporosis must take into account the characteristics of each patient and be based on a complete understanding of the cellular mechanisms involved in the aging process, ensuring that most of them are affected. Modern research has already laid the foundation for the development of a new direction in the treatment and prevention of osteoporosis, which is a combination of two agents that have a mutually potentiating effect. Such a drug, combining powerful antiresorptive and anabolic aspects of the treatment and prevention of osteoporosis, is today presented in a single form - this is the drug Fosavance, containing the original alendronate at a dose of 70 mg and vitamin D3 at a dose of 2800 IU, the frequency of dosage is 1 time per week. Such treatment today appears to be a truly effective means of slowing down the aging of bone tissue, helping to improve the quantitative and qualitative composition of bone tissue, its renewal, reducing the amount of accumulated microdamage and preventing aging/obesity of the bone marrow. Fosavance is rightfully the first choice drug for the treatment and prevention of postmenopausal osteoporosis, glucocorticoid osteoporosis and osteoporosis in men. In modern clinical practice, it should also be remembered that methods for determining BMD, such as densitometry, should be included in a comprehensive examination of patients not only with risk factors for osteoporosis, but also with diseases of the cardiovascular system.
Osteoporosis and atherosclerosis in women
Osteoporosis and atherosclerosis, the consequences of which are skeletal bone fractures and cardiovascular accidents, respectively, are the most common causes of decreased quality of life and mortality in women over 50 years of age. In this age group, the lifetime risk of osteoporetic fractures is about 20%, and the risk of vascular complications associated with atherosclerotic vascular disease is almost 50%.
In addition to estrogen deficiency and the main markers of atherosclerosis and osteoporosis (low-density lipoprotein cholesterol, triglycerides, bone mineral density), there are a number of modifiable risk factors: dietary habits, sedentary lifestyle, smoking, alcohol abuse. Therefore, timely identification of risk factors and intervention on them can help prevent both osteoporosis and cardiovascular diseases, or curb the further development of these diseases.
In our department, together with the division of the Center “Women’s Health after 40,” a comprehensive examination and treatment of postmenopausal women is carried out:
11 November 2010 | Author Boris Severyukhin
Good afternoon my dear parishioners! Today I want to give you unique information and talk about the relationship and interdependence of two negative processes . occurring in the human body. We will talk about osteoporosis and atherosclerosis . Don't be surprised by this way of asking the question. There is a direct relationship between these two serious diseases, and I will try in a short article to tell you about this seemingly paradoxical connection. First, let's understand the concepts of osteoporosis and atherosclerosis .
Osteoporosis is a systemic disease of the skeletal bones, characterized by a decrease in bone density and a decrease in their mass, manifested by microarchitectural disorders of bone tissue and leading to an increased risk of fractures. The basis of the disease osteoporosis is the loss of calcium from the bones and an increase in their fragility. Bone mass decreases gradually, hiddenly, and is often diagnosed after fractures, which has given rise to calling osteoporosis a “silent epidemic.”
Atherosclerosis is a degenerative disease of the body's arterial vessels. With atherosclerosis, cholesterol (saturated fats) and calcium are deposited in the walls of damaged vessels (mainly large arteries). Subsequently, such vascular lesions grow with connective tissue. Gradually increasing, they turn into foci of vascular destruction. Such lesions are called atherosclerotic plaques. Atherosclerotic plaques cause narrowing of the lumen of blood vessels and deformation of the area of the blood vessel, which in turn leads to disturbances in blood circulation in the internal organs. They are one of the main causes of strokes and heart attacks.
How do events develop in the body in such a way that these two pathological processes begin to stomp each other? Let's look at this issue in more detail.
The main unifying factor of these processes is a decrease in the body’s to critical levels that do not meet the functional needs of the body. We will talk about the reasons for this a little later, but now I will tell you where the missing energy is added from.
The energy of the body is the product of the energy of tissue cells and organs. If the process of energy production in cells drops to critical levels, the body sets into motion compensatory mechanisms that close this deficiency.
One of these mechanisms is the breakdown of calcium molecules in the skeletal system into atoms and its leaching from the bones into the bloodstream. Breaking the molecular bonds of calcium provides a powerful energy boost to the body . ensuring it performs vital functions.
Thus, an excess of atomic calcium appears in the blood, forcing the body to dispose of it. And the body has two main possibilities for this. The first is to “push” calcium back into the bones or release it freely through the kidneys.
