1. Impaired patency of the coronary arteries caused by their occlusion, narrowing, spasm.

2. Signs of compensation for impaired blood circulation (collateral blood flow, intense myocardiogram).

The classification of atherosclerotic lesions of the coronary arteries includes 5 characteristics:

I. Anatomical type of blood supply to the heart: right, left, balanced.

II. Localization of the lesion. Along the main trunks:

1) trunk of the left coronary artery;

2) anterior interventricular branch;

4) first diagonal branch;

5) right coronary artery;

6) marginal branch of the right coronary artery.

III. Prevalence of damage: localized (in the proximal, middle and distal third of the arteries) and diffuse forms of damage.

IV. The degree of narrowing of the artery lumen:

3) more than 75%,

4) occlusion.

Zero degree - to indicate unchanged arteries.

V. Collateral blood flow. Assessing the nature of collateral circulation therefore has important diagnostic value. Usually, with significant and widespread damage to the coronary artery and long-term course of coronary artery disease, coronary angiography reveals a well-developed network of collaterals, while in patients with a “short” ischemic history and stenosis of one coronary artery, the collateral circulation is less pronounced. The latter circumstance is of particular importance in cases of sudden thrombosis, which is usually accompanied by the occurrence of widespread and transmural necrosis of the heart muscle (for example, in relatively young patients with coronary artery disease).

Of great interest are data on the frequency and nature of damage to various coronary arteries. Lesions of the trunk of the left coronary artery were observed in 2.9% of patients, the anterior interventricular branch in 84% of patients, the right coronary artery in 62% and the circumflex branch of the left coronary artery in 48% of the examined patients.

· A feature of lesions of the anterior interventricular branch is that the pathological process in it is initially localized in the proximal areas with subsequent spread to the distal part of the vessel as the disease progresses. We identified localized lesions of the II segment of the anterior interventricular branch in 72.4% of patients, and in 27.6% of those examined, simultaneous lesions of the II and III segments of the artery were noted.

· Atherosclerotic changes in the right coronary artery are often localized. Only 12.1% of the patients we examined showed diffuse damage to the right coronary artery of the heart. Plaques are equally often localized in both the I and II segments of the artery, and the III segment (posterior interventricular branch), as a rule, is not affected by atherosclerosis.

Also in the distribution of atherosclerosis, simultaneous damage to several large branches is noted. Severe stenotic lesions of three coronary arteries simultaneously were detected in 40%, two in 41%, and one in 19%.

The degree of narrowing of the vessel is determined by a decrease in the diameter of its lumen compared to the proper one and is expressed as a percentage. Until now, visual assessment has been used, with the following characteristics: normal coronary artery, altered arterial contour without determining the degree of stenosis, narrowing< 50%, сужение на 51-75%, 76-95%, 95-99% (субтотальное), 100% (окклюзия). Существенным рассматривают сужение артерии > 50%.

In addition to the location of the lesion and its extent, coronary angiography may reveal other characteristics of arterial lesions, such as the presence of a thrombus, tear (dissection), spasm, or myocardial bridging.

Signs of coronary circulation disorders detected in patients with coronary artery disease during coronary angiography and having a particularly unfavorable prognostic value include:

1. Lesion of the left artery trunk.

2. Three-vessel lesion of the coronary artery (LAD, OB and RCA).

3. Narrowing of the lumen of the coronary arteries by 70% or more (especially coronary artery occlusion).

4. Poor development of collateral circulation.

The results of numerous examinations show a clear relationship between the nature of coronary lesions (according to angiography) and the clinical manifestations of coronary artery disease.

Left ventricular angiography (ventriculography)

Selective angiocardiography of the left ventricle (left ventriculography) is used to quantify congenital and acquired defects of the mitral and aortic valve, including subvalvular, valvular and supravalvular stenosis of the aortic mouth, aortic insufficiency, reliable radiological signs of hypertrophic cardiomyopathy and other diseases. Left ventriculography is of particular importance in the diagnosis of functional disorders of the left ventricle in ischemic heart disease.

Left ventriculography in patients with coronary artery disease allows:

1) detect regional dysfunction of the left ventricle in the form of local limited areas of akinesia, hypokinesia and dyskinesia;

2) diagnose a left ventricular aneurysm and assess its location and size;

3) identify intracavitary formations (mural thrombi and tumors);

Local disturbances in LV contractile function are an important sign of focal myocardial damage characteristic of IHD. There are three main types of such disorders, united by the concept of “asynergy”:

1. akinesia - lack of contraction of a certain (limited) area of ​​the heart muscle

2. hypokinesia - pronounced local decrease in the degree of contraction

3. dyskinesia - paradoxical expansion (“bulging”) of a limited area of ​​the heart muscle during systole

The most common causes of “asynergies” of the left ventricular myocardium are cicatricial changes, acute myocardial infarction, and severe transmural myocardial ischemia.

To calculate hemodynamic parameters, quantitative processing of images of the left ventricular cavity recorded in one of the projections at the end of systole and diastole is carried out. First, the area of ​​the cavity of the left ventricle (S) and its length, the so-called major axis (L), connecting the base and apex, are determined planimetrically. The estimated diameter along the minor axis of the ventricular cavity (D) is determined by the formula:

After this, the left ventricular volume (V) is calculated using the geometric ellipsoid model:

where V is the volume of the left ventricle, D is the estimated diameter along the minor axis, L is the length of the major axis.

Knowing the end-diastolic (EDD) and end-systolic (ESV) volumes of the left ventricle, you can easily calculate its stroke volume (SV):

УО = KDO – KSO.

Ejection fraction (EF), which reflects the percentage of shortening of the left ventricular myocardium during its contraction, is calculated as follows:

FV = UO / KDO,

where EF is the ejection fraction; SV - stroke volume; EDV - ventricular end-diastolic volume.

Another informative indicator of the contractility of the left ventricular myocardium - the average speed of circular shortening of fibers (V avg.) - is calculated by calculating the diameter along the minor axis of the ventricle (D) at the end of systole and diastole (the so-called end-systolic and end-diastolic dimensions left ventricle, or, respectively, CSR and CDR), as well as the total duration of blood expulsion (T):

V avg. = (KDR - KSR) / (KDR x T),

where EDR and ESR are the end-diastolic and end-systolic dimensions (diameters) of the left ventricle, T is the ejection time.

Normally, stroke volume (SV) is 70–110 ml, ejection fraction (EF) is 0.56–0.70, and the average rate of circular shortening of fibers is at least 1.2 s–1. An increase in left ventricular EDV of more than 90–100 ml indicates the presence of dilatation of the left ventricle caused by its volume overload (for example, with mitral or aortic insufficiency) or impaired myocardial contractility.

Selective contrasting of the ascending aorta makes it possible to clarify the location and size of the aortic aneurysm, as well as to diagnose a number of anomalies of this great vessel (para-aortic sinusoidal tract, infective endocarditis, etc.). Finally, selective injection of a radiopaque substance into the left atrium makes it possible to diagnose the presence of intracavitary formations (parietal thrombi, atrial myxoma, etc.).

Coronary angiography allows you to determine the cause - the anatomical substrate - one of the first and main constants of coronary heart disease, but cannot characterize its second component - the degree of ischemic imbalance causing functional and structural changes in heart tissue. It should be added that the degree of narrowing determined during coronary angiography does not fully correspond to the functional significance of the lesions, and in some patients with a narrowing of more than 70%, the coronary reserve may be normal, and in a patient with a narrowing of less than 50%, the coronary reserve can be significantly reduced.

ISCHEMIC CASCADE

In IHD, only those coronary circulatory disorders that lead to ischemic, necrotic or fibrotic changes in the myocardium are pathogenetically significant. Back in 1935, R. Tennant and C. Wiggers experimentally noted the appearance of disturbances in local contractility of the walls of the left ventricle when the coronary artery was clamped.

A decrease in coronary blood flow is accompanied by disruption of various parts of the functioning of the heart associated with oxygen consumption: β-oxidation, oxidative decarboxylation, oxidative phosphorylation. In turn, glycolysis is compensatory activated, which leads to excessive formation of pyruvate and a shift in the lactate-pyruvate equilibrium towards lactate. As a result, acidosis occurs, leading to disruption of ATP-dependent processes, as a result of which the intracellular concentration of calcium increases (impaired diastolic function) and myocardial contractility decreases. The opening of membrane potassium channels leads to the release of potassium from the cell. ADP present in the cell breaks down to adenosine, which, by stimulating adenosine a-receptors of afferent nerve endings in the myocardium, causes anginal pain. With prolonged ischemia, when the ATP level drops to 10% of normal, these processes become irreversible and lead to cell death. Clinically, this is manifested by a certain sequence of symptoms: diastolic dysfunction, systolic dysfunction, electrophysiological disturbances (changes in the T wave and ST segment) and, finally, pain, forming the so-called “ischemic cascade”. Angina pectoris represents its final stage, the tip of the iceberg, at the base of which lie the disturbances in myocardial metabolism that have arisen due to reduced perfusion.

However, a similar sequence of functional and morphological disorders occurs in the presence of two main conditions:

Damage to the main epicardial arteries;

Presence of stenosis of the main arteries of at least 50–70%

In most cases, local impairment of contractility of the heart walls (asynergia) occurs after impaired myocardial perfusion, but before the onset of other manifestations of ischemia, such as angina pectoris and ST segment depression. Thus, impaired local myocardial contractility is one of the earliest signs of myocardial ischemia.

Echocardiography currently plays a leading role in the diagnosis of coronary heart disease and its complications.

POSSIBILITIES OF ECHOCARDIOGRAPHY IN THE DIAGNOSIS OF IHD AND ITS COMPLICATIONS

The main areas of application of echocardiography in the diagnosis of coronary artery disease and its complications: 1) assessment of global contractility of the LV and RV myocardium (assessment of systolic function); 2) assessment of local myocardial contractility (diagnosis of areas of impaired local contractility); 3) assessment of LV and RV diastolic function; 4) diagnosis of complications of coronary artery disease.

B-mode and M-mode allow you to identify areas of local contractility impairment. The following contractility options are distinguished.

Normokinesis - all areas of the endocardium thicken evenly during systole.

Hypokinesis is a decrease in endocardial thickening in one of the zones during systole compared to other areas. Hypokinesis can be diffuse and local. Local hypokinesis, as a rule, is associated with small-focal or intramural myocardial damage; in some cases it can be noted against the background of large-focal non-extended myocardial infarction. Hypokinesis can be a consequence of frequent ischemia in any zone (hibernating myocardium) and be transient. It must be remembered that against the background of large dilatation of the heart chambers, judgments about areas of impaired local contractility may be erroneous.

Akinesis is the absence of thickening of the endocardium during systole in one of the areas. Akinesis, as a rule, indicates the presence of a large-focal lesion. Against the background of significant dilatation of the heart chambers, it is impossible to reliably judge the presence of an akinesis zone (if the LV diastolic diameter exceeds 65 mm).

Dyskinesis is a paradoxical movement of a section of the heart muscle during systole (bulging). Dyskinesis is characteristic of an aneurysm.

