Abnormal hardening of the walls of an artery: Arteriosclerosis / atherosclerosis – Symptoms and causes
Stroke Medical Terminology – Neurotrauma Program
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Acquired: Not inherited, or present at birth (congenital), but developing after birth.
Acute: Of abrupt onset, in reference to a disease; an illness that is of short duration, rapidly progressive, and in need of urgent care.
Anemia: A condition marked by deficiency of red blood cells or of hemoglobin in the blood, resulting in an unhealthy pale appearance and weakness.
Aneurysm: A localized widening (dilation) of an artery, vein, or the heart.
Arteriosclerosis: Hardening and thickening of the walls of the arteries.
Artery: A vessel that carries blood high in oxygen content away from the heart to the farthest parts of the body.
Atherosclerosis: A disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls.
Atrial Fibrillation (AFIB): A fast, irregular heart rhythm involving the upper heart chambers.
Blood clot: A mass of coagulated blood.
Blood pressure: The pressure of the blood within the arteries. Systolic pressure is measured after the heart contracts and is highest. Diastolic pressure is measured before the heart contracts and is the lowest.
Body Mass Index (BMI): A weight to height ratio, calculated by dividing one’s weight in kilograms by the square of one’s height in meters; used as an indicator of obesity and underweight.
Brain: The portion of the central nervous system that is located within the skull. The brain functions as a primary receiver, organizer, and distributor of information for the body.
Cardiovascular: Relating to the circulatory system, which comprises the heart and blood vessels and carries nutrients and oxygen to the tissues of the body and removes carbon dioxide and other wastes from them.
Carotid: Each of the two main arteries that carry blood to the head and neck.
Carotid Endarterectomy: A surgery to remove fatty deposits (plaque) that are narrowing the arteries in your neck.
Cerebral: Of or pertaining to the cerebrum or the brain.
Cerebrovascular accident (CVA): A stroke
Cholesterol: The most common type of steroid in the body.
Chronic: An illness that persists for a long time or is constantly recurring.
Coagulate: To cause a fluid, such as blood, to change into a soft, semisolid, or solid mass.
Computed tomography scan (CT Scan): Detailed images of internal organs are obtained by this type of sophisticated x-ray device.
Diabetes: A disease in which the body’s ability to produce or respond to the hormone insulin is impaired, resulting in abnormal metabolism of carbohydrates and elevated levels of glucose in the blood and urine.
Emboli: Something that travels through the bloodstream, lodges in a blood vessel and blocks it.
Embolism: Obstruction of an artery, typically by clot of blood or an air bubble.
Hemoglobin: A red protein responsible for transporting oxygen in the blood of vertebrates.
Hemorrhage: Bleeding or the abnormal flow of blood.
Hemorrhagic stroke: Occurs when a weakened vessel ruptures and bleeds into the brain.
Hypertension: Abnormally high blood pressure.
Ischemic stroke: Occurs when a blood vessel supplying blood to the brain is obstructed.
Magnetic Resonance Imaging (MRI): A procedure that uses magnetism, radio waves, and a computer to create pictures of areas inside the body.
Mechanical Thrombectomy: An emergency procedure used to remove a blood clot from a blood vessel (vein or artery).
Neurologist: A physician who specializes in the diagnosis and treatment of disorders of the nervous system.
Onset: The first appearance of the signs or symptoms of an illness.
Paralysis: Loss of voluntary movement (motor function).
Prognosis: The forecast of the probable outcome or course of a disease; the patient’s chance of recovery.
Rehabilitation: The process of helping a person who has suffered an illness or injury restore lost skills and regain maximum self-sufficiency.
Sickle Cell Disease: A severe hereditary form of anemia in which a mutated form of hemoglobin distorts the red blood cells into a crescent shape at low oxygen levels.
Sign: Any objective evidence of disease or dysfunction.
Stent: A tube designed to be inserted into a vessel or passageway to keep it open.
Stroke: The sudden death of brain cells due to lack of oxygen, caused by blockage of blood flow or rupture of an artery to the brain.
Symptom: Any subjective evidence of disease.
Telemedicine: The remote diagnosis and treatment of patients by means of telecommunications technology.
Transient Ischemic Attack (TIA): a temporary blockage of blood supply to the brain (mini stroke).
Tissue Plasminogen Activator (tPA): An enzyme that helps dissolve clots.
