Heartbreak. Symptoms and complaints. An increase in the infarct zone occurs in the pool of the same artery, the occlusion of which caused the infarction. In this case, the transition of a subendocardial infarction to a transmural one or the growth of an infarction in breadth with the capture of adjacent regions is possible.

Myocardial rupture is one of the most severe complications early myocardial infarction.

All myocardial ruptures should be divided into ( 1 ) free wall breaks And ( 2 ) internal breaks. The latter, in turn, include 2.1. ) breaks interventricular septum And ( 2.2. ) papillary muscle ruptures.

The mechanism of their effect on systemic hemodynamics is different: rupture of the free wall most often leads to cardiac tamponade, while with a rupture of the interventricular septum, shunting of blood from the left ventricle to the right occurs, and with a rupture of papillary muscles, severe mitral regurgitation occurs.

Rupture of the free wall of the left ventricle detected in 0.8-6.2% of cases acute period myocardial infarction. It is the most common cause of death after pump failure, accounting for 15% of deaths after myocardial infarction. Rupture of the free wall of the left ventricle usually occurs with myocardial infarction involving, by at least, 20% of the ventricular wall.

There are two time peaks at which rupture of the free wall of the left ventricle occurs.: the first 24 hours and 3-5 days, that is, we can talk about ( 1 ) early and ( 2 ) late breaks. Early ruptures are associated with the initial processes of the evolution of the infarct with collagen deposition in the scar zone that has not yet occurred, and late ones with the spread of the infarct to adjacent tissues.

Rupture of the free wall of the left ventricle is the most common(1 ) in patients with first myocardial infarction, ( 2 ) in the elderly and ( 3 ) among women.

Other risk factors include(1 ) arterial hypertension in the acute phase of myocardial infarction, ( 2 ) absence of angina pectoris before infarction, ( 3 ) lack of collateral blood flow in the myocardium, ( 4 ) Q-waves on ECG, ( 5 ) use of corticosteroids or non-steroidal anti-inflammatory drugs and ( 6 ) thrombolytic therapy more than 14 hours after myocardial infarction (at the same time, despite the fact that the risk of myocardial rupture increases with late thrombolysis, timely thrombolytic therapy reduces the risk of rupture).

In addition to the acute period of myocardial infarction, ruptures of the free wall of the left ventricle are described as a rare complication of dobutamine stress echocardiography. Myocardial ruptures followed by cardiac tamponade and the development of cardiogenic shock have also been described. in case of injuries of the heart by a conductor during coronary angiography. This rare complication is occasionally observed also after surgical interventions and invasive medical procedures, injuries and infections.

Clinical manifestations are diverse and depend primarily on ( 1 ) localization and ( 2 ) the size of the gap. Typically, the patient dies suddenly or rapidly from cardiac tamponade and/or electromechanical dissociation. The condition is rarely diagnosed in life. However, sometimes such a gap proceeds subacutely. This can happen in cases where the thrombus closes the hole formed and the free wall breaks gradually, “solders” to the pericardium, and thus the gap closes. If the condition is recognized, then there is a chance to surgically treat such a patient.

In most cases, rupture of the free wall of the left ventricle is manifested cardiogenic shock or severe hypotension with or without loss of consciousness. Often such a gap is preceded by a sharp increase in pain, nausea, vomiting; on the electrocardiogram, a new rise in the ST segment often occurs.

Acute rupture of the free wall of the left ventricle almost always fatal, however, under acute course there is still room for intervention, but this is less common. The dimensions of such a tear in the wall are not so large, and it can partially thrombose. Therefore, blood slowly fills the pericardium, and clinical picture hemotomponade increases gradually, over hours and even days. Sometimes this can result in the formation of a pseudoaneurysm.

Usually, the median time elapsed from the moment of myocardial infarction to the diagnosis of pseudoaneurysm is 3.9 months. During the first 6 months after formation, there is a possibility of rupture of a false aneurysm. Often, with this variant of the development of tamponade, the pain syndrome comes to the fore, which occurs several hours before the development of tamponade and is associated with a tear of the heart wall gradually spreading in the thickness of the myocardium and soaking it with blood.

Rupture of the anterior wall usually characterized by more acute violation hemodynamics and catastrophic outcome. Rupture of the posterior and tender walls often leads to the formation of a pseudoaneurysm. The accepted theory regarding the formation of pseudoaneurysms is that myocardial rupture is limited to preexisting pericardial adhesions.

Ruptures of the interventricular septum occur in 1-2% of cases of myocardial infarction and in 12% of all types of myocardial rupture. Basically, a complication occurs on the 1-5th day of a heart attack. It is believed that in patients who undergo thrombolysis, rupture of the interventricular septum occurs less frequently, but at an earlier stage of the disease, than those who do not undergo thrombolysis. At the same time, there is evidence that the frequency of ruptures of the interventricular septum is reduced precisely because of the use of thrombolytic therapy.

As a rule, ruptures of the interventricular septum occur with anterior septal myocardial infarction (60%), and in sotal cases with myocardial infarction bottom wall with rupture of the posterior basal septum. with anterior septal myocardial infarction, a septal defect occurs closer to the apex of the heart, with a postero- (lower-) septal - in basal region. Ventricular septal defect occurs, as a rule, with severe multi-vessel coronary artery disease.

The occurrence of shunting from the left ventricle to the right leads to a sharp decrease in the output from the left ventricle, as well as an increase in blood volume in the lungs, increased blood flow to the left atrium and left ventricle. The left ventricle, affected by myocardial infarction, cannot cope with the additional volume of blood. As a result of all of the above, rupture of the interventricular septum appears sharp deterioration the patient's condition with the development of pulmonary edema and / or cardiogenic shock.