Paradoxical movement of the IVS can also be observed in the following cases: 1) against the background of blockade of the branches of the His bundle (blockade of the left branch of the His bundle or a combination of blockade of the left anterior and right branches of the His bundle); 2) permanent or temporary cardiac stimulation - pacemaker (the electrode is visualized in the right sections); 3) against the background of pulmonary hypertension (IVS moves towards the LV in diastole); 4) against the background of pericarditis.

To clarify the localization of zones of impaired local contractility, the LV and RV myocardium are conventionally divided into segments. There are several options for dividing the myocardium into segments. Since the method does not allow tracing coronary blood flow and resolving the issue of the type of blood supply to the myocardium, it is practically impossible to reliably judge which coronary artery is affected. However, with the “left” type of blood supply, segments 6, 5, 12, 11 are supplied by the right coronary artery; segments 4,10,3,9 - left circumflex artery; segments 1,2,7,8, 13, 14, 15 - left anterior descending coronary artery. The LV is divided into the basal region, the middle third and the apical region. The basal section starts from the atrioventricular ring and ends at the level of the end of the papillary muscles, the middle third - from the end of the papillary muscles to their base, the apical section - from the apex to the base of the papillary muscles.

Scheme of dividing the myocardium into segments (Otto S.M., Pearlman A.S., 1995). Target type diagram (Otto S.M., Pearlman A.S., 1995). Division of the myocardium into segments.

WMSI= sum of indexes/number of segments.

To do this, the state of local contractility of each myocardial segment is assessed using a 5-point system (various versions of this classification are found in the literature): 1 - normal; 2 - slight and moderate hypokinesis; 3 - significant hypokinesis; 4 - akinesis; 5 - dyskinesis. Calculations are extremely simplified if you have a computer, since a special program allows you to do them very quickly. Normally, WMSI = 1. In the case when WMSf> 2, the ejection fraction is less than 30%.

When an area of ​​impaired local myocardial contractility is detected and its location is clarified, it can be assumed which of the coronary arteries is damaged.

Damage to the left anterior descending artery is a violation of local contractility in the area of ​​the anterior septum, anterior wall, and anterior apex of the LV. When the diagonal branches are damaged, contractility in the lateral wall area is impaired. If the anterior descending artery supplies blood to the entire apex, the apical segments of the posterior and posterolateral walls will be affected. Depending on the level of arterial damage, it is possible to identify zones of impaired local contractility in one or another part of the LV. When the lesion is localized in the distal third of the vessel, only the apex is affected, in the middle third of the vessel - the middle section of the LV and apical segments, in the proximal section - the entire wall, including the basal sections of the myocardium.

Damage to the circumflex artery leads to impaired local contractility in the area of ​​the lateral and posterior walls of the LV. In this case, individual characteristics of the blood supply to the myocardium are possible.

Damage to the posterior descending artery leads to impaired local contractility in the posterior wall of the LV.

Damage to the right coronary artery, as a rule, leads to impaired local contractility of the RV and posterior IVS.

ECHOCARDIOGRAPHIC CHANGES IN PATIENTS WITH IHD

Patients with coronary artery disease make up the largest percentage of studies, both in hospital and outpatient settings. Knowing the capabilities of the method eliminates unreasonable referral for research and greatly facilitates the selection of therapy.

In patients with exertional angina, calcification of the aortic walls, the left fibrous atrioventricular ring of varying degrees, and type I impairment of LV diastolic function can be observed. The LA may be slightly dilated in length. LV systolic function is usually preserved. There are no zones of local contractility impairment.

Against the background of unstable angina, there is also calcification of the fibrous ring and aortic walls, impaired LV diastolic function type I with a significant increase in DTE. LV systolic function is preserved or moderately reduced. A zone of hypokinesis or akinesis may be noted, which disappears while taking nitroglycerin. As a consequence of calcification of the base of the posterior leaflet of the MV, mitral regurgitation is recorded.

In the acute period, with small-focal lesions, it is possible to detect hyperkinesis of the myocardium of the intact zone, impaired diastolic function of the LV of type 1, with subsequent normalization during therapy. LV systolic function may be normal or moderately reduced. During the assessment of local contractility, in some cases a zone of hypokinesis can be identified.

Intramural or suoendocardial widespread myocardial infarction. Against the background of a widespread lesion, a zone of hypokinesis is diagnosed, impaired diastolic function of the left ventricle according to type I; impaired systolic function may be absent or moderately pronounced. Pathological mitral regurgitation is often recorded, rarely - thrombosis in the affected area. In the acute period, hyperkinesis of the intact myocardium can be observed.

Large-focal non-extended myocardial infarction. In the acute period, with large-focal lesions, hyperkinesis of the intact myocardium, hypo- or akinesis in the infarction zone can be observed. However, in some cases, the area of ​​impaired local contractility may not be visualized. LV diastolic function is impaired according to type I and can be quickly restored with therapy. LV systolic function may remain unchanged (Fig. 8).

Large focal widespread myocardial infarction. This type of myocardial infarction is characterized by the presence of a zone of akinesis or dyskinesis. With extensive damage, dilatation of the LV cavity and impaired LV systolic function of varying degrees of severity may develop. As a rule, there is pathological mitral regurgitation and type I impairment of LV diastolic function. In the acute period, the process is accompanied by hyperkinesis of the intact myocardium. In some cases, a small amount of fluid can be observed in the pericardium in the affected area - reactive pericarditis (Fig. 9).

Complications of myocardial infarction

Aneurysm formation. Currently, it is customary to distinguish two types of aneurysms - true and false. A true aneurysm is formed, as a rule, in the area of ​​the apex and IVS and is characterized by wall thinning and dyskinesis. In some cases, the aneurysm cavity is lined with a thrombus. A false aneurysm is formed, as a rule, in the region of the basal part of the posterolateral wall of the LV during extensive myocardial infarction due to thinning of the wall and its protrusion or rupture of the wall with thrombosis of the cavity. In some cases, the phenomenon of blood stagnation can be noted in the cavity of the false aneurysm. The literature describes cases of the formation of a false aneurysm in the area of ​​the LV apex. The presence of a zone of dyskinesis is not a decisive factor in the diagnosis of LV aneurysm. It is generally accepted that an aneurysm is also diagnosed if there is an extensive zone of akinesis, occupying more than 40% of the LV area.

Thrombosis of the LV cavity during myocardial infarction. The thrombus can be parietal or pedunculated. A parietal thrombus most often lines the cavity of the LV apex in the affected area. By the nature of the thrombus one can judge how old it is, since “fresh” blood clots have high echogenicity and areas of recanalization. The “old” thrombus has areas of calcification. It must be remembered that a parietal thrombus strengthens the wall of the aneurysm and in some cases saves the life of the patient.

A pedunculated thrombus floats in the bloodstream and can be a source of embolism in the systemic circulation. A pedunculated thrombus should be differentiated from the papillary muscle, which contracts during systole. It is necessary to try to lyse this thrombus, since the risk of its separation is high. We observed an effect up to complete lysis of the thrombus against the background of traditional therapy with disaggregants and anticoagulants just a few days after its start. In some cases, two or more thrombi occur in the LV cavity. Thrombosis of the cavity can be observed against the background of extensive myocardial damage, with subendocardial infarction, in patients with dilated non-ischemic cardiomyopathy and low cardiac output, as well as against the background of dyshormonal disorders.

Dressler's syndrome is a complication of extensive myocardial infarction, which is characterized by the presence of fluid in the pericardial cavity and pleural cavities; As a rule, the amount of liquid is insignificant. Adhesions form in the pericardial cavity. Systolic and diastolic functions are impaired, dilatation of the heart chambers, pathological mitral regurgitation, and pulmonary hypertension occur.

Rupture of the IVS with the formation of an acquired defect is one of the most serious complications of myocardial infarction. Most often occurs with a widespread anteroseptal infarction in the area of ​​the lower third of the septum. Characterized by a sharp disturbance of hemodynamics. The patient experiences a rough systole-diastolic murmur, the intensity of which may gradually increase due to the enlargement of the defect opening. The murmur is best heard at the right edge of the sternum. When the IVS ruptures, part of the blood will initially be discharged from left to right - from the LV to the right parts of the heart, which leads to a rapid increase in pressure in the right parts and to the formation of significant pulmonary hypertension. If the pressure in the right parts exceeds the pressure in the left parts of the heart, a pathological discharge of blood from right to left occurs. Doppler echocardiography makes it possible to clarify the location of the defect, the volume of the shunt, and the nature of the discharge. Signs of IVS rupture are: dilatation of the right side of the heart; blood shunting initially from left to right, turbulent systole-diastolic flow can be recorded using pulsed wave, continuous wave and color Doppler; paradoxical movement of the IVS and MPP due to pulmonary hypertension; pathological tricuspid regurgitation; pulmonary hypertension.

Blood stagnation (clumping of blood cells) in the form of a spontaneous contrast effect can be observed in the cavity of a large aneurysm with low output. Reminds me of a snow storm. The risk of thrombosis and embolism in this case is high.

Papillary muscle dysfunction. It is observed with extensive infarctions with damage to the lateral wall. It is characterized by dilatation of the left cavities of the heart, pathological mitral regurgitation with eccentric propagation of the jet, prolapse of the mitral valve by more than 5 mm. LV systolic function is impaired. You can observe the detachment of the valve chords and a chordal squeak. The pressure in the LA cavity increases rapidly, which leads to an increase in pressure in the pulmonary circulation

Myocardial tear or dissection is rare. Observed in the area of ​​the IVS or lateral wall. Leads to the formation of a wall aneurysm and severe hemodynamic disturbances. Requires surgical correction. The literature describes cases of dissection of the RV myocardium when it is damaged, which is most often combined with an infarction in the region of the posterior wall of the LV with extensive damage.

The coronary circulatory system, thanks to the mechanisms of autoregulation, has amazing adaptability to various influences. Often, at rest, patients, even with severe stenotic coronary atherosclerosis, do not have clinical and instrumental-laboratory manifestations of coronary artery disease. Therefore, to identify the discrepancy between the metabolic needs of the heart muscle and the state of the coronary circulation in echocardiography, various stress tests have also been used, provoking an increase in the myocardial oxygen demand and causing the appearance of instrumental signs of myocardial ischemia.

Stress echocardiography with physical activity was first proposed in 1979, only in 1985 its clinical significance was shown, and only in the last 10-15 years has the method become widespread.

STRESS ECHOCARDIOGRAPHY

The traditional method for identifying coronary artery pathology as the basis of coronary heart disease is electrocardiographic diagnostic methods, especially stress tests on a bicycle ergometer or treadmill. It is known that electrocardiographic stress tests consist of recording a series of stress ECGs until the appearance of electrocardiographic and/or clinical signs of ischemia. However, there are situations in which electrocardiographic stress tests are not diagnostically useful. Such situations are possible with an altered resting ECG, bundle branch block, WPW (Wolf-Parkinson-White) syndrome, and the presence of “silent” myocardial ischemia, in which in patients with complaints of angina, the results of an electrocardiographic stress test are negative or questionable. Stress EchoCG is an effective complement to stress ECG data. Using stress ECG, you can evaluate both general and regional kinetics of the LV walls

In everyday clinical practice, it is necessary to take into account that disorders of local and general LV function may have a number of features: a) regional contractility disorders appear much earlier than clinical and ECG signs of ischemia; 6) regional contractility disorders appear much earlier than disturbances in the global (pumping) function of the LV. An important advantage of stress echocardiography compared to other methods for diagnosing coronary heart disease is that despite the variety of clinical forms of coronary artery disease, for all its manifestations the use of stress echocardiography is currently extremely informative and often the determining diagnostic procedure.