Vein: A blood vessel that carries blood that is low in oxygen content from the body back to the heart.
Warfarin: An anticoagulant drug.
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Pathological deformities of the carotid arteries
The problems of treatment and prevention of cerebrovascular diseases remain one of the most urgent, since cerebrovascular accidents continue to occupy a leading position among the causes of persistent disability and mortality of the population throughout the world. Vascular diseases of the brain are the main cause of ischemic stroke. It has been proven that lesions of the extracranial internal carotid (ICA) and vertebral arteries in 65-70% of cases lead to ischemic disorders of cerebral circulation. Pathological deformities (PD) of the ICA are among the most common diseases of brachiocephalic vessels, second only to atherosclerosis in frequency. PD of the ICA lead to cerebrovascular accidents of varying severity [1-6]. The overall frequency of PD ICA among the adult population, according to the results of angiographic and pathomorphological studies, varies from 10 to 40%.
In children with manifestations of brain failure, this pathology occurs in 14-30% [2, 7, 8].
The etiology and pathogenesis of PD ICA are not fully understood. Most authors believe that their origin may be congenital or acquired. Evidence of the congenital origin of PD ICA is the presence of deformities of the carotid arteries in childhood and young age, frequent bilateral lesions, a combination of carotid artery lesions with other manifestations of systemic connective tissue dysplasia [9-11] – Marfan and Elars-Danlos syndromes [12], coarctation of the aorta, vascular hypoplasia [13—16]. The causes of acquired PD are considered to be a weakening of the elastic skeleton of the artery wall, atherosclerosis, age-related changes in the cervical spine, hypertension, diabetes mellitus, and obesity [1, 2, 5, 17, 18].
Congenital PD ICA occupy the 1st place among the causes of cerebrovascular accident in childhood. According to Yu.V. Smirnova [8], PD ICA occurs in 26.
9% of children with neurological symptoms. M.A. Lobov et al. [7] identify PD as one of the main causes of vasopathic headaches in childhood, registering them in 1/3 of cases. The incidence of PD in boys and girls is comparable.
Initial manifestations of cerebrovascular insufficiency usually occur in children 4-6 years of age. These include a delay in speech development, late formation of self-service skills, impaired adaptation in a team, hyperexcitability and irritability. Later, by 5-6 years of life, headaches join. The described symptoms are non-specific and may mask vascular anomalies of the carotid arteries, so an ultrasound examination of the vessels of the neck in the presence of such a clinic is mandatory. Acute cerebrovascular accidents in children occur quite rarely: transient cerebrovascular accidents – in 4.3% of cases, ischemic stroke with the development of focal lesions of the brain substance is observed even less often – in 2.1% [7, 8, 10, 15-17] . A feature of the clinical picture of PD in children is epileptic seizures (in 19.
3% of cases).
The predominant types of ICA PD are couling, C- and S-shaped crimps (20-30%). This is due to intrauterine development disorders [1, 13, 18-20]. Back in 1925, A. Kelly [21] believed that the loops are formed at the 5-6th week of embryo development. The ICA originates from the third gill arch and the dorsal aorta, at the junction of which a distinct inflection is formed, which manifests itself in a 5-week-old embryo. In the process of further development of the fetus, due to the lowering of the heart into the chest cavity and its vertical turn along the axis, the carotid artery straightens. If this straightening or turning turns out to be incomplete, this leads to the formation of bends, loops, and kinks of varying severity. Another factor contributing to the deformities may be a more pronounced growth of the arteries of the aortic arch compared to the growth of the neck. This is confirmed by the presence of tortuosity of the ICA in embryos and children at the level of the location of the glossopharyngeal nerve [13, 19].
The frequency of such anomalies in newborns ranges from 5 to 10% [2, 10, 11].
Data on the etiological factors leading to dysembryogenesis and the development of congenital vascular deformities are not available in the literature. It should be noted that bends and loops can also be found in the cerebral, coronary, retinal and vertebral arteries, but they are more often acquired. Bends of the coronary arteries are associated with hypertension and myocardial infarction, retinal arteries with retinopathy in malignant hypertension and diabetes mellitus, muscle and heart capillaries with arterial hypertension and diabetes mellitus, and veins with varicose disease [22].