Most often, the body uses both of these possibilities, which in any case contributes to the development of a new pathology.
Look what's happening. To “corral” excess free calcium into the bones, the body begins to intensively produce cholesterol (cholesterol ) . What is it for? The mechanism is as follows: when cholesterol enters the skin under the influence of ultraviolet radiation from the sun, it forms vitamin D, which “pushes” calcium back into the bones, strengthening their internal structure and, to some extent, restoring them.
Part of the calcium leaves through the kidneys and settles in the tubules and pelvis to form urinary stones, which is the cause of the development of urolithiasis.
We found out the reasons for the development of osteoporosis and the formation of urolithiasis. Now let's return to atherosclerosis.
You probably already realized that by turning on compensatory mechanisms and producing large amounts of cholesterol, the body triggers atherosclerosis. By the way, it must be said that cholesterol is not as bad as it is trumpeted in all instances. The main damaging factor for blood vessels is thick, acidic blood released into the aorta under high pulsating pressure . Under such conditions, blood acts as an abrasive, damaging the inner lining of large arterial vessels. Micro-abrasions and micro-tears in the intima of blood vessels appear.
Normally, cholesterol comes in and tries to cover up these damages, like biological glue, thereby trying to maintain the integrity of the damaged arteries. Unfortunately, when the internal environment of the body remains pathological for a long time, this does not help. The process of vascular damage increases, and freely “dangling” calcium is involved here. Internal “proliferations” of blood vessels appear, consisting of a detached inner membrane (intima). cholesterol and calcium. Subsequently, these formations grow with connective tissue and real atherosclerotic plaques are formed.
Excess cholesterol increases the growth of plaques and accelerates and aggravates the course of atherosclerosis.
Thus, we traced the relationship and interdependence of these three pathological processes.
And now I’ll tell you that the main reason for all these disgraces in the body is INVOLUTIONARY CHRONIC DEHYDRATION OF THE BODY. But this topic is so vast that it’s worth stopping for today. Understand the material presented and wrap your knowledge around yourself :) Bye.
Atherosclerosis is a chronic disease in which arteries are affected as a result of disturbances in protein and fat metabolism in vascular tissues. The disease is characterized by the formation of atherosclerotic plaques in the walls of blood vessels, narrowing and deforming the vessels, which causes circulatory disorders and damage to internal organs. Vascular atherosclerosis is one of the most pressing diseases of our time. It ranks among the top four causes of illness, disability and premature death. Several factors are involved in the formation of atherosclerosis: age, metabolic disorders, chronic diseases.
The cause of atherosclerosis is that large arteries become clogged with so-called atherosclerotic plaques, which prevents normal blood supply to organs. An atherosclerotic plaque is a formation consisting of a mixture of fats (primarily cholesterol) and calcium. This “growth” on the inner shell of the vessel is covered on the outside with a capsule. Violation of the integrity of this tire (that’s what it’s called in medicine) leads to the fact that a blood clot—a conglomerate of cells (mainly platelets) and blood proteins—begins to be deposited on the plaque. The thrombus, firstly, further narrows the lumen of the artery, and secondly, a piece can come off from it, which is carried further along the vessel by the blood flow until the diameter of the latter becomes so small that the thrombus gets stuck.
In this case, a severe circulatory disorder occurs: blood simply stops flowing to any organ (or part of it) and it may die. The latter situation occurs in the following diseases:
The atherosclerotic plaque constantly grows, gradually narrowing the lumen of the artery. At the beginning, symptoms appear only with arterial spasm (sharp contraction), and then with relaxed arteries.
The causes of atherosclerosis are not fully understood, but the risk factors for the development of this disease are precisely known:
Elimination of these factors is the key to successful treatment of atherosclerosis.
Atherosclerosis of cerebral vessels is the most common disease of the brain, affecting vessels of the muscular-elastic type, with the formation of single or multiple foci of lipid, mainly cholesterol, deposits - atheromatous plaques - in the inner lining of brain vessels. The subsequent proliferation of connective tissue in it (sclerosis) and calcification of the vessel wall lead to slowly progressive deformation and narrowing of its lumen until complete emptying (obliteration) of the vessel and thereby cause a chronic, slowly increasing insufficiency of the blood supply to the organ fed through the affected brain vessel. Atherosclerosis of cerebral vessels occurs in people over 20 years of age, but with the greatest frequency in men aged 50-60 years and in women over 60 years of age. The pathogenesis is complex and not fully deciphered. Pathological features of the metabolism and transport of fats and fat-protein complexes, on the one hand, and violations of the functional and structural integrity of the inner lining of the arteries, on the other, play a role.