The diagnostic capabilities of the stress echocardiography method allow, from a clinical point of view, to make certain judgments about the pathology of the coronary arteries, the functioning of the ischemic myocardium and its viability. Based on the characteristics of the development of pathophysiological and pathomorphological changes in ischemic heart disease, it is possible to formulate a list of diagnostic capabilities of stress echocardiography.

DIAGNOSTIC CAPABILITIES OF STRESS ECHOCARDIOGRAPHY METHOD

1. Assessment of the functional significance of pathological changes in the main coronary arteries and pathology of the myocardial blood supply not associated with damage to the main coronary arteries:

Anatomical stenoses of the coronary arteries, their localization, prevalence and severity;

- “dynamic” stenoses of the coronary arteries (transient thrombotic occlusions);

Predisposition of the coronary arteries to spasm (Prinzmetal's angina); pathology of small coronary arteries (syndrome "X");

Insufficiency of myocardial blood supply and subendocardial ischemia with arterial hypertension and other causes of increased end-diastolic pressure in the LV.

2. Assessment of pathological changes and features of myocardial functioning during ischemia:

changes in the functioning of morphologically unaffected myocardium during ischemia that occurs against the background of various stress tests in individuals with stenotic lesions of the coronary arteries;

changes in the functioning of the myocardium in the syndrome of “fatigued” chronic myocardial ischemia (“hibernation” syndrome);

changes in the functioning of the myocardium in the syndrome of “stunned” acute myocardial ischemia (C “stunning” syndrome) without the development of necrotic changes;

changes in the functioning of the myocardium in various types and forms of ischemic necrosis, mainly in myocardial infarction;

changes in myocardial functioning before and after cardiac revascularization operations (coronary artery and mammary coronary bypass grafting, coronary angioplasty and stenting).

3. Assessment of pathological changes and features of the functioning of the “non-viable” myocardium with cicatricial, severe cardiosclerotic, as well as with severe inflammatory (myocarditis), myocardial-dystrophic changes and various cardiomyopathies.

Clinical indications for the use of stress echocardiography are actually determined by the ability of this method to obtain data on the pathology of various parts of the coronary blood supply, information on the nature of the functioning of the myocardium in the syndromes of “fatigued” and “stunned” myocardial ischemia, and on the characteristics of the functioning of viable and non-viable myocardium.

Contraindications to stress echocardiography are divided into 3 main groups:

a) general clinical contraindications used when conducting all types of stress testing;

b) electrocardiographic contraindications used when conducting all types of stress testing;

c) contraindications related to the characteristics of the physical, pharmacological and other stress agents used during stress echocardiography.

BASIC STANDARD ULTRASONIC POSITIONS AND PROJECTIONS. USED ​​FOR STRESS ECHOCARDIOGRAPHY

For stress echocardiography, as a rule, three main transthoracic positions of the sensor are used: parasternal (section along the long axis, along the short axis at the level of the mitral valve, papillary muscles and apex of the heart), apical (five-, four-, three-, two-chamber projections ) and subcostal (section along the long and short axes). The generally accepted scheme of division into 16 segments, adopted by the American Association of Echocardiography, is when each segment corresponds to about 6% of the LV area of ​​the heart. There is a good relationship between the isolated segments and the coronary arteries supplying blood to these segments.

Ultrasound projections	Evaluated segments of the LV	Coronary arteries, predominantly* supplying blood to the assessed segments
Parasternal left ventricular long axis (PLAX)	Interventricular septum Posterolateral wall	Permanent residence permit (PCA)
Perasternal left ventricular short axis (PSAX)	All walls of the heart at the level of the papillary muscles	Permanent residence. OV. PKA
Apical four-chamber (MS)	Interventricular septum Lateral wall	Permanent residence. PKA Ov
Apical (A2C) two-chamber	Front wall Rear wall	Permanent residence PKA(OV)

DIAGNOSTIC CRITERIA FOR TERMINATION OF STRESS ECHOCARDIOGRAPHIC STUDY

There are three main groups of criteria for stopping a stress echocardiogram:

Stress EchoCG criteria for implementing the research protocol - achieving the maximum possible dose of a pharmacological stress agent, submaximal physical (electrophysiological) load;

Achieving the maximum permissible heart rate;

Positive data from stress echocardiography - the appearance and worsening of asynergies.

2) clinical criteria for stopping the stress echocardiography study;

3) electrocardiographic criteria for stopping a stress echocardiography study.

ANALYSIS OF STRESS ECHOCARDIOGRAPHIC STUDIES

Normal and pathological reaction of the LV myocardium in response to various types of stress.

In healthy individuals, the normal LV response to stress testing causes hyperdynamic (hyperkinetic) movement of all LV walls; increased systolic thickening of the LV walls; increased ejection fraction; reduction in LV size (measured in the SAX projection). Hyperkinetic wall motion and sufficient systolic thickening of the LV myocardium are the main signs of myocardium not affected by ischemia.

Pathological response of the LV to a stress test. The pathological reaction of the LV to a stress test is the appearance of regional, global and hemodynamic disturbances.

The actual ultrasound markers of ischemia are: a) local disturbances in the kinetics of the LV myocardium (akinesis, hypokinesis, dyskinesis, aneurysmal bulging of the wall); b) LV remodeling (dilatation of cavities, change in LV shape, decrease in the rate of circular shortening of myocardial fibers); c) a decrease in the speed and change in the phase characteristics of blood flow in the aorta and through the mitral valve with various types of Doppler recording of blood flow.

Analysis of regional contractility

It has been shown that in transient regional ischemia, echocardiographic indicators of regional asynergy of the LV myocardium have the greatest sensitivity, specificity, clinical significance and diagnostic capabilities. In routine clinical practice, stress echocardiography is also assessed primarily based on the analysis of regional contractility of the LV myocardium. Analysis of the kinetics of myocardial walls is the main subject of stress echocardiography studies.

Analysis of the works of various researchers shows that stress echocardiographic criteria for myocardial ischemia include:

The appearance of areas of regional asynergy of the LV myocardium that were absent before the stress test study;

Worsening of the disturbances in the kinetics of the LV myocardial walls that existed before the stress test study;

No changes in the kinetics of the walls of the left ventricle of the heart, remaining hypokinetic, akinetic or dyskinetic, despite the stress test effect on the myocardium; - absence of a proper increase in the kinetics of the LV walls against the background of a dobutamine stress test (considered by a number of researchers as abnormal myocardial ischemia).

Arterial and pulmonary hypertension, cardiomyopathies, treatment with beta blockers, and low levels of exercise can distort the normal hyperdynamic response. Left bundle branch block also complicates the interpretation of wall kinetics. Practical experience shows that it can be difficult to identify zones of active ischemia within the area of ​​a previous infarction in the first days after heart surgery, including revascularization operations, during a stress echocardiography study for various reasons.

Currently, various methods are used to analyze regional contractility, which depend on the capabilities of the available ultrasound equipment, computer software, and the goals and objectives facing the study.

Methods for analyzing regional contractility

1. A qualitative or descriptive method of analysis, when during the study, disturbances in the kinetics of the heart walls are visually assessed on a five-point scale of changes in contractility in 16 segments identified in the LV.

2. A semi-quantitative method of analysis, when the regional contractility disorder index (INRS, or WMSI - wall motion score index) is calculated on a five-point scale in 16 left ventricular segments.

3. Automated analysis method using specialized computer programs (center line method and radial wall-motion method) and specialized ultrasonic technologies (color kinesis and acustic quantification).

Assessment of the severity of regional contractility disorders

The severity and severity of regional disturbances in the kinetics of the heart walls depend on the number of affected segments and the type of asynergic disturbances. The integral indicator of the severity of local contractility disorders is considered to be the regional contractility disorder index (INRS. or WMSI). The regional contractility impairment index is calculated as the sum of the LV local contractility impairment indices divided by the number of analyzed segments, i.e. at 16. It was accepted that, depending on the severity of disturbances in the kinetics of the LV myocardium, each type of regional asynergia, based on an analysis of the direction and severity of systolic movement of the endocardium, the nature and degree of systolic thickening of the myocardium, is assigned its own index. Some authors also identify such a violation of the kinetics of the LV walls as an “aneurysm with a scar,” assigning it an index of 6.

Table 2. System of indices for assessing the severity of regional contractility disorders

Wall movement	Contractility impairment indices	Sleep topical movement of the endocardium	Systolic myocardial thickening
Normoi"ez	1	Normal, inside	Normal (not less than ZON)
Hypokines	2	Moderately reduced, inside	Reduced, but but absent
Akinee	3	Absent	Absent
Dyskinesis	4	Absent or outward protrusion of the wall	Absent or decreased systolic thickening
Aneurysm	5	Diastole and scalp deformation	Absent

According to the values ​​of the INRS indicator, 4 degrees of severity of violations of regional contractility are distinguished. Assessment of the severity of disturbances in regional contractility of the LV:

1) INRS = 1.0 or less - normal regional contractility;

2) INRS = 1.1-1.49 - mild disturbances of regional contractility;

3) INRS = 1.5-1.99 - moderate severity of regional contractility impairment;

4) INRS = 2.0 or more - severe disturbances of regional myocardial contractility.

Assessment of the severity of myocardial ischemia occurring during a stress echocardiography study and the diagnostic value of the method depend not only on the type of asynergic disturbances in the kinetics of the heart walls and on the number of affected muscles, but also on a comprehensive accounting of all the main clinical and instrumental data of the stress test .

The severity of ischemia depends on:

1) type of regional asynergy

2) the severity of the emerging asynergia

3) the time of occurrence of positive or other criteria for stopping the test

4) recovery time

Stress echocardiography is a clinical diagnostic method for identifying coronary artery disease, in which clinical, ECG, and echocardiography changes certainly play an important role. The final assessment of stress echocardiography should give an integral answer to the task assigned to the study.

When stress echocardiography, various types of loads are used, which allow inducing myocardial ischemia in different ways. The most commonly used types of loads are:

1. Exercise tests:

Dynamic - VEM, treadmill test,

Static load – isometric stress echocardiography.

2. Pharmacological stress tests with different mechanisms of action:

Adrenergic stimulation - test with dobutamine;

Vasodilation - test with dipyridamole;

Vasoconstriction of the coronary arteries - test with ergonovine;

Combined pharmacological loads - sequential use of drugs with different mechanisms of action).

3. Non-pharmacological stress tests that induce vasoconstriction of the coronary arteries:

Test with hyperventilation;

Cold test

Stress tests with electrical stimulation of the heart: - TEES.