B. Callewaert et al. [23] describe a special “arterial tortuosity syndrome”. This is a congenital disease with an autosomal recessive type of inheritance (defect of the gene SLC2A10 ), which is characterized by tortuosity, elongation and the formation of aneurysms of large arteries due to a violation of the structure of the elastic fibers of the media of the vascular wall.
The combination of tortuosity and arterial aneurysms is the main feature of Loeys-Dietz syndrome, a congenital disease with a mutation in the TGF β receptor. At the same time, the aneurysm is primary and becomes the background for the development of tortuosity.
Yu.V. Smirnova [11] proved that the trait of a tortuous ICA can be inherited in an autosomal dominant or autosomal recessive manner. An association of polymorphism A80807T of the transcription factor gene 8p4 with pathological tortuosity of the carotid arteries was established. The probability of having PD ICA in homozygotes A80807/A80807 compared to carriers of the other two genotypes (A80807/T80807, T80807/T80807) is 1.64 times higher.
M.A. Lobov et al. [10, 24] also indicate the hereditary determinism of PD ICA in children. According to them, the frequency of familial cases is 50%. Segregation analysis of these cases demonstrates that PD ICA can be either isolated or a manifestation of hereditary syndromic connective tissue pathology.
The segregation frequency is 45% [24]. Hypoplasia, aplasia and anomalies in the position of the arteries are regarded by researchers as nonspecific signs of dysembryogenesis and are classified as precerebral angiodysplasias.
In recent years, the issue of the role of congenital inferiority of connective tissue in the formation of PD ICA has been discussed. Clinical observations of a combination of elongation and deformities of the carotid and vertebral arteries with phenotypic signs of hereditary connective tissue pathology, Elars-Danlos, Marfan, Sturge-Weber syndromes are presented [5, 9, 12, 15]. At the same time, combinations of PD ICA with the above syndromes are described in isolated cases. It should be noted a higher incidence (60%) of small forms of connective tissue dysplasia in children with PD ICA, such as joint hypermobility, skin hyperextensibility, muscle hypotension, posture disorder, flat feet, mitral valve prolapse, abnormal chords, abnormal growth and development of teeth.
However, the degree of “phenotypic tension” of the signs does not reach the severity corresponding to the established criteria for diagnosing the syndrome of connective tissue pathology [24]. Therefore, the question whether PD ICA in children can be considered a manifestation of connective tissue dysplasia syndrome remains open.
The pathomorphological features described by P.O. Kazanchyan et al. [1], including degenerative changes in elastic fibers, compensatory hyperelastosis, multiplication of the internal elastic membrane, development of mucoid edema, proliferation of smooth muscle cells.
The most acceptable hypothesis of the pathogenesis of carotid anomalies is the appearance of defects in the structure of elastin and collagen due to endogenous or genetically determined increase in the activity of degradative enzymes – collagenase and elastase [20, 25-27]. It is worth emphasizing that the same changes in the structure of elastin and collagen are considered the main pathogenetic factor in the development of vascular pathology, both congenital and acquired.
A possible cause of the development of PD ICA in children may be a birth injury, overstretching of the neck structures during childbirth. It is known that collagen fibers under conditions of uniaxial tension are the main factor preventing deformations. Collagen concentration correlates positively with tensile strength and negatively with maximum relative elongation. The experiment proved that when collagen is removed from the vascular wall, the tensile strength and stiffness decrease, and when elastin is removed, the wall strength and relative deformation decrease. A significant content of elastin in the wall of the carotid artery determines its greater reserves of extensibility compared to the vertebral artery. O.V. Kalmin [28] proposed a hypothesis about the sequence of damage to the structures of the neck during hyperextension, hyperflexion and longitudinal stretching during childbirth. The nerve trunks have relatively little extensibility and the least rigidity, while the wall of the common carotid artery (CCA), on the contrary, has the greatest extensibility and the least rigidity.
With hyperextension, the phrenic nerve has the highest risk of damage, followed by the vagus, and damage to the carotid artery wall is unlikely. With hyperflexion, the spinal cord can be damaged first of all, and only after the rupture of the ligaments of the spine will massive damage to the walls of the arteries occur. With longitudinal stretching of the neck, the main part of the deforming load will fall on the vertebral trunk and its ligaments, then the nerve trunks, the vertebral artery and, lastly, the carotid artery. OSA has the largest elongation reserve – 33.8%, without disturbing the structure and functions of the neck structures. Based on the foregoing, it follows that damage to the CCA during childbirth is unlikely [1, 18]. At the same time, ICA remains outside the attention of researchers. With longitudinal stretching during childbirth, in our opinion, the greatest load occurs on the area where the carotid artery enters the skull, which can lead to the development of deformities.