Predisposition to cerebral atherosclerosis is often hereditary; Risk factors contribute to the spread of the disease:
The clinical picture varies depending on the predominant localization and extent of the process, but is always determined by the manifestations and consequences of tissue or organ ischemia, depending both on the degree of narrowing of the lumen of the main arteries and on the development of collaterals. Since symptoms pathognomonic for atherosclerosis itself are unknown, the diagnosis is based on signs of damage to individual vascular areas or vessels.
Most often, atherosclerosis affects the vessels of the lower extremities in the places of branching, the aorta and coronary vessels, the superficial femoral and popliteal arteries. Inside the vessel, a mushy mass of lipids accumulates on its walls. The lumen of the vessels narrows, the walls of the vessels become ulcerated, blood clots form, and scar tissue grows. Granular masses of lime salts are deposited on the walls of blood vessels - vascular calcification occurs. Subsequently, the entire wall of the vessel becomes calcified. The most striking manifestation of obliterating atherosclerosis of the lower extremities is intermittent claudication. When walking, severe pain occurs in the calf muscles, thigh muscles and even in the hip joint.
When you stop, the pain in the legs subsides and the patient can continue on his way. However, when movements are resumed, sharp pain occurs again. Since even with complete blockage of the vessel, collateral circulation develops through the deep femoral artery and its branches, the clinical picture may be blurry. Coldness in the legs, cramps in the calf muscles at night, numbness of the toes, fatigue when walking - all these are quite early symptoms of obliterating atherosclerosis of the lower extremities. Pale and cyanotic skin is also characteristic of the onset of the disease. Plantar symptom is a way to assess anemization of leg tissues. In the supine position, the patient raises his legs to 45° without bending his knees. At the same time, he is asked to bend his ankle joints - the speed at which the feeling of fatigue appears and the appearance of pallor of the soles shows the degree of vascular damage and the development of anemia in the tissues.
Symptoms of atherosclerosis depend mainly on the malnutrition of the organ supplied by the artery altered by sclerosis. Poor circulation is one of the main negative manifestations of atherosclerosis, which leads to various complications in the functioning of the heart, brain and other organs. The characteristic symptoms accompanying circulatory disorders in the body include the following:
A person suffering from atherosclerosis constantly feels tired, apathy manifests itself, frequent fainting occurs, dizziness and a general deterioration in health are observed.
The greatest danger is a pathological disorder of cerebral circulation, which develops due to atherosclerotic damage to the carotid arteries and other blood flow pathways that deliver blood to the brain (for example, the carotid artery and aorta). Insufficient oxygen supply to the brain is accompanied by a wide range of symptoms listed below:
Atherosclerosis of cerebral vessels is also manifested by permanent redness of the face, increased sweating and general malaise of the body.
During the development of atherosclerosis, the most common damage to the coronary cardiac blood flow, which leads to disruption of the heart muscle - a weakening of the force of contractions and an increase in pulse with rhythm disturbances. This ultimately leads to the development of coronary heart disease and the manifestation of the following symptoms of the disease:
The above symptoms can be aggravated by an unhealthy lifestyle, bad habits, poor diet and overwork.
Insufficient blood flow, which is an integral effect of atherosclerosis on the body, leads to the fact that blood does not flow in sufficient volumes to areas of the body remote from the heart - the upper and lower extremities. The manifestation of symptoms is most pronounced in the lower part of the legs, as in the furthest from the heart:
A characteristic feature of leg pain with atherosclerosis is that it is observed in the muscles. This is an important point, since pain in the lower extremities also accompanies a disease such as arthrosis, but in this case the pain is observed not in the muscles, but in the joints.
The diagnosis of atherosclerosis is based on signs of damage to individual vascular areas or arteries and always consists of several main stages:
At the first stage, the doctor compares the patient’s complaints with the symptoms of the disease. Symptoms of atherosclerosis, depending on the location and stage of development of the disease, vary greatly, but a number of common ones can be identified:
Professional specialists, along with studying the patient's complaints, always conduct an external examination for the presence of xanthomas and xanthelasmas - neoplasms on the skin of a characteristic yellow color. The examination may also include palpation (palpation) of all accessible arteries (iliac, popliteal, femoral, carotid and others) and listening to murmurs in the aorta.