In our country, during stress echocardiography, exercise tests, pharmacological tests and TEE are the most widely used.

The advantages of TEES compared to physical activity are as follows:

The test can be carried out in patients who are unable to perform physical activity,

The patient does not move during exercise, thereby not interfering with obtaining an image of better quality,

The test is not accompanied by a hypertensive reaction and is safer compared to physical exercise (immediate return to the original heart rate after cessation of stimulation, the possibility of stopping paroxysmal supraventricular tachycardias, and a significantly lower likelihood of ventricular arrhythmias).

The disadvantages are:

Non-physiological nature of the test, some discomfort for the patient associated with stimulation, the possibility a-v development II degree blockade in approximately 1/3 patients.

The static load was not chosen by chance, since during stress tests with dynamic load, due to significant tachycardia and tachypnea, it is impossible to analyze changes in LV diastolic function, namely, diastolic function reacts much earlier to negative processes occurring in the functionally defective myocardium.

The main advantage of pharmacological stress tests is the ability to perform them on patients who, for any reason, are unable to perform physical activity or achieve the required level of physical activity. It is also important to be able to record echoCG positions throughout the entire test.

Pharmacological drugs used for stress echocardiography allow inducing myocardial ischemia by various mechanisms of action, are relatively safe, have a short half-life and are comparable to physical exercise in sensitivity and specificity in the diagnosis of stenotic lesions of the coronary bed. It is also significant that in patients with systolic dysfunction of the left ventricle, pharmacological stress tests can identify viable myocardium.

PROGNOSTIC VALUE OF STRESS ECHOCARDIOGRAPHY

The ability of stress echocardiography, both in normal and in extreme (stressful) situations for the body, to identify the nature and characteristics of damage to the coronary arteries, features of the development of myocardial ischemia, to assess the viability and non-viability of the myocardium allows its use for prognostic purposes in patients with coronary artery disease in a variety of forms . This is a prognosis for the course of chronic forms of coronary heart disease; prognosis (probability assessment) of the development of acute coronary insufficiency or myocardial infarction; prognosis for the development of complications after acute myocardial infarction; assessment and prognosis of the degree of cardiac risk and the development of cardiac complications during surgical operations of myocardial revascularization, percutaneous transluminal angioplasty, installation of stents in the coronary arteries, as well as during all other heart operations; assessment of the risk level of the feasibility of heart transplantation. Patients with a positive stress echocardiogram have a significantly higher risk of developing life-threatening coronary complications.

Thus, methods for diagnosing transient myocardial ischemia are numerous. When determining the objective value of a particular method, it is necessary to focus on its sensitivity and specificity. They differ for different methods. Equally important is taking into account the cost of the study. However, the low cost of the method should not be the determining argument when choosing it. Taking into account the specific features of the methods, including their diagnostic value, as well as based on practical expediency, the examination should begin with simpler methods (VEM, daily ECG monitoring). If they cannot be performed or do not solve the assigned tasks, stress echocardiography is necessary. And only if this study does not solve the problem, it is advisable to use more complex examination methods.

CT scan

Improvements in technology in recent years have expanded the use of computed tomography (CT), which was limited due to low resolution and artifacts in cardiac image registration. New software has appeared for analyzing and interpreting the resulting images, which has simplified and unified the method. There is ultra-high-speed, or electron beam, and multislice (multilayer) CT. The use of both methods reliably confirmed the ability to assess the degree and extent of coronary vessel calcification. The sensitivity of CT for diagnosing CAD ranged from 85 to 100%, but the specificity was only 41 to 76%; positive predictive value ranges from 55 to 84%, and negative predictive value ranges from 84 to 100%.

Calcium is deposited in the coronary arteries in atherosclerotic plaques. Coronary calcification increases with age. The extent of coronary calcification correlates more with the total number of plaques than with the degree of stenosis or the location of the stenoses. However, several studies have shown a marked difference with repeated CT measurements of coronary calcification levels. Thus, detection of coronary artery calcification may be useful in identifying patients at higher risk of coronary artery disease, but cannot be recommended as a method for routine diagnosis of coronary artery disease. The use of serial CT scans in individual patients to determine and subsequently analyze regression or progression of calcification remains problematic.

CT image quality can be significantly improved with the use of intravenous contrast agents. However, CT has proven to be a promising non-invasive method for imaging the coronary arteries with the ability to identify and characterize atherosclerotic plaques. Thus, the sensitivity and specificity of CT angiography for detecting CAD are 95 and 98%, respectively, when using a 16-layer scanner. Studies using 64-slice scanners have shown 90-94% sensitivity and 95-97% specificity, and a negative predictive value of 93-99%.

Magnetic resonance imaging (MRI) with contrast of the coronary arteries

As in the case of CT, the use of MRI has found application with additional intravenous administration of contrast agents. Currently, MRI is the subject of scientific study and is not recommended for routine clinical use for the diagnosis of CAD.

Radionuclide studies

In 1995, the ACC/AHA published a detailed review on the use of radionuclide imaging for the diagnosis of CAD and localization of myocardial lesions. The most widely used radioisotope in patients with suspected CAD for the purpose of visualizing myocardial perfusion is the 201 Tl radioisotope, but new isotopes - 99m Tc-sestamibi and 99m Tc-tetrofosmin - have been shown to have similar diagnostic accuracy. Thus, in most cases, for diagnosing coronary artery disease, all three isotopes can be used with the same degree of diagnostic value.

Both planar and single photon emission computed tomography (SPECT) can be used to visualize myocardial perfusion with visual analysis or technical quantitative calculations. Calculations (eg, those made using horizontal or peripheral contours) may improve the sensitivity of the test, especially in patients with single-vessel disease. For 201 Tl planar scintigraphy, the mean published sensitivity and specificity values ​​were 83 and 88%, respectively, for visual analysis, and 90 and 80%, respectively, for quantitative analysis. 201 T SPECT is generally more sensitive than planar imaging for diagnosing CAD, localizing hypoperfused areas of the myocardium, identifying stenoses of the left anterior descending and left circumflex arteries, and is also more likely to detect the presence of multivessel lesions in CAD. The average sensitivity and specificity of load SPECT with 201 Tl were within 89 and 76%, respectively, for qualitative analysis, and 90 and 70%, respectively, for quantitative analysis.

Thrombolytic therapy. Almost significant markers of myocyte death are the activities of enzymes - AST, CPK, LDH. Table 4 Some indicators of the lipid spectrum of blood serum of men from Kataysk, patients with arterial hypertension I, II degrees and coronary heart disease, M±m Indicators Groups Total cholesterol, N – 5.2-6.5 mmol/l Triglycerides, N – 0 .51-1.86 mmol/l...

Functional class of CHF. 12. The preliminary diagnosis can be formulated as follows: Main: Hypertension of the III degree, III stage, a very high risk group for complications. Complications: Coronary heart disease: Stable rest angina of functional class IV. Chronic heart failure stage I, functional class II. II. Plan for additional...

Drug therapy. Treatment is prescribed in repeated courses under the control of serum lipid levels (cholesterol, triglycerides, etc.) until a stable lipolytic effect is achieved. CORONARY HEART DISEASE The WHO Expert Committee defines coronary artery disease (CHD) as acute or chronic damage to the heart muscle caused by a decrease or cessation of blood delivery to the myocardium in...

Pathologies of the circulatory system lead in the entire structure of diseases, among the main causes of disability and mortality. This is facilitated by the prevalence and persistence of risk factors. Diseases do not always affect the heart and blood vessels at the same time; some of them develop in the veins and arteries. There are quite a few of them, but occlusion of the arteries of the lower extremities is the most dangerous.

Impaired blood flow due to vascular occlusion

Blockage of the arteries of the lower extremities leads to the cessation of oxygen supply and nutrients to the organs and tissues they supply. More often affected popliteal and femoral arteries. The disease develops abruptly and unexpectedly.

The lumen of the vessel may be blocked blood clots or emboli of various origins. The diameter of the artery, which becomes impassable, depends on their size.

Wherein tissue necrosis develops rapidly in the area below the blocked artery.

The severity of the signs of pathology depends on the location of the occlusion and the functioning of the lateral - collateral blood flow through healthy vessels running parallel to the affected ones. They deliver nutrients and oxygen to ischemic tissues.

Arterial blockage is often complicated gangrene, stroke, heart attack that lead the patient to disability or death.

It is impossible to understand what leg vascular occlusion is, to understand the severity of this disease, without knowing its etiology, clinical manifestations, and treatment methods. We must also take into account the importance of preventing this pathology.

More 90 % of cases of blockage of the leg arteries have two main causes:

1. - blood clots form in the main vessels, are delivered by the blood flow to the arteries of the lower extremities and block them.
2. - a thrombus as a result of atherosclerosis appears in the artery, grows and closes its lumen.

Etiology

The etiology of the remaining cases is as follows:

Risk factors

Vascular occlusion is a disease for the development of which the presence of risk factors. Minimizing them reduces the possibility of obstruction. They are:

• alcoholism, drug addiction, smoking;
• heredity;
• surgery on the blood vessels of the legs;
• unbalanced diet;
• pregnancy, childbirth;
• excess weight;
• sedentary lifestyle;
• gender - men are more often affected, age - more than 50 years.

Impact of underlying causes and risk factors more often accumulates for a long time.

Important! Experts note the spread of leg vascular occlusion among young people, many of whom sit in front of computers and gadget monitors. Therefore, when the first signs of occlusion occur, regardless of age category, you must immediately consult a doctor.

Types and signs of the disease

Blockage of the arteries can occur in any part of the lower limb; various diameters of the vessels overlap. In accordance with this, they distinguish varieties occlusions:

1. Obstruction large and medium arteries. The blood supply to the femoral and adjacent areas is disrupted.
2. Blockage small vessels, supplying blood to the legs and feet.
3. Mixed obstruction of large and small arteries simultaneously.

According to the etiological factors that provoked the appearance and development of the disease, occlusions are divided into the following types:

• air - blockage of the vessel with air bubbles;
• arterial - obstruction is caused by blood clots;
• fatty - blockage of an artery with particles of fat.

Obstruction of the blood vessels of the legs occurs in two forms:

1. Spicy.
2. Chronic.

Acute occlusion occurs when an artery is blocked by a blood clot. Develops suddenly and quickly. Chronic illness proceeds slowly, manifestations depend on the accumulation of cholesterol plaques on the vessel wall and a decrease in its lumen.

Symptoms

The first sign of obstruction of the leg arteries is symptom of intermittent claudication. Intense walking begins to cause pain in the limb, the person, sparing the leg, limps. After a short rest, the pain disappears. But as the pathology develops, pain appears from minor loads on the limb, lameness intensifies, and long rest is necessary.

Over time they appear 5 main symptoms:

1. Constant pain, aggravated by even a slight increase in loads on the leg.
2. Pale and cold to the touch skin on the affected area, which eventually develops a bluish tint.
3. The pulsation of blood vessels at the site of blockage cannot be felt.
4. Decreased sensitivity in the leg, a feeling of goosebumps, which gradually disappears, leaving numbness.
5. The onset of limb paralysis.