The question of the appropriateness of surgery for PD ICA in children remains open. There is evidence that in some children in the process of growth, the straightness of the vessel path is restored, and in some patients the deformity persists with leveling of local hemodynamic disorders [1, 8]. It should be taken into account that generalized epileptic seizures, which often occur with anomalies of the carotid arteries, are a contraindication to surgery [6, 8, 11]. Still, conservative therapy is considered to be a priority direction in the treatment of children [7, 15, 17]. With its ineffectiveness, an increase in neurological symptoms and a decrease in the rate of cerebral blood flow, surgical intervention is necessary. Reconstructive elimination of the deformity leads to a decrease in the manifestations of chronic brain failure in the immediate postoperative period in all patients [2, 4]. At the same time, among the literature data, we did not find scientific studies evaluating the impact of surgical or conservative treatment of children with PD ICA on their quality of life in the postoperative period.
Acquired pathological deformities of the ICA rank second among the causes of ischemic disorders of cerebral circulation, second only to atherosclerosis [1, 4—6, 18, 20, 22, 25]. PD ICA occur predominantly in patients over 60 years of age. It is believed that kinking is detected in 5-16% of patients, more often in men [1, 4, 29, 30], although there are reports of a prevalent lesion in women, which is explained by damage to the elastic framework of blood vessels associated with hormonal changes [31-33] . L. Del Corso et al. [34] based on study 469patients with PD (tortuosity, kinking and bending) confirm the high incidence of lesions among women. E. Ballotta et al. [35] consider that asymptomatic carotid kinking in women progresses with age and becomes symptomatic after 60 years of age. R. Zanetti et al. [6] indicates that in adults, changes in the length and shape of the carotid arteries most often appear in the sixth decade of life, while the ratio of men and women is 4:1. Perhaps such disagreements are related to the presence of concomitant pathology in patients – atherosclerosis, hypertension, diabetes mellitus, hyperlipidemia, hormonal changes, as well as the influence of toxic substances and smoking.
The clinical picture is characterized by disorders of cerebral circulation. The most common symptoms are dizziness, cochlear, sensory and cognitive impairment, ischemic retinopathy. Symptoms of cerebral ischemia in the hemisphere on the side of the ICA tortuosity occur in 26% of patients, cerebral manifestations – in 41.75%, their combination – in 27.5%. There are data on the dependence of the clinical picture on the type of PD ICA. C- and S-deformities most often occur asymptomatically – about 70% of cases, kinking, loop- and spiral-shaped tortuosity have severe clinical symptoms – in more than 80% of cases [18, 35, 36]. The development of symptoms also depends on the severity of the angle in the kinking segment – the sharper the angle, the more severe the lesions. At an angle of less than 45°, all patients have severe cerebral symptoms requiring surgical intervention [18, 19, 36].
Among the types of PD ICA, kinking, elongations and kinks are most often described, which is associated with the peculiarities of the origin of acquired deformities.
So, Z.K. Mackevicius et al. [37] distinguish a group of causes of PD ICA, subdividing them into 2 subgroups. The first is a kink at the site of the carotid artery in the area of the end of an atherosclerotic plaque, the second is kinks and deformities based on age-related destructive changes in the muscular-elastic skeleton of the arterial wall. Arterial hypertension that appears with age contributes to the aggravation of PD, since vascular deformities become a functional device to reduce the pulse wave and ensure blood flow uniformity [4, 19, 25]. However, P.A. Paulyukas and E.M. Barkauskas [29] believe that in these cases, hypertension is secondary, has a reflex character and develops in response to cerebral ischemia. As hemodynamic studies show, elimination of kinks and loops of brachiocephalic vessels reduces systemic arterial pressure [5, 9, 18, 25].
According to N.V. Vereshchagin and A.N. Koltover [20], hypertension is the primary cause of PD ICA. In response to increased pressure in the walls of the carotid arteries, adaptive changes occur in the form of focal and circular muscular-elastic thickening of the intima, sclerosis of the inner and middle membranes with destruction of the elastic framework.