To diagnose the disease, the attending physician must clarify the risk factors for developing the disease (smoking, obesity, diabetes, unbalanced diet, etc.). However, even after examination and identification of external signs of the disease, as well as the patient being at risk, making a diagnosis is impossible without laboratory blood tests and instrumental diagnostics.
The main purpose of a blood test is to detect elevated levels of lipids (cholesterol, triglycerides). Each age has its own norm, since their accumulation, even with a balanced diet, is inevitable. Blood sampling is done in the morning and on an empty stomach, since it is under such conditions that various biochemical indicators are not influenced by the liquid drunk throughout the day, food taken, and physical activity.
This is an inexpensive, painless, safe and informative (with an accuracy of 99%) method of examining the blood flow in the neck that supplies the brain. For this procedure, we use the MyLab 50 ultrasound system. When scanning with an ultrasound sensor, the diagnostician receives a holistic picture of the state of the blood flow in the neck: lumen, presence of cholesterol plaques, blood flow speed. Diagnostic results are ready within a few minutes after the procedure.
If there is a suspicion of atherosclerosis affecting the arteries of the arms or legs, duplex scanning of the extremities will help to refute or confirm the diagnosis. This method is similar to scanning the brachiocephalic arteries; it allows you to find blood clots and diagnose venous insufficiency. The main advantage of the procedure is the absence of contraindications and complete safety.
This method is used to assess the state of cerebral blood flow. It is based on ultrasound scanning using special equipment - the RIMED Digi-Life Doppler. Using this method, it is possible to diagnose cerebral atherosclerosis in the early stages and prevent stroke.
The essence of this method is to inject a radiopaque substance into the arteries and veins through a special catheter and study the arteries in which the blood flow is impaired. This method is one of the most accurate in studying arteries that are inaccessible to duplex scanning. The method is often used to diagnose coronary heart disease, the most common disease that develops as a result of atherosclerosis.
The ankle-brachial index (ABI) is an important indicator in the diagnosis of atherosclerotic bloodstream lesions. This is the ratio of blood pressure in the lower leg to the pressure in the arm. At certain ABI values, a professional physician can detect atherosclerosis of peripheral vessels in the early stages and prevent its development.
X-ray, MRI and CT to diagnose the disease are prescribed to the patient, as a rule, in cases where highly specialized methods for identifying atherosclerosis of the peripheral arteries, blood flow of the heart and brain were not enough. They provide the diagnostician with information about various injuries, aneurysms (dilation of arteries) and other pathologies.
An ECG is used if coronary heart disease is suspected, the consequence of which is most often atherosclerosis. This is a universal method in cardiology, and no doctor can prescribe treatment without it. In order to make the heart work in a stressful situation, for example, during physical activity, a stress ECG is used. Simulating cycling gives the doctor an understanding of how the vessels that supply the heart with blood work during exercise.
Echocardiography (EchoCG) is an informative way to examine the heart and coronary arteries with ultrasound. A diagnostician can assess in real time the nature of wall damage, the presence of blood clots, and the speed of blood flow.
Success in the treatment of atherosclerosis depends entirely on timely diagnosis. Since this disease cannot be cured, the patient needs to monitor his health for the rest of his life, see a doctor and undergo periodic examinations of the vascular system.
Treatment of atherosclerosis aims to prevent the progression of the process and stimulate the development of circuitous pathways of blood flow to the affected organ or part of the body. The treatment regimen for atherosclerosis considers both drug and non-drug methods.
Surgical treatment is carried out depending on the location of atherosclerotic plaques. For atherosclerosis of the coronary arteries (the heart's own arteries), a number of measures are used.
Percutaneous methods of intervention (that is, without opening the chest, medical instruments are inserted through vessels under the control of an X-ray machine):
For atherosclerosis of the brachiocephalic arteries, the following are used:
For atherosclerosis of the lower or upper extremities, the following are used:
In case of atherosclerosis of the intestinal arteries, only part of the intestine is removed during its infarction (death of a section of the intestine with a complete cessation of blood flow to it).
The most popular traditional medicine that can be used to cure a disease such as atherosclerosis.
This remedy is used for some symptoms of atherosclerosis such as dizziness and sharp pain in the heart area; it can be used to improve vision and hearing.
You will need 500 grams of vodka, which we pour into a three-liter jar. Also add twenty-five grams of clove seasoning and 500 grams of sugar to the vodka in a jar, add four small lemons with peel, previously grated. Thoroughly mix the ingredients in the jar until the sugar is completely dissolved and fill the remaining volume with warm, boiled warm water.