Important be aware that a few hours after the appearance of characteristic signs of blockage, tissue necrosis begins at the site of vessel occlusion, and gangrene may develop.

These processes are irreversible, therefore, untimely treatment will lead to amputation of the limb and disability of the patient.

If signs of intermittent claudication or at least one main occlusive symptom appear, this is a reason to urgently consult a doctor.

Treatment methods

Conducts the necessary studies to confirm the diagnosis. After this, he prescribes treatment. In the initial stages of the disease, it is conservative and carried out at home. Drug therapy used:

• , thinning the blood and reducing its viscosity (Cardiomagnyl, Plavix, Aspirin Cardio);
• antispasmodics, relieving vascular spasms (No-Shpa, Spazmol, Papaverine);
• (fibrinolytics) that destroy blood clots (Prourokinase, Actylase);
• painkillers, relieving attacks of pain (Ketanol, Baralgin, Ketalgin);
• cardiac glycosides that improve heart function (Corglicon, Digoxin, Strophanthin);
• antiarrhythmic drugs, normalizing heart rhythms (Novocainamide, Procainamide).

Anticoagulant action is used for local treatment of occlusion. Vitamin complexes are prescribed. Physiotherapy is used.

Electrophoresis accelerates and ensures maximum penetration of drugs to the site of arterial damage.

Relieves pain, improves blood circulation, increases blood saturation with oxygen.

In case of severe development of occlusion and ineffective drug therapy, surgical treatment is used:

1. Thrombectomy- removal of blood clots from the lumen of the vessel.
2. Stenting— by introducing a special balloon, the lumen of the artery is opened and a stent is installed to prevent its narrowing.
3. Bypass surgery- creation of a bypass artery to replace the affected area. An implant or a healthy limb vessel can be used for this.

When gangrene develops, partial or complete amputation of the limb is performed.

Prevention

Performing simple prevention rules significantly reduce the risk of developing the disease:

1. Lead an active lifestyle, use moderate physical activity.
2. Visit skating rinks, swimming pools, gyms.
3. Quit smoking and alcohol or reduce the consumption of strong drinks to a minimum.
4. Eat the right foods that contain enough vitamins and microelements. Avoid foods that increase blood cholesterol, blood viscosity, blood pressure, and those containing large amounts of fat.
5. Avoid significant weight gain and maintain normal weight.
6. Avoid stress, learn to get rid of it.
7. Monitor the course and treatment of chronic diseases that can cause obstruction of the blood vessels of the legs.

Conclusion

Blockage of the arteries of the lower extremities in most cases develops over a long period of time, so early symptoms appear in the initial stages of the disease. They signal problems with blood vessels. You must not miss this moment and visit a specialist. This is the only way to correctly determine the cause of vascular occlusion, eliminate it, stop the development of pathology, and have a favorable prognosis for recovery.

If timely treatment is not carried out in the case of the acute stage of the disease, it may become irreversible.

Symptoms

A number of symptoms can serve as a sign that the disease has manifested itself. The main symptom when the disease occurs in the extremities (lower or upper) is the absence of pulsation of the arteries that are located further from the center of the body in relation to the location of the potential problem.

After this, the limb begins to turn pale, then a marble pattern appears on it. The skin becomes cold to the touch. Sometimes ischemic signs occur, for example, brittle nails, dry and noticeable wrinkling of the skin, lack of hair on it, and so on.

Sensitivity may be impaired, tactile sensations are reduced, tingling sensations are felt on the skin, overall muscle strength decreases, and in extreme cases, immobility of the affected limb may occur. If surgical treatment is not carried out (and in the case of an acute form of the disease, treatment should be as prompt as possible), then gangrene of the limb cannot be avoided.

• pain;
• lack of pulse;
• pallor;
• decreased tactile sensitivity;
• paralysis.

All these symptoms in English language start with the letter "p", so you may see the disease under an alternative name - the five P complex.

Classification

Occlusion that occurs in vessels can be classified according to various criteria. First of all, it varies according to the type of its localization and the type of vessels affected.

Based on the type of vessels affected, the following are distinguished:

According to localization, occlusion occurs:

• affecting nutritional organs;
• affecting the set of great vessels;
• affecting the central nervous system;
• affecting some of the limbs (lower or upper).

Most often, in approximately fifty percent of all cases, occlusion occurs in the lower extremities. Damage to the vessels of the central nervous system and the vessels of the head section, that is, supplying blood to the head, occurs much less often.

The internal carotid artery is most often affected. Then a lack of nutrition of the brain and central nervous system cells develops. As a result, a serious pathology may occur, which will lead to a cerebral infarction - an ischemic stroke, so that after this a significant part of the activity of the body's systems may be disrupted - all this can lead to dementia and paralysis.

This disease can also occur in the vertebral artery, which affects the occipital part of the brain.

In this case, if treatment is not carried out, damage to part of the brain can lead to paralysis, dizziness, problems with vision, speech, and fainting.

Unlike the manifestation of this disease in the lower extremities and brain, occlusion of the vessels that supply the retina can begin suddenly and painlessly, but ultimately leads to almost complete loss of vision in the eye that was affected. This problem usually occurs in men after fifty years of age - and it requires surgical treatment.

Causes

There are a number of reasons that may result in vascular occlusion in the lower extremities, brain and other places.

There are several main ones:

Embolism. This name hides the blockage of a vessel by a dense formation located in the bloodstream. In turn, embolism can have various causes, most often infectious.

There are several subspecies of it:

• air embolism – entry of an air bubble into the vessels, which can occur due to lung injury or an incorrect injection;
• arterial embolism - blockage of blood vessels with the help of mobile blood clots that are formed due to pathology in the valve apparatus of the heart - usually occlusion in the lower extremities, vessels of the heart and brain (brain) occur precisely for this reason;
• fat embolism - occurs due to metabolic disorders, but sometimes can also occur as a result of injury - consists of the accumulation of tiny particles of fat in the blood into a larger fat clot.

Thrombosis. This is a process in which the lumen of the arteries regularly decreases, as the number and size of blood clots on the inner walls constantly increases.

The cause may be vascular atherosclerosis, but injuries and infections can also trigger this problem. Not only can occlusion occur due to thrombosis, but it also creates conditions for the development of embolism, which also increases the risk of the described disease. Aneurysm.

This vascular problem can similarly cause occlusion to occur. This is an anomaly, which is expressed in a sharp expansion or protrusion of part of the walls of blood vessels. It can be either congenital or acquired. Potential consequences include the embolism and thrombosis described above.

Injuries. Finally, occlusion can occur when bone or muscle tissue is damaged, resulting in compression of large blood vessels, making normal blood flow much more difficult. Where the artery is pinched, thrombotic processes can begin, as well as embolism - so treatment after injuries must be started promptly, regardless of whether the injuries are to the lower extremities, brain or anything else.

Diagnostics

To diagnose the disease, it is necessary to carry out a number of examinations, which include palpation of the pulse in problem areas, functional tests, laboratory blood tests, duplex scanning, CT arteriography, MR angiography.

It is necessary to try to carry out a diagnosis at the first manifestations of signs of the disease, because it (in its acute form) develops quickly, and therefore can lead to amputation of the lower or upper extremities, and in a situation where the problem has arisen in the brain or manifested itself in the retina, further action must be taken more quickly, because the possibility of surgical intervention, in the case of the same brain, is minimal.

Treatment

If signs of the described disease are detected, it is necessary to undergo urgent hospitalization and consultation with a doctor specializing in blood vessels. It all depends on what stage of ischemia began to develop due to this disease:

1. Tension ischemia and grade IA. At this early stage, it is sufficient to carry out conservative treatment. Thrombolics, fibrinolytic agents, antiplatelet agents and antispasmodics are administered intravenously. Various physiotherapeutic treatments are carried out, including barotherapy, magnetic therapy, and diadynamic therapy.
2. Ischemia IB-IIB degree. In this case, you cannot do without emergency intervention, which should help quickly restore blood flow. Bypass surgery, thrombectomy or embolectomy is performed. If the occlusion is not extensive, then prosthetics of a segment of the artery can be performed.
3. Ischemia IIIA-IIIB degrees. Emergency thrombectomy or embolectomy, as well as bypass surgery, are performed, but in addition to them, treatment such as fascitotomy is mandatory. Low-level amputation is possible.
4. Ischemia IIIB degree. Vascular operations in this case are strictly contraindicated, because they can lead to post-ischemic syndrome and potential death. At this stage, amputation of the affected upper or lower limbs is mandatory.

To prevent recurrence of the problem, treatment continues for some time after surgery, namely anticoagulant therapy.

Prevention

To avoid the need for treatment, it is best to resort to a set of preventive measures that will help reduce the likelihood of this extremely unpleasant problem occurring:

1. Reduce or, if possible, stop drinking alcohol and smoking. Sometimes the disease can manifest itself precisely from this.
2. Maintain a healthy lifestyle that includes physical activity appropriate to your current health and age.
3. Try to avoid stress, various nervous shocks, and so on as much as possible.
4. Bring your weight back to normal. If you are at all overweight, this can place quite a significant amount of unnecessary strain on your entire cardiovascular system.
5. Eat healthy - reduce the number of foods that are too fatty and contain a lot of cholesterol. After forty years, it is generally recommended to undergo cholesterol tests at least approximately once every six months.
6. Increase the consumption of natural products containing a large supply of vitamins.
7. It is reasonable to consume strong tea and coffee, as well as salty and spicy foods. You cannot provoke the development of hypertension, which can start small.

Contact a vascular surgeon - angiosurgeon, preferably at a regional clinic.

My mother is diagnosed with occlusion of the SFA on the right. Occlusion of the RCA, 3BBA, PBBA on the right. On the left there is stenosis of the SFA, GBA, RCA. I'm looking for information.

• Diseases
• Body parts

A subject index to common diseases of the cardiovascular system will help you quickly find the material you need.

Select the body part you are interested in, the system will show materials related to it.

© Prososud.ru Contacts:

Use of site materials is possible only if there is an active link to the source.

Signs and treatment of coronary artery occlusion

Occlusion is a sudden vascular obstruction. The cause is the development of pathological processes, blockage by a blood clot, and traumatic factors. According to localization they distinguish different types occlusion, for example, it can affect the arteries of the heart. It is supplied with blood by two main vessels - the left and right coronary arteries.

Due to their obstruction, the heart does not receive the required amount of oxygen and nutrients, which leads to serious problems. Often there are only minutes, sometimes hours, to take emergency measures, so it is necessary to know the causes and symptoms of occlusion.

Causes

The processes that occur during the formation of coronary-type occlusion largely determine the morphology. Most often, chronic occlusion begins to form from the moment of formation of a fresh intraluminal thrombus. It is this that fills the lumen after the fibrous capsule of an unstable atherosclerotic plaque ruptures in acute coronary syndrome.

Thrombus formation occurs in two directions from the plaque. The length of the occlusion is determined by the location of the large lateral branches in relation to the occluding plaque.

There are several stages in the formation of structures of chronic occlusion of the cardiac arteries.