As sclerotic changes develop, the muscular and elastic elements of the arteries are lost, their tone is lost, as a result of which, against the background of arterial hypertension, pathological tortuosity and kinks of these vessels with pronounced septal stenosis are formed. The latter, by restricting blood flow, can act as an independent pathogenetic factor of cerebrovascular accidents. Hypertension, according to J. White et al. [27], leads to stretching of the smooth muscle cells of the vessel media, loss of elastin and fragmentation of elastomers. The progression of these processes is the cause of pathological elongation of the vessel. Data from P. Pancera et al. [38] demonstrate a clear predominance of hypertension in patients with kinking compared with individuals without vascular anomalies. However, D. Radak et al. [39] believe that there is still no clear understanding of the pathogenetic relationship between known vascular risk factors and the development of kinking.
The main cause of the development of acquired PD ICA in patients over 60 years of age is atherosclerosis.
The question remains open – what is primary, atherosclerosis or PD? There is no consensus among researchers on this matter. Some believe that atherosclerosis leads to the development of destructive changes in the elastic skeleton of the vessel and, together with arterial hypertension, contributes to the development of deformities such as elongation and kinking [4—6, 19, 20, 22, 31, 32, 37, 40-42]. Other authors call atherosclerosis an aggravating disease in PD ICA. Violation of local hemodynamics in the bending zone of a deformed vessel leads to trauma to the intima, damage to the endothelium and the launch of a pathological process [1, 5, 20, 29, 34, 38]. Based on this, early atherosclerosis should develop in the carotid arteries, clinically and angiographically manifested before the age of 40, which is not confirmed by the literature data [2, 19, 37, 40, 41]. Other researchers have proven that when bending, a pressure difference is created at the outer and inner radius, leading to the development of hemodynamic flow turbulences and, as a result, the growth of the endothelium and connective tissue in the vessel.
At the same time, signs of proliferative-sclerotic remodeling are found in the vessel due to the activation of the immune system – high apoptotic activity of smooth muscle cells and the development of chronic inflammation in the tortuosity zone [42]. At the same time, in a series of morphological studies, there are no data on inflammation and the presence of vasculitis [20, 37, 38, 43].
It is important that it is atherosclerosis in PD that increases the risk of stroke by several times. This combination is observed in 40-70% of patients with cerebrovascular accidents [1, 4, 19, 22, 31, 34, 38, 41, 43].
Fibromuscular dysplasia is considered one of the important causes of the development of PD ICA. Accurate data on its incidence of dysplasia in PD ICA are not available. It is believed that fibromuscular dysplasia and PD ICA occur more often in middle-aged people, although there are data on patients over 60 years of age. The mechanism of development of carotid deformities in this disease is unknown.
Fibromuscular dysplasia is a non-atherosclerotic and non-inflammatory disease of the arteries with a predominant lesion of the renal arteries and ICA, which develops predominantly in young women. The predominant pathomorphological variant of carotid lesions in fibromuscular dysplasia without PD is medial fibroplasia. It is characterized by fibrosis with partial or total damage to the media, complete or partial loss of elastic fibers. This leads to the formation of multiple aneurysms, as a result of which the vessel resembles a “string of beads”. In addition to the development of aneurysms, vascular bundles, occlusion of the vascular lumen, and vascular ruptures are possible. It can be assumed that the commonality of the pathological process in fibromuscular dysplasia and PD ICA – the loss of the elastic framework of the vessel, is probably a significant factor for the development of pathological flexures in fibromuscular dysplasia [44-47].
Age-related changes in the vertebrae of the cervical spine are considered an important factor in the development of acquired AP ICA.
Vertebrogenic compression contributes to hemodynamic disturbances and the development of ICA PD. In patients with tortuosity, there is a forward displacement of the head, smoothing of the cervical lordosis, kyphosis in the thoracic region, a pronounced tension of the sternocleidomastoid, scalene muscles and muscles located above and below the hyoid bone. Shortening of the muscles of the anterior surface of the neck and deformation of the fascia lead to extravasal effects on the carotid and vertebral arteries [18, 48]. Thus, mechanical deformations of the fascia against the background of disorders in the cervical spine can be considered as one of the reasons for the formation of arterial deformities. R. Wirbel et al. [49] proved that hyperextension and rotation effects on the cervical spine that occur during manual therapy sessions, sports, such as wrestling, can lead to damage to the vertebrobasilar vessels. A number of authors believe that although most injuries of the neck vessels occur without a cause visible to the patient, a minor injury of the cervical region is detected in 80% of cases [50].