A sign of a ruptured interventricular septum such patients will have a rough pan systolic murmur to the left of the base of the sternum or between it and the apex of the heart. An echocardiographic study confirms the presence of a shunt and determines the volume of blood passing through the defect.

Rupture and avulsion of the papillary muscle leads to severe mitral regurgitation. More often than complete separations, tears of the heads of the papillary muscles are observed. Usually severe mitral insufficiency in myocardial infarction occurs on the 2nd-7th day of the disease (from 1 to 14 days). It should be borne in mind that much more often acute mitral regurgitation is a consequence of acute dysfunction of the papillary muscle, and not its rupture.

Clinically, the condition manifests itself pulmonary edema and/or cardiogenic shock. The characteristic pansystolic murmur of mitral regurgitation may not be due to an acute rise in pressure in the non-enlarged left atrium. At the same time, with any deterioration in the condition of a patient with myocardial infarction, accompanied by pulmonary edema or cardiogenic shock, acute mitral insufficiency should be excluded. X-ray examination in such cases quickly reveals pulmonary congestion.

If there is a suspicion of rupture of the free wall of the myocardium of the left ventricle an emergency echocardiogram should be performed. When detecting fluid in the pericardium and with ultrasound and clinical symptoms tamponade, the patient should undergo an emergency pericardial puncture, administer drugs with a positive inotropic effect (dopamine) and / or conduct counterpulsation. The patient should be immediately transferred to the cardiac surgery department. Emergency pericardiocentesis is best performed on Larrey or Marfan.

All these measures (evacuation of fluid from the pericardium and inotropic support) have only a temporary effect, and the patient is indicated for emergency cardiac surgery, which gives him a chance for survival. Unfortunately, mortality in emergency surgery for rupture of the myocardium of the free wall of the left ventricle remains high - up to 60%. However, this is better than 100% mortality with drug treatment.

With signs of rupture of the interventricular septum echocardiography should be performed immediately.

If an acute interventricular shunt is detected, you should:

(1 ) at severe violations hemodynamics to establish intra-aortic counterpulsation;

(2 - if necessary, introduce drugs with a positive inotropic effect and / or vasodilators (nitrates);

(3 - if respiratory disorders are transferred to artificial ventilation of the lungs;

(4 ) to perform emergency coronary angiography, since urgent revascularization has been shown to improve the prognosis of such patients;

(5 ) cardiac surgery should be performed urgently if the patient has a relatively stable state of hemodynamics, and immediately in cases of cardiogenic shock.

Acute mitral regurgitation, accompanied by unstable hemodynamics, requires the installation of an intra-aortic balloon for counterpulsation. It has been shown that the mortality rate of such patients receiving drug therapy reaches 70%, while with surgical treatment it is 40%.

Cardiac surgery should be carried out urgently, since there is always a risk of developing cardiogenic shock or other complications. Emergency mitral replacement is usually performed, although there are reports of plastic, valve-sparing operations.

Apparently, intra-aortic counterpulsation should become a routine technique in the treatment of acute heart failure resulting from any rupture of the left ventricular myocardium.

Classification of complications of myocardial infarction

Hospital mortality due to myocardial infarction is mainly due to heart failure due to severe left ventricular systolic dysfunction and other complications of myocardial infarction. These complications can be divided into

• mechanical,
• electrical (arrhythmic),
• ischemic,
• embolic and
• inflammatory (eg pericarditis).

Mechanical complications

These include such dangerous complications, How

• rupture of the interventricular septum,
• papillary muscle rupture,
• rupture of the free wall of the left ventricle,
• large aneurysm of the left ventricle,
• left heart failure,
• cardiogenic shock,
• dynamic obstruction of the outflow tract of the left ventricle,
• right ventricular failure.

Rupture of the interventricular septum

Prior to the advent of thrombolysis, this complication occurred in 1-2% of patients and was the cause of 5% of deaths in the acute period of myocardial infarction. With the advent of thrombolysis, the frequency of ruptures of the interventricular septum has decreased significantly. In the GUSTO-1 study, it was approximately 0.2%. Ventricular septal ruptures are more common in the elderly, in women, in non-smokers, as well as in arterial hypertension, anterior infarcts, high heart rate, and left ventricular failure at admission. Previously, ruptures occurred on the 2-5th day of infarction, but with the advent of thrombolysis, they began to occur earlier: half of the ruptures occur on the first day. However, thrombolysis does not increase the risk of rupture of the interventricular septum.

Clinical picture

At the beginning, the rupture of the interventricular septum can proceed almost asymptomatically, without orthopnea and stagnation in the small circle. The recurrence of chest pain, pulmonary edema, hypotension, and shock may appear later and increase very rapidly. However, hemodynamics may worsen and gradually: hypotension, right and left ventricular failure develops; in this case, the appearance of a new noise will be the first symptom.

Physical examination

A ventricular septal rupture should be suspected when new pansystolic murmur, especially with simultaneous deterioration of hemodynamics and the development of heart failure in both circles of blood circulation. The results of the physical examination at admission should be accurately recorded so that later there is something to compare with. Physical examination for infarction is regularly repeated.

• The murmur is usually best heard from below at the left edge of the sternum, in half of the cases it is accompanied by systolic trembling. With a large tear and severe heart failure or shock, the murmur may be quiet or absent, so the absence of noise does not allow to exclude a rupture of the interventricular septum.
• Differences in noise during rupture of the interventricular septum and mitral insufficiency due to rupture of the papillary muscle are shown in the table. Noise can be carried out to the base and to the apex of the heart. Perhaps the appearance of a III heart sound, a loud pulmonary component of the II tone and signs of tricuspid insufficiency.