Place the jar with the product in a dark place for two weeks. After two weeks, our ready-made remedy must be taken regularly 15 minutes before meals, 25 grams three times a day. We do not stop drinking the product until it runs out, after which we take a seven-day break and repeat. The full course, which leads to recovery, will be completed after three such cans have been consumed.
This folk remedy is recommended for use not only for atherosclerosis, but also for cardiovascular diseases. To prepare the product, you will need 250 grams of garlic, which must be chopped on a grater or through a garlic press. Mix garlic with 350 grams of honey. Place the mixed mass in a dark place for a week. After seven days, the infused mass should be taken one teaspoon 15 minutes before meals three times a day. Garlic has a positive effect on the human body, it is useful for cardiovascular diseases, and can be taken in any form.
The folk remedy not only has general strengthening properties, but also helps cure the disease of atherosclerosis. You will need 300 grams of garlic squeezed through a garlic press, which you need to put in a small jar and add to it the juice of three medium-sized lemons just squeezed. The jar does not need to be closed, just tie it with gauze.
Before taking the product, the infusion should be shaken thoroughly. Take a teaspoon of infusion and dilute it in a glass of boiled water and drink. Within two weeks after taking the tincture, patients feel better, memory improves, immunity is strengthened and performance returns.
Another popular method of folk treatment for atherosclerosis, which was used in Rus', is prepared on the basis of rose hips. You will need a half-liter jar of rose hips, which must be crushed. Fill a half-liter bottle 2/3 full with crushed rose hips, and fill the rest of the bottle with vodka. We leave the bottle in a dark place for two weeks so that the product infuses, but the bottle must be shaken daily. This remedy must be taken with the help of refined sugar. Add 20 drops of infusion to the refined sugar and dissolve.
Sophora japonica perfectly washes away organic salt from the walls and cleanses the blood. To prepare this method, you will need 50 grams of Japanese sophora, which must be infused with 500 grams of vodka in a dark place for thirty days. This remedy should be taken one teaspoon three times a day. If drinking alcohol is contraindicated for a person, there is a way out - Japanese Sophora should be brewed in boiling water. We brew it like tea: for a glass of water we need a teaspoon of sophora. This infusion should be infused for a day in a thermos and consumed 2 tablespoons twice a day.
Like any other disease, atherosclerosis is easier to prevent than to treat. Prevention of the development of the disease, as well as its treatment, has similar methods, the main task of which is a qualitative change in lifestyle.
Smokers should give up this bad habit. Nicotine and tar, which are contained in cigarettes, disrupt microcirculation in the walls, promote blood clots and replace oxygen cells with carbon monoxide. Smoking a cigarette after a meal interferes with the normal process of lipid metabolism, as a result of which excess cholesterol is deposited on the inner walls.
You should also sharply limit or stop drinking alcohol. It does not directly contribute to the development of atherosclerosis, but it creates additional stress on the heart and increases blood pressure. But hypertension has a negative effect on blood vessels, causing them to constantly increase in diameter, thereby accelerating the development of pathology.
Another important therapeutic and preventive method is physical activity. They will be useful not only for overweight people, but also for those whose activities involve sedentary work. There are special therapeutic physical education programs aimed at preventing cardiovascular diseases.
People with symptoms of atherosclerosis are recommended to take walks in the fresh air. There are special breathing exercises that train the patient’s body.
A balanced diet is one of the most important components of non-drug treatment and prevention of the disease. A diet for atherosclerosis includes avoiding fatty and salty foods, fried foods, and bread made from premium flour. The daily diet should be enriched with vegetables, herbs and fruits. Nuts, sea fish, dried fruits are useful.
The diet prescribed for atherosclerosis excludes refractory fats, red meat, and any fatty and fried foods. Sausages and pates, rich broths are excluded. It is not recommended to eat offal (brains, liver, etc.). Fatty dairy products fall into disgrace (the permissible fat content of cheese is no more than 30%). You should not include baked goods, confectionery products with cream, or fatty sauces into your diet.