With significant displacements of the vertebrae or their parts, abrupt changes in the normal course of the vessels are detected, while macroscopically observed twisting, compaction and overextension of the vertebral and carotid arteries.
Other causes of PD ICA include diabetes mellitus, hyperlipidemia, and other vascular risk factors [2, 5, 6, 20, 34, 38, 41].
Possible factors contributing to the development of PD ICA are smoking, taking contraceptives, and toxic effects [5]. According to the new theory of D.D. Zerbino [51, 52], heavy metals damage the muscular-elastic skeleton of the arteries and lead to the development of arteriosclerosis and arterial hypertension [51]. It has been proven that the toxic effect of cadmium leads to massive elastolysis of the media due to the activation of elastase and the development of aortic aneurysms. It is known that heavy metals contained in cigarettes cause irreversible changes in the coronary arteries, leading to the development of atherosclerosis and myocardial infarctions in patients under 40 years of age.
Smoking and many years of professional contact with toxic substances are important causes of the development of vascular pathology in middle age.
Some authors mention vasculitis among the possible causes of the development of PD ICA in young patients [20, 37, 43]. Z.K. Mackevicius and P.A. Paulukas [37] describe angiitis vasa vasorum , which is explained by ischemic damage vasa vasorum with the development of inflammation and subsequent severe sclerosis.
The mechanism of development of PD ICA in patients 40-50 years old remains unclear. In literary sources, the prevailing opinion is that they are the result of a violation of embryogenesis [2, 5, 22, 32, 35, 43]. Based on the foregoing, it follows that congenital deformities in children are characterized by loop-like deviations (couling), C- and S-shaped tortuosity, and for patients older than 60 years, kinking, elongations, and kinks. Whether the transition of one type of AP to another is possible remains unexplored.
Yu.V. Rodin et al. [53], with the help of mathematical modeling methods, a hypothetical assessment of the development of S-shaped crimp was given – any bend under certain conditions tends to an angular inflection. The results obtained are also valid for other types of tortuosity, since they usually contain an S-shaped tortuosity. At the same time, this hypothesis completely refutes the possibility of transition from one type of crimp to another and requires further research.
The pathomorphological picture of ICA PD is characterized by pronounced sclerotic changes in the vessel wall, destruction of the elastic framework, proliferation of connective tissue around the vessel [13, 20, 37, 38]. Since such changes contribute to stable irreversible deformations that increase with age, the question of whether changes in the configuration of deformations are possible remains open.
Surgical intervention is recognized as the most effective treatment for acquired PD ICA.
An indication for surgery is considered to be a hemodynamically significant PD of the ICA, commensurate with circulatory disorders characteristic of stenoses of 70% or more, regardless of the presence of neurological symptoms and / or hemodynamically significant atherosclerotic stenosis, as well as embologenic plaques that stenose the lumen of more than 50%, and plaques with pronounced surface and parietal thrombosis. The high efficiency of surgical intervention in patients with symptomatic PD of the ICA is known, at the same time, the question of the appropriateness of surgical intervention in patients with asymptomatic deformities remains open [1, 3, 4, 6, 19, 29, 35, 36, 42, 54].
In conclusion, we mention that a comparative analysis of the literature on congenital and acquired PD ICA showed that they have many distinctive features not only in origin and pathogenesis, but also in the clinic, treatment and prognosis. It is appropriate to assume that congenital and acquired PD ICA are two different diseases, the relationship between which has not been proven.
This review of the literature demonstrates the relevance of studying this disease, the presence of unresolved and controversial issues not only in the genesis, but also in the treatment tactics of managing patients, the need for a comprehensive clinical and pathomorphological study of this important vascular pathology.
Echocardiography: Cardiac Ultrasound – Vascular Innovation Center
Diagnosis in brief
Echocardiography (EchoCG) is a test that uses high-frequency sound waves (ultrasound) to examine the structure and function of the heart. The common non-medical name for this study is cardiac ultrasound. The study is absolutely harmless to humans.