Morphology

The defect usually occurs at the border of myocardial infarction. With anterior infarction, this is most often the apical part of the septum, and with the lower one, its basal part. Ventricular septal ruptures almost always occur in transmural myocardial infarction. As a result of the gap, one large defect is not necessarily formed; in 30-40% of cases, a network of tortuous passages is found. Multiple defects are especially common in lower myocardial infarctions.

• On ECG in about 40% of cases, AV block or intraventricular conduction disturbances are detected.

• echocardiography

1. EchoCG with color Doppler study is best method diagnosis of ventricular septal rupture.

A. Basal ruptures of the interventricular septum are visible from the parasternal approach along the long axis of the left ventricle with the deviation of the scanning plane medially and from the apical and subcostal approaches along the long axis of the left ventricle.

b. Apical ruptures of the interventricular septum are best seen from the four chamber position.

2. Sometimes, to clarify the size of the defect, a transesophageal echocardiogram is performed.

3. EchoCG allows you to determine the size of the defect and the amount of blood discharge from left to right. The discharge is calculated from the ratio of blood flow through the pulmonic valve and the aortic valve.

4. In addition, with using echocardiography evaluate systolic ventricular function, which largely determines mortality.

• Right heart catheterization(see details)

An increase in oxygen saturation in the pulmonary artery and right ventricle allows the diagnosis of ventricular septal rupture to be made. It is very important to accurately determine the level at which the increase in blood oxygen content occurs, since an increase in oxygen content in the branches of the pulmonary artery has been described in acute severe mitral insufficiency. Under the control of fluoroscopy, blood oxygen saturation is measured in the superior and inferior vena cava, right atrium, right ventricle and pulmonary trunk.

1. Normally, blood oxygen saturation in the superior vena cava is 64-66%, in the lower - 69-71%, and in the right atrium, right ventricle and pulmonary artery - 64-67%.

2. Left-to-right shunting through a ventricular septal defect usually results in an increase in oxygen saturation between the right atrium and right ventricle, or pulmonary artery 8% or more.

3. The reset value is calculated by the formula:

Qp - pulmonary blood flow,

Qs - systemic blood flow,

SaO2 - oxygen saturation of arterial blood,

S v O 2 - mixed venous blood,

S PV O 2 - blood in the pulmonary veins,

S PA O 2 - blood in the pulmonary artery.

In congenital malformations, a shunt with a Qp/Qs of 2.0 or more is considered large and usually requires surgical closure of the defect. In myocardial infarction, any rupture of the interventricular septum requires surgical treatment regardless of the reset value.

4. With intracardiac shunting, thermodilution gives an inaccurate estimate of cardiac output, so the Fick method must be used. For correct assessment cardiac output, the oxygen content in mixed venous blood is determined immediately before the level of discharge (that is, with a ventricular septal defect - in the right atrium or vena cava).

According to the Fick equation, cardiac output (l/min) is calculated using the formula:

where V O 2 - oxygen consumption in ml / min,

1.34 is the volume of oxygen in ml that binds to 1 g of hemoglobin; oxygen saturation of arterial and venous blood (S a O 2 and S v O 2) is taken in fractions.

Treatment

• Early surgical treatment shown to all patients, even with stable hemodynamics.

• Medical treatment

1. Previously, it was believed that the results are better with delayed surgery, this was explained by the healing of fragile myocardial tissue. However, apparently, such an idea is erroneous: the least severe patients survive before the operation with this tactic. Mortality with rupture of the interventricular septum in the first 72 hours is 24%, and in the first 3 weeks. – 75%. The operation should be carried out as soon as possible.

2. Vasodilators reduce left-to-right shunt and increase cardiac output by reducing peripheral vascular resistance, but a preferential decrease in pulmonary vascular resistance may lead to an increase in shunt. The best remedy – sodium nitroprusside IV in the initial dose of 5-10 mcg / kg / min, followed by its increase to achieve an average blood pressure of 70-80 mm Hg. Art.

• Endovascular methods

If there is no expressed aortic insufficiency, then in anticipation of the operation, intra-aortic balloon counterpulsation is started as soon as possible. She reduces systolic pressure in the aorta, the shunt fraction, increases coronary blood flow and maintains blood pressure. In addition, it becomes possible to select the dose of vasodilators under invasive hemodynamic control.

• Surgical closure of the defect is the best method of treatment, even with stable hemodynamics.

1. In case of cardiogenic shock and multiple organ failure, the lethality of the operation is high, which serves as an additional argument in favor of early surgical intervention - before the development of these complications.

2. Mortality is also high in basal ruptures of the septum in inferior infarcts. It is 70%, and with anterior infarcts - 30%. This is due to the technical complexity of the operation and the often occurring need for simultaneous plasty. mitral valve about its insufficiency, not uncommon in these patients.

3. In patients with stable hemodynamics, mortality was lower with early surgical treatment than with expectant management with delayed surgery.

4. Surgical closure of the ventricular septal defect is the best treatment. However, endovascular methods are now emerging, which may be a good alternative to surgical closure when the latter is ineffective or in very severe patients.

Mitral insufficiency

According to the GUSTO-I study, mitral insufficiency worsens the prognosis of myocardial infarction. Mild and moderate mitral insufficiency in myocardial infarction develops quite often - in 13-45% of patients. Even mild mitral regurgitation worsens the prognosis.

Mitral regurgitation in myocardial infarction can have several causes:

• expansion of the mitral annulus with dilatation of the left ventricle
• dysfunction of the inferomedial papillary muscle due to impaired contractility of the left ventricular wall at the site of its attachment
• partial or complete break chords or papillary muscles.