1. Stage 1 lasting up to two weeks. There is a sharp inflammatory reaction to acute thrombosis, rupture of an unstable plaque. Vascular microtubules are formed. Infiltration of thrombotic material by inflammatory cells and myofibroblasts occurs. In the arterial lumen of a fresh thrombus there are platelets and red blood cells in a fibrin framework. Almost immediately they begin to infiltrate inflammatory cells. Endothelial cells also migrate in the fibrin mesh and participate in the formation of fine structures, microscopic tubules inside the thrombus, which begins to organize. At this stage, structured tubules do not form in thrombotic occlusion.
2. The duration of the next, intermediate stage is 6-12 weeks. Negative remodeling of the arterial lumen occurs, that is, the cross-sectional area decreases by more than 70%. The elastic membrane ruptures. Microscopic tubules are formed in the thickness of the occlusion. Thrombotic material continues to form. Other pathological processes also occur. Active inflammation develops, the number of neutrophils, monocytes, and macrophages increases. The formation of the proximal capsule of occlusion begins, which consists of almost only dense collagen.
3. The maturity stage lasts from 12 weeks. Inside the occlusion, soft tissue is almost completely displaced. There is a decrease in the number and total area of ​​the tubules compared to the previous period, but after 24 weeks it does not change.

Formation of atherosclerosis plaques on the coronary artery

Why do such processes begin to develop? Of course, the above does not happen in a healthy person with good blood vessels. In order for the vessels to become suddenly obstructed or the occlusion to become chronic, some factors must act on the heart and coronary arteries. Indeed, normal blood flow is impeded for several reasons.

1. Embolism. Emboli or clots can form inside arteries and veins. This is the most common cause of arterial obstruction. There are several types of this condition. Air embolism is a condition when an air bubble penetrates into the blood vessels. This often happens with serious damage to the respiratory organs or an incorrectly performed injection. There is also a fat embolism, which can be traumatic in nature, or result from deep metabolic disorders. When small fatty particles accumulate in the blood, they are able to combine into a fat clot, which causes occlusion. Arterial embolism is a condition in which the vascular lumen is blocked by mobile blood clots. They usually form in the valve apparatus of the heart. This happens in various pathologies of cardiac development. This is a very common cause of occlusion of arteries in the heart.
2. Thrombosis. It develops when a blood clot appears and begins to grow. It is attached to the venous or arterial wall. Thrombosis often develops with atherosclerosis.
3. Vascular aneurysm. This is the name given to pathology of the walls of arteries or veins. They expand or bulge.
4. Injuries. Tissues that are damaged due to external reasons begin to put pressure on the vessels, causing blood flow to be disrupted. This causes the development of thrombosis or aneurysm, after which occlusion occurs.

If you start living this wrong way from a young age, serious problems can arise. Unfortunately, they are observed even in those who once led an unhealthy lifestyle; of course, the degree of disease is not so acute. If you eliminate negative factors from your life as early as possible, the likelihood of developing occlusion will be much less.

Symptoms

The manifestation of symptoms is directly dependent on the work of the heart, because it is the heart that is being damaged. Since as a result of occlusion it ceases to receive nutrition and oxygen, this cannot go unnoticed by a person. The work of the heart suffers, and this manifests itself in soreness in this area. The pain can be very severe. The person begins to experience difficulty breathing. As a result of oxygen starvation of the heart, floaters may appear in the eyes.

The person becomes sharply weaker. He may grab the heart area with his right or left hand. As a result, this situation often leads to loss of consciousness. It should be taken into account that the pain can radiate to the arm or shoulder. The signs are very pronounced. In any case, first aid must be provided.

Treatment

It is necessary to relieve pain and spasm. To do this, you should give an anesthetic. It’s good if it is possible to inject papaverine. If a person has heart medication with him, it must be given in the correct dose.

After rendering assistance by emergency medical specialists, the victim is taken to the hospital. There the patient is examined. An ECG is available in any medical institution. When it is deciphered, the depth and height of the teeth, the deviation of the isoline and other signs are taken into account.

An ultrasound of the heart and blood vessels and arteries is also performed. This study helps to identify the consequences of occlusion and blood flow disturbances. It is useful to perform coronary angiography of the heart vessels with the introduction of a contrast agent.

Treatment of acute manifestations of occlusions is a complex matter. Its success depends on the timely detection of the first signs of damage to the coronary arteries. Basically you have to resort to surgical intervention in order to clean the internal cavities of the arteries and remove the affected areas. Arterial bypass is performed.

In order not to bring the body to this, it is necessary to maintain the cardiovascular system in normal condition. To do this, a number of preventive measures should be taken:

1. You need to monitor your blood pressure levels. It is best to be smart about drinking strong tea, coffee, salty and spicy foods.
2. It's important to eat right. This means that you need to reduce your intake of fatty foods that contain a lot of cholesterol. After forty years, it is necessary to take cholesterol tests at least once every six months. Every day you should eat natural foods that contain a lot of vitamins and essential microelements.
3. Need to get rid of excess weight, as it puts a serious strain on the heart and blood vessels.
4. You should give up bad habits. This applies to smoking and alcoholic beverages. In medical practice, there have been cases when sharp spasmodic occlusion occurred, which was caused by alcohol or nicotine.
5. Stress and mental turmoil must be avoided.

Thanks to such simple measures, you can protect yourself from dangerous consequences. It is important to understand that occlusion poses a real threat to human health and life. We need to prevent it or provide first aid!

The information on the site is provided for informational purposes only and does not constitute a guide to action. Do not self-medicate. Consult your healthcare provider.

PCA cardiology

Circumflex branch of the left coronary artery. Right coronary artery

The circumflex branch of the left coronary artery begins at the bifurcation (trifurcation) of the left artery trunk and runs along the left atrioventricular (coronary) groove. For simplicity, we will further call the circumflex branch of the left artery the left circumflex artery. This is exactly what, by the way, it is called in English literature - left circumflex artery (LCx).

From one to three large (left) marginal branches depart from the circumflex artery, running along the obtuse (left) edge of the heart. These are its main branches. They supply blood to the lateral wall of the left ventricle. After the marginal branches depart, the diameter of the circumflex artery decreases significantly. Sometimes only the first branch is called the (left) marginal branch, and the subsequent ones are called the (posterior) lateral branches.

The circumflex artery also gives off one to two branches going to the lateral and posterior surfaces of the left atrium (the so-called anterior branches to the left atrium: anastomatic and intermediate). In 15% of cases with a left (non-right) coronary form of blood supply to the heart, the circumflex artery gives off branches to the posterior surface of the left ventricle or posterior branches of the left ventricle (F. H. Netter, 1987). In approximately 7.5% of cases, the posterior interventricular branch also departs from it, feeding both the posterior part of the interventricular septum and partially the posterior wall of the right ventricle (J. A. Bittl, D. S. Levin, 1997).

The proximal portion of the circumflex branch of the LCA is the segment from its mouth to the origin of the first marginal branch. There are usually two or three marginal branches to the left (obtuse) edge of the heart. Between them is the middle part of the circumflex branch of the LCA. The last marginal, or as it is sometimes called (posterior) lateral, branch is followed by the distal portion of the circumflex artery.

Right coronary artery

In its initial sections, the right coronary artery (RCA) is partially covered by the right ear and follows along the right atrioventricular groove (sulcus coronarius) towards the chiasm (the place on the diaphragmatic wall of the heart where the right and left atrioventricular grooves, as well as the posterior interventricular groove of the heart (sulcus) meet interventricularis posterior)).

The first branch to arise from the right coronary artery is the branch to the conus arteriosus (in half of the cases it arises directly from the right coronary sinus of the aorta). When the anterior interventricular branch of the left artery is blocked, the branch to the conus arteriosus is involved in maintaining collateral circulation.

The second branch of the RCA is the branch to the sinus node (in 40-50% of cases it can arise from the circumflex branch of the LCA). Departing from the RCA, the branch to the sinus angle goes posteriorly, supplying blood not only to the sinus node, but also to the right atrium (sometimes both atria). The branch to the sinus node goes in the opposite direction in relation to the branch of the conus arteriosus.

The next branch is the branch to the right ventricle (there can be up to three branches running in parallel), which supplies blood to the anterior surface of the right ventricle. In its middle part, just above the acute (right) edge of the heart, the RCA gives rise to one or more (right) marginal branches running towards the apex of the heart. They supply blood to both the anterior and posterior walls of the right ventricle, and also provide collateral blood flow during blockage of the anterior interventricular branch of the LCA.

Continuing to follow the right atrioventricular groove. The RCA goes around the heart and already on its posterior surface (almost reaching the intersection of all three grooves of the heart) gives rise to the posterior interventricular (descending) branch. The latter descends along the posterior interventricular groove, giving rise, in turn, to small lower septal branches, supplying blood to the lower part of the septum, as well as branches to the posterior surface of the right ventricle. It should be noted that the anatomy of the distal RCA is very variable: in 10% of cases there may be, for example, two posterior interventricular branches running in parallel.

The proximal portion of the right coronary artery is the segment from its origin to the branch leaving the right ventricle. The last and most inferior branch (if there is more than one) borders the middle part of the RCA. This is followed by the distal portion of the RCA. In the right oblique projection, the first - horizontal, second - vertical and third - horizontal segments of the RCA are also distinguished.

This section of the site is outdated, go to the new site

Internet consultations

Topic: RCA subocclusion

Please answer my questions.

Complaints: aching, constricting pain in the left half of the chest, occurring with little physical activity and at rest, radiating to the left shoulder blade and arms, relieved by taking nitroglycerin after 1-2 minutes, headaches when blood pressure rises to 180/100 mm rt. Art., dizziness, shortness of breath with little physical exertion.

Predominance of coronary arteries

The term predominance is applied to the artery supplying the posterior diaphragmatic part of the interventricular septum and the diaphragmatic surface of the LV. When these branches originate from the PKA, the system is said to be right-dominant; when they originate from the left circumflex artery, the left dominant node system in this case also originates from the LOA).

Mixed dominance or codominance occurs when clear dominance of the PCA or LOA is not determined. The coronary circulation is right dominant in approximately 85% of people, left dominant in 8%, and codominant in 7%. Dominance in the absence of coronary artery disease does not have any particular clinical significance.

The main trunk of the LCA originates in the upper part of the left sinus of Valsalva, has a diameter of 3-6 mm and a length of up to 10 mm. It passes behind the outflow tract of the right ventricle, after which it divides into the left anterior interventricular artery and the LOA.

The left LAD runs along the anterior interventricular groove towards the apex of the heart and the septal perforating and diagonal branches extend from it. The first septal perforating branch marks the connection between the proximal and middle segments of the LAD. In a small number of patients, the main trunk of the LCA undergoes “trifurcation,” namely, a median artery, the ramus intermedius, appears between the LCA and LCA. This artery supplies the free wall along the lateral border of the LV.

The LOA appears at the bifurcation of the main trunk of the LCA and passes through the left AV sulcus. The obtuse margin marginal arteries arise from the LOA and supply the lateral wall of the LV. The site of appearance of the first marginal artery corresponds to the junction between the proximal and middle segments of the LOA. If it is dominant, the LOA gives rise to the PNA, PPA, and often the AV node artery. In 30% of people, a large left atrial branch arises from the proximal LOA and gives rise to the sinus node artery. In patients with coronary artery disease, it may be an important conduit for collateral blood flow into the RCA system.