Echocardiography uses reflected ultrasound waves to create an image of the heart, its chambers, valves, walls, and blood vessels (aorta, pulmonary arteries, and veins). The sensor of the ultrasound machine is located on the chest and sends ultrasonic waves that are reflected from the heart and are again captured by the sensor, after which the signal is transmitted to the machine, where it is converted into an image that is understandable to a specialist.
If it is necessary to assess the coronary reserve, stress echocardiography methods (stress echocardiography) are used.
Diagnosis at ISC
Our clinics have high-quality ultrasound equipment for performing cardiac ultrasound, which allows performing a full examination in outpatient and inpatient conditions. Our specialists have significant experience in such studies and enjoy a well-deserved reputation among colleagues and patients.
Indications and contraindications for diagnosis
Echocardiography is prescribed to detect heart disease and evaluate its function. Most often, an ECHOCG is prescribed by a cardiologist, in preparation for major vascular operations, an ultrasound of the heart can also be prescribed by the attending physician, or an anesthesiologist-resuscitator.
Echocardiography reveals:
- The size and shape of your heart, the thickness and movement of the walls of the heart.
- Assess the pumping function of the heart – ejection fraction
- Check the condition of the heart valves, whether the leaflets close, whether there is a narrowing in the area of the valves.
- The presence of aneurysms of the heart, blood clots in the cavities of the heart.
- Abnormal openings between the atria or ventricles.
- Check for infection on the valves.
- Echocardiography can assess the pressure in the pulmonary artery and its size
- Identify aneurysms of the ascending aorta.
- Fluid accumulation or disease of the outer lining of the heart (pericardium).
- Tumors of the heart.
Echocardiography is a safe test and has no contraindications.
Preparation for diagnosis
Echocardiography does not require any preparation. You can eat and drink as usual.
Diagnosis procedure
During cardiac ultrasound, the patient is placed on his back or left side. The sensor during echocardiography can be located in different planes for better visualization of the heart chambers. The sensor and the patient’s skin are wetted with a special water-soluble gel, which ensures tight contact between the sensor plane and the body.
Our cardiac ultrasound machines offer a variety of echocardiography options. One-dimensional echocardiography in M-mode allows you to reproduce the movement of the heart walls and valves in the form of a graph, which makes it possible to evaluate the function of the ventricles.
Two-dimensional echocardiography shows a section of the heart in a certain projection and allows you to determine the size of the cavities of the ventricles and atria, the thickness of their walls, evaluate the movements of the valves and walls of the ventricles, and detect thrombosis of the heart cavities.
Doppler mapping can reveal the speed and direction of blood flow in the cavities of the heart, which makes it possible to determine valvular insufficiency or stenosis, atrial and ventricular septal defects.
The usual procedure for echocardiography involves first identifying the heart valves; heart walls. Further, the nature of the movement of the valve leaflets is revealed, the thickness of the walls and the dimensions of the cavities of the heart are measured.
In conclusion, Doppler echocardiography reveals stenosis or insufficiency of the heart valves and pathological holes in the heart septa.
After diagnosis
Within half an hour, the doctor will prepare a conclusion on the results of an ultrasound examination of the heart. If a serious pathology is detected, a consultation with a cardiologist or cardiac surgeon will be offered.
Possible complications
Echocardiography has no complications and can be performed without restrictions.
Diseases
Echocardiography is regularly used in the diagnosis and treatment of patients with heart disease. It is one of the most widely used diagnostic tests in cardiology. It gives a lot of useful information, including the size and shape of the heart, the ability to contract various parts of the heart. An echocardiogram can also give doctors other important information about heart function, such as calculating cardiac output, ejection fraction, and diastolic function (how well the heart relaxes).
Echocardiography can help detect cardiomyopathies such as hypertrophic cardiomyopathy, dilated cardiomyopathy, and many others. The use of stress echocardiography can also help determine if any chest pain or related symptoms are related to heart disease. The biggest advantage of echocardiography is that it is non-invasive (does not require entry into body cavities) and has no known risks or side effects.
Echocardiogram can not only create ultrasound images of heart structures, but also accurately assess blood flow through the heart with Doppler echocardiography using pulsed or continuous Doppler ultrasound. This allows assessment of both normal and abnormal blood flow through the heart. Color Doppler, like spectral Doppler, is used to visualize any abnormal connections between the left and right sides of the heart, any leakage of blood through the valves (valvular regurgitation), and assess how well the valves are opening (or not opening in the case of valvular stenosis).