In most cases, mitral insufficiency is transient, asymptomatic and does not lead to serious consequences. Severe mitral insufficiency with rupture of the papillary muscle - life threatening but a treatable complication of myocardial infarction. Previously, it was believed that the rupture of the papillary muscle most often occurs on the 2nd-7th day of a heart attack. However, according to the SHOCK register, rupture of the papillary muscle occurs on average 13 hours after the onset of a heart attack. Rupture of the papillary muscle is the cause of cardiogenic shock in 7% of cases and death due to myocardial infarction in 5% of cases. The frequency of this complication is 1%.

Clinical picture

Rupture of the papillary muscle is more common in lower infarcts. Thrombolysis reduces the number of ruptures, but they occur earlier. Sometimes, with the existing predisposition, hemodynamic overload that occurs during myocardial infarction can lead to rupture of the notochord.

• Symptoms and complaints

Complete rupture of the papillary muscle is rare and usually results in immediate shock and death. With a rupture of one or two heads of the papillary muscle, severe shortness of breath suddenly occurs, pulmonary edema and cardiogenic shock develop.

• Physical examination

A new pansystolic murmur appears at the apex of the heart, radiating to the axillary region or to the base of the heart. With a rupture of the inferomedial papillary muscle, the murmur is carried along the left edge of the sternum, and it can be mistaken for a murmur with a ruptured interventricular septum or aortic stenosis. The loudness of the noise does not allow to judge the severity of mitral insufficiency. With low cardiac output or high left atrial pressure, the pressure gradient drops rapidly, so the murmur may be quiet or absent.

Pathogenesis

Rupture of the papillary muscle often occurs with lower infarcts. In this case, the inferomedial papillary muscle suffers, since it receives blood supply only from the posterior descending branch. The anterolateral papillary muscle has a dual blood supply: from the anterior descending and circumflex arteries.

In half of the cases, rupture of the papillary muscle occurs with relatively small infarcts.

Additional research methods

• The ECG usually shows signs of inferior or posterior myocardial infarction.
• A chest x-ray may show signs of venous congestion in the pulmonary circulation. Sometimes venous stasis can only be in upper lobe right lung due to a jet of regurgitation directed into the right pulmonary veins.

Diagnostics

• Doppler echocardiography is the best diagnostic method.

1. In severe mitral insufficiency, a flailing (dangling) leaflet of the mitral valve is usually visible.

2. Color Doppler examination distinguishes papillary muscle rupture with severe mitral regurgitation from ventricular septal rupture.

3. If the jet of regurgitation is directed backwards, it may be difficult to assess its magnitude during transthoracic echocardiography. In these cases, transesophageal echocardiography helps to assess the severity of mitral insufficiency and understand its cause.

• Pulmonary artery catheterization

High V waves may appear on the PAP curve. However, the same V waves occur with rupture of the interventricular septum due to a sharp increase in venous return from the lungs to the undistended left atrium. In severe mitral insufficiency, simultaneously with V waves, an increase in the oxygen content in the pulmonary artery compared to the right atrium is possible. This introduces additional difficulties in differential diagnosis of mitral insufficiency and ventricular septal rupture. To distinguish between these two states, the following circumstances should be considered.

1. A pronounced V wave on the pulmonary artery pressure curve, preceding incisura, almost always indicates severe mitral regurgitation.

2. Blood to determine the oxygen content should be taken from the pulmonary trunk, and not from the branches of the pulmonary artery; for this, the position of the catheter is determined using fluoroscopy.

Treatment

• Tactics

First of all, rupture of the papillary muscle is excluded, since this condition requires active drug treatment and emergency surgery.

• Medical treatment

1. Vasodilators are very effective in acute mitral regurgitation. Sodium nitroprusside reduces peripheral vascular resistance, reduces regurgitation fraction and increases stroke volume and cardiac output. The initial dose is 5-10 mcg / kg / min, then the dose is selected so that the average blood pressure is 70-80 mm Hg. Art.

2. Vasodilators are not prescribed for arterial hypotension; in this situation, intra-aortic balloon counterpulsation is indicated. It reduces left ventricular afterload, improves coronary perfusion, and increases cardiac output. With arterial hypotension, vasodilators can be prescribed after the installation of an intra-aortic balloon. In moderate mitral regurgitation after myocardial infarction, vasodilators are usually sufficient.

• Coronary angioplasty

An improvement in hemodynamics and a decrease in mitral insufficiency can occur after coronary angioplasty in the event that severe mitral insufficiency is caused not by rupture of the papillary muscle, but by its ischemia. With a true rupture of the papillary muscle, endovascular methods are useless.

• Surgery

When the papillary muscle is ruptured, urgent operation.

1. Without surgery, the prognosis is extremely unfavorable. Despite the fact that mortality in urgent operations is higher than in planned operations, and reaches 20-25%, surgical treatment is indicated for all patients.

2. Before the operation, coronary angiography is performed, since coronary artery bypass surgery improves immediate and long-term prognosis after mitral valve surgery.

3. For mild mitral regurgitation that does not respond to vasodilators, mitral valve repair may help. Valve replacement is often avoided.

Rupture of the free wall of the left ventricle

This complication occurs in 3% of patients with myocardial infarction. Rupture of the free wall of the left ventricle Cause of every tenth death due to myocardial infarction. In the first 5 days after a heart attack, half of the ruptures occur, in the first 2 weeks. – 90% breaks. Rupture of the free wall of the left ventricle occurs only in transmural myocardial infarctions.

Risk factors include:

• elderly age,
• female,
• arterial hypertension ,
• first ,
• poorly developed collateral circulation.

Clinical picture

1. Acute course

In an acute course, cardiac tamponade develops, electromechanical dissociation and instant death occurs. An incipient tear may be indicated by the sudden onset of chest pain after straining or coughing.