The RCA originates in the right coronary sinus at a point that is slightly lower than the origin of the LMCA in the left sinus. The RCA runs along the right AV sulcus towards the chiasm. The first branch of the RCA, the conal artery, can serve as a source of collateral circulation in patients with LAD occlusion. In two thirds of patients, the sinus node artery arises from the proximal RCA, just distal to the conus artery. This artery supplies the sinus node, often the right atrium or both atria. Like the LOA, which also courses in the AV groove, the RCA gives rise to marginal arteries, the first of which marks the connection between the proximal and middle segments of the RCA. Occlusion of the RCA proximal to the marginal branch of the right ventricle can cause right ventricular infarction with its hemodynamic consequences. In the area of ​​the distal chiasm, the RCA is divided into the PCA and the PCA. Several small septal perforating arteries arise from the PNA and supply the lower third of the septum. As with the LAD, the right-angle origin of the septal perforating arteries helps identify the LAD. The apex of the PLA flexure is often the origin of the arteries of the AV node.

Valsalva

Medical server named after. Antonio Maria Valsalva

• Administrator

• Index of cases

RCA occlusion and angina: tactics

I think that we need to convince the patient to lower his quality of life requirements and observe. Very tight to watch.

Re: RCA occlusion and angina: tactics

I would choose OMT without revascularization and “observe”, then depending on the situation (if OMT does not bring relief, you can try to open the RCA)

In this case, there is already occlusion of a large RCA.

The patient received a quota and was sent by regional specialists to the RKNPK (we sent him to the RSCH).

In July 2008, an operation was performed at the RKNPK OSSH: coronary artery bypass grafting of the diagonal artery, obtuse edge artery, posterior interventricular artery (from the right coronary artery), mammary coronary bypass grafting of the anterior descending artery.

Who's at the conference now?

This forum is currently viewed by: Google , Mariam Mayilian and 0 guests

Occlusion (vascular obstruction) is a serious manifestation of vascular insufficiency

Cardiovascular pathologies firmly occupy a leading place among diseases leading to death or permanent disability of a person. A decrease in the conductive capacity of large blood vessels can paralyze the functioning of many organs and systems of the body. One of the most terrible manifestations of vascular insufficiency is vascular occlusion.

What is occlusion and why does it occur?

Occlusion is a sudden obstruction of blood vessels due to the development of pathological processes in them, blockage by a blood clot, or due to traumatic causes. It is imperative to know the causes of this phenomenon and its symptoms, since in most cases the time to take emergency measures is extremely limited - literally hours and minutes count.

Occlusion using the example of a hand

Depending on their location, there are different types of occlusion - venous or arterial, affecting the great vessels that feed organs, limbs, and the central nervous system. They can be caused by a number of circumstances:

Embolism is a blockage of a vessel by a dense formation located in the bloodstream.

1. An embolism can be caused by an infectious lesion when the vessel is closed by an accumulation of microorganisms or inflammatory purulent blood clots.
2. Air embolism is the consequence of an air bubble entering the blood vessels. It often appears with complex injuries to the respiratory organs (lungs); it may be a consequence of improper injection.
3. Fat embolism can also be traumatic in nature, but often occurs with deep metabolic disorders in the body. Tiny particles of fat that accumulate in the blood can form a fat clot, leading to occlusion.
4. Arterial embolism is a blockage of blood vessels by mobile blood clots, which, as a rule, form in the valvular apparatus of the heart in a number of pathologies of its development. Usually it is this reason that leads to occlusion of the arteries of the lower extremities, vessels of the heart and brain.

Most often, emboli lead to occlusion in places of narrowing or branching of blood vessels - the so-called bifurcations.

Thrombosis is the process of gradual narrowing of the lumen of an artery due to the formation and growth of blood clots on its internal walls. Often the reason for this is atherosclerosis of blood vessels (in particular, the legs), but traumatic or infectious formations are also possible. In addition to the fact that thrombosis itself can lead to occlusion, it creates a very vulnerable site that is most susceptible to embolism (thromboembolism).

Vascular aneurysm can also cause occlusion. A congenital or acquired anomaly of the walls of blood vessels, leading to their sharp local expansion or protrusion, is a very characteristic site of future thrombosis and embolism.

Trauma – Occlusion occurs when damaged muscle or bone tissue compresses large blood vessels, preventing normal blood flow. At the site of compression of the artery, thrombotic processes occur, and the likelihood of embolism is high.

Lower extremity lesions

Such vascular damage can be included in a separate section, since according to medical statistics, in approximately half of all known cases, occlusion of the femoral artery and popliteal artery is recorded.

The symptoms of such occlusion have been studied and described in detail, and in the English-language medical literature there is even a rule of “five R” - characteristic manifestations, if at least one of them occurs, emergency diagnostics and treatment are required:

• Pain - pain - diffuse, extensive area below the affected area, intensifying and not relieved by changing the position of the leg.

• Pulselessness is the disappearance of the pulse in characteristic places close to the arteries. Doctors use a similar symptom to more accurately determine the location of occlusion.

• Pallor – pallor, the color of the skin below the affected area initially turns pale, then spots of cyanosis appear. The temperature of such areas is rapidly decreasing.

• Paresthesia – paresthesia, a feeling of numbness, tingling, “pins and needles” are sure signs of vascular damage. Sensitivity to touch disappears, complete numbness may occur with the disappearance of painful sensations.

• Paralysis – paralysis of a limb, impairment of its motor function - a manifestation of extensive ischemia of the area.

Failure to take measures in a timely manner (over 4–6 hours) can lead to irreversible necrotic changes in tissues and the development of a gangrenous process. Occlusion of the arteries of the extremities is one of the main causes of disability and leg amputation, especially in men over 60 years of age.

Occlusion of vessels supplying the head and central nervous system

Less likely, but still quite often, large vessels that deliver blood to the human head are affected. The most typical occlusion of the internal carotid artery.

With such a lesion, an acute lack of brain nutrition and oxygen starvation of the cells of the central nervous system (CNS) develop. This leads to pathological changes in the membranes, the development of areas of cerebral infarction - ischemic stroke, which can result in extensive damage to the central nervous system with subsequent disruption of the functioning of organs and systems of the body as a whole, paralysis, a sharp decrease in intellectual abilities and dementia.

Another vulnerable spot is the vertebral artery, the development of occlusion in which leads to damage to the occipital part of the brain. Precursors to the formation of large areas of stroke are the so-called TIAs (transient ischemic attacks). This can be expressed by extraterrestrial numbness of the limbs up to temporary paralysis, frequent dizziness, memory loss, speech and vision disorders, and periodic fainting.

Occlusion of the eye, or more precisely, of the vessels supplying its retina, can appear completely suddenly and absolutely painlessly, but, as a rule, leads to complete immediate loss of vision in the affected eye. Men who have reached age are more often susceptible to this disease.

Treatment and prevention of occlusion

Treatment of acute manifestations of occlusion is a very complex matter, the success of which depends on the timely detection of the very first symptoms. Most often, it is necessary to resort to surgical intervention in order to clean the internal cavities of the arteries, remove the affected areas, and perform arterial bypass surgery. In advanced cases, it is often necessary to amputate the affected limbs to avoid the spread of gangrenous processes and the occurrence of sepsis.

In order not to push your body to extremes, you must definitely maintain your vascular system in normal condition by performing a set of preventive measures:

1. Constantly monitor your blood pressure levels. Hypertension is the first step to serious cardiovascular failure. You should be reasonable about the consumption of coffee, strong tea, spicy and salty foods.
2. Proper nutrition - reduce as much as possible in your daily diet the amount of fatty foods with high cholesterol content. After 40 years of age, cholesterol tests should become mandatory at least once every six months.
3. Eat natural foods rich in vitamins every day.
4. Get rid of extra pounds. Excess weight is a very sensitive excess load on the entire cardiovascular system as a whole.
5. Give up bad habits - smoking and drinking alcohol. Medicine knows cases of sharp spasmodic occlusion caused by nicotine or alcohol.
6. A correct lifestyle, including regular physical activity, commensurate with age and general health.
7. Try to avoid unnecessary stress and mental shock.

To finish the topic of vascular occlusion, a few words about the similar meaning of this term. It's about about endovascular occlusion. Unlike everything described above, this is not the name of the pathology, but a method of surgical treatment of an aneurysm, when an artificial blockage of the area of ​​protrusion of the artery or artificial thrombosis at the site of its significant expansion is surgically created, which protects against a possible rupture of the great vessel.

Occlusion is a sudden vascular obstruction. The cause is the development of pathological processes, blockage by a blood clot, and traumatic factors. There are different types of occlusion based on location; for example, it can affect the arteries of the heart. It is supplied with blood by two main vessels - the left and right coronary arteries.

Due to their obstruction, the heart does not receive the required amount of oxygen and nutrients, which leads to serious problems. Often there are only minutes, sometimes hours, to take emergency measures, so it is necessary to know the causes and symptoms of occlusion.

Causes

The processes that occur during the formation of coronary-type occlusion largely determine the morphology. Most often, chronic occlusion begins to form from the moment of formation of a fresh intraluminal thrombus. It is this that fills the lumen - after the fibrous capsule of an unstable atherosclerotic plaque ruptures.

Thrombus formation occurs in two directions from the plaque. The length of the occlusion is determined by the location of the large lateral branches in relation to the occluding plaque.

There are several stages in the formation of structures of chronic occlusion of the cardiac arteries.

1. The first stage lasts up to two weeks. There is a sharp inflammatory reaction to acute thrombosis, rupture of an unstable plaque. Vascular microtubules are formed. Infiltration of thrombotic material by inflammatory cells and myofibroblasts occurs. In the arterial lumen of a fresh thrombus there are platelets and red blood cells in a fibrin framework. Almost immediately they begin to infiltrate inflammatory cells. Endothelial cells also migrate in the fibrin mesh and participate in the formation of fine structures, microscopic tubules inside the thrombus, which begins to organize. At this stage, structured tubules do not form in thrombotic occlusion.
2. The duration of the next, intermediate stage is 6-12 weeks. Negative remodeling of the arterial lumen occurs, that is, the cross-sectional area decreases by more than 70%. The elastic membrane ruptures. Microscopic tubules are formed in the thickness of the occlusion. Thrombotic material continues to form. Other pathological processes also occur. Active inflammation develops, the number of neutrophils, monocytes, and macrophages increases. The formation of the proximal capsule of occlusion begins, which consists of almost only dense collagen.
3. The maturity stage lasts from 12 weeks. Inside the occlusion, soft tissue is almost completely displaced. There is a decrease in the number and total area of ​​the tubules compared to the previous period, but after 24 weeks it does not change.

Formation of atherosclerosis plaques on the coronary artery

Why do such processes begin to develop? Of course, the above does not happen in a healthy person with good blood vessels. In order for the vessels to become suddenly obstructed or the occlusion to become chronic, some factors must act on the heart and coronary arteries. Indeed, normal blood flow is impeded for several reasons.