In small quantities, you can introduce various vegetable oils and dietary meats into the diet (this is veal, lean poultry without skin, game, rabbit meat). You are allowed to eat cheeses little by little (mild and low-fat). Eggs can be consumed, but not more than 2 pieces. in Week. You can season your food with soy sauce. Sweets are allowed in small quantities. Dry wine can also be included in the patient’s diet - it is believed that it has a beneficial effect on the cardiovascular system (resveratrol, present in wine, fights blockages in blood vessels). Fish (various types) is welcome. It is worth consuming low-fat dairy products. Vegetables, berries and fruits are beneficial. The diet may include dietary types of bread, dry cookies, wholemeal pasta, and various cereals (except semolina). Nuts and sugar-free drinks are beneficial.
Atherosclerosis can have different localizations. If the vessels of the extremities are affected, then it is worth limiting the intake of vitamin D. The diet for atherosclerosis of the vessels of the brain and neck is enriched with B vitamins (B6, B12), E, C. It is useful to eat tomatoes. If the carotid arteries are affected, you definitely need to cut back on calories. It is recommended to unload on vegetables. The diet prohibits baking, sweets, pickles, and smoked foods. For obliterating atherosclerosis, it is recommended to eat a varied diet (the bulk of animal fats should be obtained from dairy products). If the aorta is affected, it is recommended to increase the rate
Question: Hello, please tell me, my 73-year-old grandfather has atherosclerosis of the lower extremities, they say cut off his leg above the knee, is there anything else that can be done?
Nowadays, gentle techniques are widespread and available to almost everyone who is not in critical condition and does not need emergency amputation against the background of spreading gangrene.
Angioplasty and stenting is an operation during which a balloon at the end of a long catheter is inserted into the affected (narrowed) vessel.
Classic stenting is an intervention that involves the introduction of a stent (a metal tubular prosthesis that ensures normal blood flow) in order to preserve the vascular lumen.
Bypass surgery is a surgical procedure aimed at creating an additional bypass when an artery is blocked by a blood clot or atherosclerotic plaque.
Question: A 29-year-old man has pain in his legs not when walking, but at night, closer to the morning. Every night my legs are spinning. Is this a symptom of atherosclerosis? What diseases does this look like?
Question: Please tell me, are there any folk remedies for the treatment of obliterating atherosclerosis of the vessels of the lower extremities? Thanks in advance for your answer!
Question: Hello! My dad is 59 years old. He has atherosclerosis, critical stenosis of the iliac artery, occlusion of the superficial femoral artery. He also has tachycardia. ischemic disease stage 2. In November he was in the hospital, he was given IV drips and sent to Krasnodar for surgery, but he is afraid. Tell me if I should have surgery or if I can treat it with other methods. Regards, Tatiana
Question: I am 33 years old. After a TBI, a diagnosis was made: grade 3 hypertension, risk 4. Atherosclerosis of cerebral vessels, grade 2. Against the background of a decrease in venous outflow by 80% and thickening of the aorta. Cholesterol 4.7. Is such a diagnosis possible at my age?
Question: How to treat atherosclerosis using traditional methods?
Question: A 58-year-old woman, a year ago she underwent abdominal aortic replacement, the postoperative period was without complications, when monitored by ultrasound, a cholesterol plaque closed the lumen by 30-40%. Is there any drug treatment?
Question: Hello, please answer the question: My father is 57 years old, he was diagnosed with atherosclerosis of the lower extremities, he underwent tests and was sent for surgery, is it necessary or not? Is it possible to do without surgery? Thank you.
Question: Hello! My dad is 68 years old, he was diagnosed with obliterating atherosclerosis of the lower extremities, at first they treated his big toe for two months, they said it was a fungus, and when the toes turned dark and red, they decided that it was atherosclerosis, now he is in the hospital receiving a course of treatment, but the doctor says that soon All I have to do is amputate my leg, because... there is no pulse on it, we didn’t have a consultation with a vascular surgeon, but reading other people’s questions about the signs are very similar, tell me if there is an alternative treatment without surgery, what would you advise on what to do. He will be discharged but the pain will not stop. Are there any painkillers that could help? Thanks in advance for your answer.
Question: Male, 56 years old, cardiac ultrasound showed atherosclerosis of the aorta. Has bad habits: he smokes a lot for a long time, drinks alcohol (but does not abuse it). I did not carry out prophylaxis; after I learned the diagnosis, I have not yet been treated with anything. What treatments can help him?
Question: Hello! Please tell me whether a slow reaction, memory loss, and incomprehension can be signs of atherosclerotic lesions? The suspected patient is a 55-year-old man. He always answers questions after a long pause. If yes, how can this be treated?
Question: Is it possible to engage in physical exercise with atherosclerosis?