2. Subacute course

Sometimes the rupture of the free wall of the left ventricle can proceed subacutely due to the formation of a false aneurysm of the left ventricle. Characterized by the same pain as in pericarditis, nausea and hypotension. In a retrospective analysis of a large number of patients with myocardial infarction, rupture of the free wall of the left ventricle occurred in 6.2% of cases. In about a third of cases, it proceeded subacutely. Echocardiography may show a pericardial effusion and a false aneurysm.

Physical examination

A subacute rupture may be indicated by jugular venous distention, paradoxical pulsation, muffled heart sounds, and a pericardial friction rub. In addition, when the free wall ruptures and a false aneurysm is formed, a new two-component systolic-diastolic murmur may appear.

Pathogenesis

Ruptures of the free wall of the left ventricle are partly due to the increase in mortality in the first 24 hours after thrombolysis. However common frequency ruptures of the free wall of the left ventricle during thrombolysis does not increase. The rupture can occur anywhere, but is most prone to it lateral wall of the left ventricle.

Ruptures of the free wall of the left ventricle are divided into three types.

• Type I ruptures occur in the first 24 hours of myocardial infarction, they occur in the myocardium that has not yet been thinned. The frequency of such ruptures increases with thrombolysis.
• Type II ruptures occur due to myocardial erosion in the infarction area.
• Type III ruptures are late ruptures that occur in a thinned myocardium. The frequency of type III ruptures decreases with thrombolysis. Type III ruptures are thought to be caused by dynamic obstruction of the left ventricular outflow tract, which increases stress in the left ventricular wall.

Additional research methods

In addition to signs of myocardial infarction on the ECG, there may be an AV nodal or idioventricular rhythm, a decrease in the amplitude of the teeth, and high T waves in the chest leads. Rupture is often preceded by bradycardia.

Diagnostics

In the acute course of a rupture of the free wall of the left ventricle, there is usually no time for diagnosis.

• echocardiography in subacute course, it allows to identify signs of cardiac tamponade:
  • collapse of the right atrium for more than a third of systole,
  • right ventricular collapse in diastole
  • expansion of the inferior vena cava and the disappearance of its collapse on inspiration,
  • pronounced dependence top speed early diastolic filling of the left (more than 25%) and right (more than 40%) ventricles from the respiratory phases.

• Cardiac catheterization

Equalization of right atrial pressure, right ventricular end-diastolic pressure, and PAWP indicates cardiac tamponade.

Treatment

• Tactics

The main goal is to quickly diagnose and perform an emergency operation.

• Medical treatment in itself ineffective, but necessary in anticipation of the operation.
• Pericardiocentesis

Ischemic complications of myocardial infarction

Clinical picture

1. Enlargement of the infarction area occurs in the basin of the same artery, the occlusion of which caused a heart attack. In this case, the transition of a subendocardial infarction to a transmural one or the growth of an infarct in breadth with the capture of adjacent areas is possible.

• Characterized by persistent or recurrent chest pain, the appearance of new ECG changes and a prolonged increase in CPK activity.
• With echocardiography or myocardial scintigraphy, you can see an increase in the affected area compared to what was immediately after a heart attack.

2. Postinfarction angina

• Postinfarction is called in the period from several hours to 30 days after myocardial infarction. It occurs in 24-60% of patients and is more common in non-ST elevation infarcts and after thrombolysis.
• Postinfarction angina increases the risk sudden death, repeated heart attacks and other complications.
• The pathogenesis of postinfarction angina pectoris is the same as unstable angina so treatment should be appropriate.

3. Re-infarction

Usually occurs when re-occlusion of the artery, in the basin of which a heart attack occurred. However, re-occlusion does not always cause re-infarction. With coronary angiography, re-occlusion is found in 5-30% of patients, it worsens the prognosis. Diagnosis of a second heart attack in another area in the first 24-48 hours after the first heart attack can be difficult. It is difficult to distinguish it from an increase in the area of ​​the initial infarction. Repeated heart attacks develop in approximately 4.7% of patients. Risk factors include age over 70, female gender, diabetes and a history of myocardial infarction.

• It can be difficult to recognize ECG signs of recurrent infarction against the background of changes caused by the original infarction.
• CPK and its MB fraction are more important than troponins for the diagnosis of recurrent infarction. A re-infarction is indicated by an increase in the activity of the CPK MB fraction after its normalization or its increase by more than 2 times compared to the previous values.
• With echocardiography, you can see new zones of impaired local contractility.

Treatment

Medical treatment

In case of repeated myocardial ischemia, active treatment aspirin, heparin, nitrates and beta-blockers.

Endovascular methods

• Intra-aortic balloon counterpulsation used for arterial hypotension and severe left ventricular failure.
• After the condition is stabilized, coronary angiography. If the condition remains unstable, it is carried out urgently. Coronary angioplasty and coronary bypass surgery improve the prognosis.

Thromboembolism

Thromboembolism of the arteries great circle blood circulation with obvious clinical manifestations occurs in 2% of patients with myocardial infarction, more often with anterior infarcts. Parietal thrombosis of the left ventricle occurs in 20% of cases of myocardial infarction. With large anterior infarcts, this frequency reaches 60%.

Clinical picture

Symptoms

The most common manifestation of thromboembolism is stroke, but limb ischemia, renal infarction, and mesenteric ischemia are also possible. Thromboembolism most often occurs in the first 10 days of a heart attack.

Physical examination

The manifestations of thromboembolism depend on its location.

• With strokes, neurological symptoms appear.
• With thromboembolism of the arteries of the arms and legs, there is a cooling of the affected limb, pain and the absence of a peripheral pulse.
• Renal infarction may be accompanied by hematuria and back pain.
• Mesenteric ischemia causes abdominal pain and bloody diarrhea.