1. Embolism. Emboli or clots can form inside arteries and veins. This is the most common cause of arterial obstruction. There are several types of this condition. Air embolism is a condition when an air bubble penetrates into the blood vessels. This often happens with serious damage to the respiratory organs or an incorrectly performed injection. There is also one, which can be traumatic in nature, or arise as a result of deep metabolic disorders. When small fatty particles accumulate in the blood, they are able to combine into a fat clot, which causes occlusion. Arterial embolism is a condition in which the vascular lumen is blocked by mobile blood clots. They usually form in the valve apparatus of the heart. This happens in various pathologies of cardiac development. This is a very common cause of occlusion of arteries in the heart.
2. . It develops when a blood clot appears and begins to grow. It is attached to the venous or arterial wall. Thrombosis often develops with atherosclerosis.
3. Vascular aneurysm. This is the name given to pathology of the walls of arteries or veins. They expand or bulge.
4. Injuries. Tissues that are damaged due to external reasons begin to put pressure on the vessels, causing blood flow to be disrupted. This causes the development of thrombosis or aneurysm, after which occlusion occurs.

It is important to remember that some of these reasons are due to lifestyle. Atherosclerosis and blood clots form due to the fact that a person abuses alcohol, smokes, eats poorly, moves little, and experiences frequent stress. All this has a very bad effect on both the entire body and its blood vessels.

If you start living this wrong way from a young age, serious problems can arise. Unfortunately, they are observed even in those who once led an unhealthy lifestyle; of course, the degree of disease is not so acute. If you eliminate negative factors from your life as early as possible, the likelihood of developing occlusion will be much less.

Symptoms

The manifestation of symptoms is directly dependent on the work of the heart, because it is the heart that is being damaged. Since as a result of occlusion it ceases to receive nutrition and oxygen, this cannot go unnoticed by a person. The work of the heart suffers, and this manifests itself in soreness in this area. The pain can be very severe. The person begins to experience difficulty breathing. As a result of oxygen starvation of the heart, floaters may appear in the eyes.

The person becomes sharply weaker. He may grab the heart area with his right or left hand. As a result, this situation often leads to loss of consciousness. It should be taken into account that the pain can radiate to the arm or shoulder. The signs are very pronounced. In any case, first aid must be provided.

Treatment

It is necessary to relieve pain and spasm. To do this, you should give an anesthetic. It’s good if it is possible to inject papaverine. If a person has heart medication with him, it must be given in the correct dose.

The main thing is not to panic. If the room is stuffy and hot, you need to open the window and ventilate it. Remove clothing that may make breathing difficult. There is no way to avoid calling an ambulance! She needs to be called immediately as soon as a person becomes ill.

After rendering assistance by emergency medical specialists, the victim is taken to the hospital. There the patient is examined. An ECG is available in any medical institution. When it is deciphered, the depth and height of the teeth, the deviation of the isoline and other signs are taken into account.

An ultrasound of the heart and blood vessels and arteries is also performed. This study helps to identify the consequences of occlusion and blood flow disturbances. It is useful to perform coronary angiography of the heart vessels with the introduction of a contrast agent.

Treatment of acute manifestations of occlusions is a complex matter. Its success depends on the timely detection of the first signs of damage to the coronary arteries. Basically, it is necessary to resort to surgical intervention in order to clean the internal cavities of the arteries and remove the affected areas. They carry out arterial.

In order not to bring the body to this, it is necessary to maintain the cardiovascular system in normal condition. To do this, a number of preventive measures should be taken:

1. You need to monitor your blood pressure levels. It is best to be smart about drinking strong tea, coffee, salty and spicy foods.
2. It's important to eat right. This means you need to reduce your intake of fatty foods. After forty years, it is necessary to take cholesterol tests at least once every six months. Every day you should eat natural foods that contain a lot of vitamins and essential microelements.
3. You need to get rid of excess weight, as it puts a serious strain on the heart and blood vessels.
4. You should give up bad habits. This applies to smoking and alcoholic beverages. In medical practice, there have been cases when sharp spasmodic occlusion occurred, which was caused by alcohol or nicotine.
5. Stress and mental turmoil must be avoided.

Thanks to such simple measures, you can protect yourself from dangerous consequences. It is important to understand that occlusion poses a real threat to human health and life. We need to prevent it or provide first aid!

Occlusion is a sudden vascular obstruction. The cause is the development of pathological processes, blockage by a blood clot, and traumatic factors. There are different types of occlusion based on location; for example, it can affect the arteries of the heart. It is supplied with blood by two main vessels - the left and right coronary arteries.

Due to their obstruction, the heart does not receive the required amount of oxygen and nutrients, which leads to serious problems. Often there are only minutes, sometimes hours, to take emergency measures, so it is necessary to know the causes and symptoms of occlusion.

Causes

The processes that occur during the formation of coronary-type occlusion largely determine the morphology. Most often, chronic occlusion begins to form from the moment of formation of a fresh intraluminal thrombus. It is this that fills the lumen - after the fibrous capsule of an unstable atherosclerotic plaque ruptures in acute coronary syndrome.

Thrombus formation occurs in two directions from the plaque. The length of the occlusion is determined by the location of the large lateral branches in relation to the occluding plaque.

There are several stages in the formation of structures of chronic occlusion of the cardiac arteries.

1. The first stage lasts up to two weeks. There is a sharp inflammatory reaction to acute thrombosis, rupture of an unstable plaque. Vascular microtubules are formed. Infiltration of thrombotic material by inflammatory cells and myofibroblasts occurs. In the arterial lumen of a fresh thrombus there are platelets and red blood cells in a fibrin framework. Almost immediately they begin to infiltrate inflammatory cells. Endothelial cells also migrate in the fibrin mesh and participate in the formation of fine structures, microscopic tubules inside the thrombus, which begins to organize. At this stage, structured tubules do not form in thrombotic occlusion.
2. The duration of the next, intermediate stage is 6-12 weeks. Negative remodeling of the arterial lumen occurs, that is, the cross-sectional area decreases by more than 70%. The elastic membrane ruptures. Microscopic tubules are formed in the thickness of the occlusion. Thrombotic material continues to form. Other pathological processes also occur. Active inflammation develops, the number of neutrophils, monocytes, and macrophages increases. The formation of the proximal capsule of occlusion begins, which consists of almost only dense collagen.
3. The maturity stage lasts from 12 weeks. Inside the occlusion, soft tissue is almost completely displaced. There is a decrease in the number and total area of ​​the tubules compared to the previous period, but after 24 weeks it does not change.

Formation of atherosclerosis plaques on the coronary artery

Why do such processes begin to develop? Of course, the above does not happen in a healthy person with good blood vessels. In order for the vessels to become suddenly obstructed or the occlusion to become chronic, some factors must act on the heart and coronary arteries. Indeed, normal blood flow is impeded for several reasons.

1. Embolism. Emboli or clots can form inside arteries and veins. This is the most common cause of arterial obstruction. There are several types of this condition. Air embolism is a condition when an air bubble penetrates into the blood vessels. This often happens with serious damage to the respiratory organs or an incorrectly performed injection. There is also fat embolism, which can be traumatic in nature, or result from deep metabolic disorders. When small fatty particles accumulate in the blood, they are able to combine into a fat clot, which causes occlusion. Arterial embolism is a condition in which the vascular lumen is blocked by mobile blood clots. They usually form in the valve apparatus of the heart. This happens in various pathologies of cardiac development. This is a very common cause of occlusion of arteries in the heart.
2. Thrombosis. It develops when a blood clot appears and begins to grow. It is attached to the venous or arterial wall. Thrombosis often develops with atherosclerosis.
3. Vascular aneurysm. This is the name given to pathology of the walls of arteries or veins. They expand or bulge.
4. Injuries. Tissues that are damaged due to external reasons begin to put pressure on the vessels, causing blood flow to be disrupted. This causes the development of thrombosis or aneurysm, after which occlusion occurs.

It is important to remember that some of these reasons are due to lifestyle. Atherosclerosis and blood clots form due to the fact that a person abuses alcohol, smokes, eats poorly, moves little, and experiences frequent stress. All this has a very bad effect on both the entire body and its blood vessels.

If you start living this wrong way from a young age, serious problems can arise. Unfortunately, they are observed even in those who once led an unhealthy lifestyle; of course, the degree of disease is not so acute. If you eliminate negative factors from your life as early as possible, the likelihood of developing occlusion will be much less.

Symptoms

The manifestation of symptoms is directly dependent on the work of the heart, because it is the heart that is being damaged. Since as a result of occlusion it ceases to receive nutrition and oxygen, this cannot go unnoticed by a person. The work of the heart suffers, and this manifests itself in soreness in this area. The pain can be very severe. The person begins to experience difficulty breathing. As a result of oxygen starvation of the heart, floaters may appear in the eyes.

The person becomes sharply weaker. He may grab the heart area with his right or left hand. As a result, this situation often leads to loss of consciousness. It should be taken into account that the pain can radiate to the arm or shoulder. The signs are very pronounced. In any case, first aid must be provided.

Treatment

It is necessary to relieve pain and spasm. To do this, you should give an anesthetic. It’s good if it is possible to inject papaverine. If a person has heart medication with him, it must be given in the correct dose.

The main thing is not to panic. If the room is stuffy and hot, you need to open the window and ventilate it. Remove clothing that may make breathing difficult. There is no way to avoid calling an ambulance! She needs to be called immediately as soon as a person becomes ill.

After rendering assistance by emergency medical specialists, the victim is taken to the hospital. There the patient is examined. An ECG is available in any medical institution. When it is deciphered, the depth and height of the teeth, the deviation of the isoline and other signs are taken into account.

An ultrasound of the heart and blood vessels and arteries is also performed. This study helps to identify the consequences of occlusion and blood flow disturbances. It is useful to perform coronary angiography of the heart vessels with the introduction of a contrast agent.

Treatment of acute manifestations of occlusions is a complex matter. Its success depends on the timely detection of the first signs of damage to the coronary arteries. Basically, it is necessary to resort to surgical intervention in order to clean the internal cavities of the arteries and remove the affected areas. Arterial bypass is performed.

In order not to bring the body to this, it is necessary to maintain the cardiovascular system in normal condition. To do this, a number of preventive measures should be taken:

1. You need to monitor your blood pressure levels. It is best to be smart about drinking strong tea, coffee, salty and spicy foods.
2. It's important to eat right. This means that you need to reduce your consumption of fatty foods that contain a lot of cholesterol. After forty years, it is necessary to take cholesterol tests at least once every six months. Every day you should eat natural foods that contain a lot of vitamins and essential microelements.
3. You need to get rid of excess weight, as it puts a serious strain on the heart and blood vessels.
4. You should give up bad habits. This applies to smoking and alcoholic beverages. In medical practice, there have been cases when sharp spasmodic occlusion occurred, which was caused by alcohol or nicotine.
5. Stress and mental turmoil must be avoided.

Thanks to such simple measures, you can protect yourself from dangerous consequences. It is important to understand that occlusion poses a real threat to human health and life. We need to prevent it or provide first aid!