Treatment

1. In case of large anterior infarctions and parietal thrombosis, heparin infusion is carried out intravenously for 3-4 days, APTT is maintained at the level of 50-65 s.

2. Warfarin for 3-6 months is prescribed for parietal thrombosis and large areas of impaired contractility according to echocardiography.

3. One study showed that after major infarcts, anticoagulant therapy with heparin followed by warfarin (INR 2 to 3) reduced the incidence of embolic stroke within a month from 3 to 1%

Pericarditis

Early (epistenocarditic) pericarditis

This complication occurs in about 10% of cases. Inflammation usually develops within 24-96 hours after myocardial infarction.

Clinical picture

Epistenocarditis pericarditis occurs with transmural infarcts. In most cases, it is asymptomatic, sometimes a pericardial friction rub can be heard.

• Symptoms

1. Patients complain of progressive, severe, prolonged chest pain. The pain depends on the position of the body: it increases in the supine position and weakens when the patient sits down and leans forward. The pain resembles pleural pain in nature: it intensifies on inspiration, coughing and swallowing.

2. Irradiation of pain to the anterior edge of the trapezius muscle is almost pathognomonic for acute pericarditis and does not occur with angina pectoris. In addition, the pain may radiate to the neck and, less commonly, to the arm or back.

• Physical examination

A pericardial friction rub is pathognomonic for pericarditis, but it may be intermittent.

1. It is best heard from below at the left edge of the sternum when auscultated with a phonendoscope membrane.

2. Noise consists of three phases, corresponding to atrial systole, ventricular systole and ventricular diastole. In about 30% of cases, the noise is two-phase, in 10% it is single-phase.

3. With the appearance of a pericardial effusion, the volume of the murmur may become unstable, but it can be heard even with a significant amount of effusion.

Pathogenesis

Pericarditis is usually fibrinous inflammation, which occurs in the area of ​​​​the pericardium adjacent to the infarct zone. Pericardial friction rub is more common in large infarcts and indicates the possibility of hemodynamic disturbances.

Additional research methods

• ECG is the main method for diagnosing pericarditis. However, ECG changes caused by myocardial infarction can make it difficult. Unlike ischemia, which is characterized by focal changes ECG, with pericarditis, changes are visible in almost all leads.

1. On the elevated ST segment with pericarditis, there is sometimes a concavity, then it has a saddle shape.

2. With pericarditis, negative T waves form after the return of the ST segment to the isoline, while with myocardial infarction, negative T waves can appear even with an elevated ST segment.

3. ECG changes Pericarditis usually goes through four stages:

• Chest x-ray has no diagnostic value.
• Echocardiography can detect pericardial effusion high probability indicates pericarditis. However, the absence of effusion does not exclude this diagnosis.

Treatment

• Aspirin

This is the main remedy for epistenocarditis pericarditis, it is given at a dose of 650 mg every 4-6 hours.

• Other NSAIDs and glucocorticoids are not used. They can interfere with myocardial healing and promote stretching of the infarct zone.

Late pericarditis (Dressler's syndrome)

The frequency of this complication is 1-3%. Dressler's syndrome occurs 1-8 weeks after a heart attack. Its pathogenesis is unknown, it is believed that autoimmune reactions are the basis.

Clinical picture

Chest pain, including pleural pain, fever, arthralgia, malaise, and an increase in the number of leukocytes and ESR are characteristic. Echocardiography may show pericardial effusion.

Treatment

The same as in epistenocarditis pericarditis - aspirin. NSAIDs and glucocorticoids can be used 4 weeks after myocardial infarction in severe cases. Colchicine may help with recurrent pericarditis.

Literature:

1. B. Griffin, E. Topol "Cardiology" M. 2008

2. M. Fried, S. Grines "Cardiology" M. 1996

3. V.N. Kovalenko "Guide to cardiology" K. 2008

4. Textbook of Cardiovascular Medicine (March 2002): By Eric J Topol MD, Robert M Califf MD, Jeffrey Isner MD, Eric N Prystowsky MD, Judith Swain MD, James Thomas MD, Paul Thompson MD, James B Young MD, Steven Nissen MD By Lippincott Williams & Wilkins

5. John R. Hampton "The ECG in practice" Fourth edition, 2003

Rupture of the wall of the left ventricle with cardiac tamponade occurs in 1-3% of patients with myocardial infarction. Of these, in 30-50% of patients, the gap occurs within the first hour, in 80-90% - during the first 2 weeks. As a rule, rupture of the heart leads to death. In 25% of cases, a subacute rupture of the left ventricular wall occurs, which can simulate myocardial reinfarction, since pain and ST segment elevation recur with a decrease in blood pressure. The clinical picture of cardiac tamponade, verified by echocardiography, develops. The only method treatment is surgery. In this article, we will look at the symptoms of left ventricular free wall rupture and the main signs of left ventricular free wall rupture in humans.

Signs of rupture of the wall of the left ventricle

Rupture of the free wall of the left ventricle often occurs when extensive heart attack myocardium, as well as against the background of arterial hypertension or in the absence of previous angina pectoris.

Symptoms of rupture of the wall of the left ventricle

Clinically, the gap is manifested by the sudden disappearance of the pulse, sharp drop Blood pressure (with sphygmomanometry is not determined) and loss of consciousness while maintaining the ECG, which is called electromechanical dissociation.

Rupture of the interventricular septum

Rupture of the interventricular septum occurs in 1-3% of patients with myocardial infarction, and in 20-30% of cases it develops within the first 24 hours. After 2 weeks, the likelihood of a rupture of the interventricular septum is low. A lethal outcome without surgical intervention is recorded in 54% of patients during the first week and in 92% during the first year. The main clinical signs of acute rupture of the interventricular septum are a loud systolic murmur radiating to the right of the sternum and clinical deterioration of the patient's condition due to severe left ventricular failure (hypotension, pulmonary congestion). It should be remembered that the noise with an acute tear may be mild or completely absent. The main method confirming the presence of a defect is Doppler echocardiography.

Mitral valve insufficiency of a minor degree in myocardial infarction is observed in almost 50% of patients, while a pronounced degree is present in 4%; in the latter case without surgical treatment death occurs in 24%. The causes of mitral valve insufficiency may be dysfunction or rupture of the papillary muscles.

Papillary muscle dysfunction

Papillary muscle dysfunction occurs more frequently. As a rule, the posterior papillary muscle is affected, since the anterolateral muscle is supplied with blood from two arteries. Transient dysfunction of the papillary muscles is possible with ischemia of the nearest segment of the left ventricle. The clinical manifestation of papillary muscle dysfunction is a systolic murmur at the apex of the heart due to mitral valve insufficiency. Dysfunction is detected by echocardiography, and it usually does not require special interventions.

Rupture of the papillary muscles occurs in 1% of patients with myocardial infarction. The posterior papillary muscle is most commonly affected. Clinically, the rupture is manifested by the sudden onset of a coarse systolic murmur and pulmonary edema on days 2-7 from the onset of myocardial infarction. The severity of pulmonary edema exceeds that with a rupture (defect) of the interventricular septum. The diagnosis is confirmed by echocardiography: a "thrashing" leaflet of the mitral valve is detected, and the degree of severity of mitral valve insufficiency is determined by Doppler echocardiography. Mortality without surgery is 50% in the first 24 hours and 94% within 2 months.

Rhythm and conduction disorders in case of rupture of the wall of the left ventricle

Rhythm and conduction disturbances can be fatal.

Sinus bradycardia with rupture of the left ventricular wall

Sinus bradycardia occurs frequently, especially in myocardial infarction of the inferior wall of the left ventricle. With severe arterial hypotension, it is necessary to administer 0.3-0.5 mg of atropine IV, if necessary, repeated injections (maximum total dose of 1.5-2 mg).

AV block in left ventricular wall rupture

First-degree AV block usually does not require treatment. The occurrence of AV block II degree type 1 (with Wenckebach periodicals) in myocardial infarction of the inferior wall of the left ventricle rarely leads to hemodynamic disturbances. With an increase in signs of hemodynamic disturbances, atropine is administered or a temporary pacemaker is installed. Type II AV block (Mobitz) and AV block III degree require the installation of a temporary pacemaker.

Ventricular disorders heart rate with rupture of the wall of the left ventricle

Single and paired ventricular extrasystoles, short "runs" of ventricular tachycardia without hemodynamic disturbances do not require treatment. With arrhythmias with pain syndrome, arterial hypotension, manifestations of acute heart failure requires intravenous bolus administration of lvdocaine at a dose of 50 mg for 2 minutes, followed by infusion up to a total dose of 200 mg. In case of arrhythmia against the background of bradycardia, in order to increase the heart rate, the introduction of atropine is recommended. With the development of ventricular fibrillation, as well as with cardiac arrest, resuscitation in accordance with the recommendations of the European Resuscitation Council, 1998.

Supraventricular arrhythmias in the rupture of the wall of the left ventricle

Atrial fibrillation occurs in 15-20% of patients with myocardial infarction. Quite often it stops on its own. With a low rate of rhythm and no changes in hemodynamics, atrial fibrillation does not require special treatment. With a frequent rhythm, signs of heart failure, it is necessary to administer amiodarone at a dose of 300-450 mg IV drip or electrical defibrillation. Other supraventricular arrhythmias are rare and do not require special intervention.

January 23, 2019 No comments

Ventricular septal rupture (IVS) is a rare but fatal complication of myocardial infarction (MI). The event occurs 2-8 days after the infarction and often provokes cardiogenic shock. The differential diagnosis of postinfarction cardiogenic shock should exclude free rupture of the ventricular wall and rupture of the papillary muscles.

To avoid the high morbidity and mortality associated with this disorder, patients must undergo emergency surgical treatment. In modern medical practice, postinfarction rupture of the IVS is recognized as an emergency surgical care, and the presence of cardiogenic shock is an indication for intervention. Long-term survival can be achieved in patients who undergo operative surgery. Concomitant coronary artery bypass grafting (CABG) may be required. The use of additional CABG can improve long-term survival.

The operation is performed with a trans-infarction approach and the entire reconstruction is done using prostheses to avoid strain. Advances in myocardial protection and improved prosthetic materials have made significant contributions to successful treatment IVS rupture. Improved surgical techniques (eg, infarctectomy) and better perioperative mechanical and pharmacological support have helped reduce mortality. In addition, the development surgical methods to repair perforations in various areas of the septum led to improved results.

In current practice, patients undergoing shunt repair tend to be older and with more likely received thrombolytic agents, which may complicate recovery. After successful recovery, survival and quality of life are excellent, even in patients over 70 years of age.

Pathophysiology

The septal supply comes from branches of the left anterior descending coronary artery, the posterior descending branch of the right coronary artery, or the peripheral artery when it is dominant. The infarction associated with IVS rupture is usually transmural and extensive. About 60% of cases occur with infarction of the anterior wall, 40% with infarction of the posterior or lower wall. Rear gap IVS may be accompanied by mitral valve insufficiency secondary to infarction or papillary muscle dysfunction.

At autopsy, patients with IVS rupture usually have complete occlusion coronary artery with little or no collateral flow. The absence of collateral blood flow may be secondary to comorbidities arteries, anatomical abnormalities, or myocardial edema. Sometimes there are multiple perforations of the septum. This can happen at the same time or within days of each other.

Ventricular aneurysms are commonly associated with ventricular septal rupture after infarction and contribute significantly to hemodynamic compromise in these patients. The reported incidence of ventricular aneurysms ranges from 35% to 68%, while the incidence of ventricular aneurysms alone after MI without IVS rupture is significantly lower (12.4%).

On a natural history of postinfarction rupture of the IVS big influence hypertension, anticoagulant therapy, advanced age, and possibly thrombolytic therapy. The natural history of patients with ventricular septal rupture after infarction is well documented and concise. Most patients die within the first week, and nearly 90% die within the first year; Some reports indicate that less than 1% of patients are alive after 1 year.

This bleak prognosis is a consequence of acute volume overload caused by both ventricles of a heart already affected by major myocardial infarction and sometimes extensive coronary artery disease (CAD) in locations other than those already infarcted. In addition, superimposed ischemic mitral valve regurgitation, ventricular aneurysm, or a combination of these conditions may be present, further impairing heart function. Suppressed left ventricular function usually results in impaired perfusion of peripheral organs and death in most patients.

Several sporadic reports indicate that some individuals with postinfarction IVS rupture who received medical treatment live for several years. Although many medical advances have been made in the non-surgical treatment of these patients, including intra-aortic balloon pumping, these methods have not eliminated the need for surgery.

Rupture of the interventricular septum is a rare complication of myocardial infarction. Although autopsy studies show 11% of cases of myocardial wall rupture after myocardial infarction, perforation of the septal wall is much less common, occurring at an incidence of approximately 1-2%.

Diagnostics

Radiography

According to chest x-ray, 82% of patients with ventricular septal rupture after infarction have left ventricular enlargement, 78% have pulmonary edema, and 64% have pleural effusion. These findings are nonspecific and do not exclude other causes such as papillary muscle rupture.

M-mode transthoracic echocardiography and transesophageal echocardiography are also used to diagnose postinfarction IVS rupture. Echo-CG results have been improved using color Doppler imaging techniques. In addition, echocardiography allows you to study the presence of any pathology of the mitral valve.

Electrocardiography

No electrocardiographic (ECG) signs can serve as diagnostic criteria for postinfarction IVS rupture, although an ECG may indeed provide some useful information. Permanent increase ST segment associated with ventricular aneurysm is common. ECG can reveal atrioventricular block in one third of patients. An ECG can also be performed to predict the anatomical location of a septal tear.

Catheterization and pressure measurement

Left heart catheterization with coronary angiography is recommended for all stable patients. This procedure is time consuming and has some degree of complications; accordingly, common sense is required when prescribing this diagnostic method.

An important diagnostic test for differentiating IVS rupture from mitral valve insufficiency is catheterization of the right heart with a catheter. In the presence of a rupture of the interventricular septum, the oxygen concentration between the right atrium and the pulmonary artery increases. In addition, monitoring of pulmonary capillary wedge pressure is useful in differentiating acute mitral regurgitation from IVS rupture.

Left and right pressure measurements are helpful in assessing the degree of biventricular insufficiency and are useful in monitoring response to perioperative therapy. While right-sided insufficiency is more common in patients with IVS rupture after infarction, left-sided insufficiency and refractory pulmonary edema are more pronounced in patients with papillary muscle rupture. However, one third of patients with postinfarction IVS rupture also have some degree of MR secondary to left ventricular dysfunction. Only rarely is an IVS rupture also associated with papillary muscle rupture.

Treatment

Pharmacological therapy

Initiate pharmacological therapy in an attempt to ensure the hemodynamic stability of the patient. The goal is to reduce afterload on the heart and increase cardiac forward output.

Vasodilators can be used to reduce left-to-right shunting associated with a mechanical defect and therefore increase cardiac output. Intravenous nitroglycerin may be used as a vasodilator and may improve myocardial blood flow in individuals with severe coronary artery disease.

When used alone, inotropic agents may increase cardiac output; however, without changes in the ratio of pulmonary to systemic blood flow (Qp-to-Qs ratio), they markedly increase left ventricular work and myocardial oxygen consumption. The profound level of cardiogenic shock in some patients precludes treatment with vasodilators, which often requires the support of vasopressors.

Vasopressors markedly increase left ventricular function and myocardial oxygen consumption. In addition, they increase systemic afterload and further increase the Qp to Qs ratio, thereby lowering cardiac output and significantly increasing myocardial oxygen consumption.

Intra-aortic balloon counterpulsation provides the most important means temporary hemodynamic support. Intra-aortic balloon pumping reduces left ventricular afterload, thus increasing systemic cardiac output and decreasing the ratio of pulmonary to systemic blood flow.

Surgical therapy

Indications and contraindications

In view of the poor prognosis for patients receiving medical treatment, the diagnosis of postinfarction rupture of the interventricular septum is in itself an indication for surgery. Currently, most surgeons agree that early operation effective in minimizing the risk of mortality and morbidity. The success of surgical treatment depends on the rapid medical stabilization of the patient and the prevention of cardiogenic shock.

Relative safety of repair was established after 2-3 weeks or more after perforation. Since the edges of the defect have become stronger and more fibrous, the repair becomes safer and easier to carry out. A successful clinical outcome is associated with adequate closure of the IVS; therefore, if possible, look for multiple defects both before and during surgery.

Initially, recovery should be delayed only when the patient is hemodynamically stable condition, but there must be a high degree of confidence that the patient is indeed stable. In such patients, the condition may suddenly worsen and death may occur. Criteria for delayed surgical treatment include the following:

Adequate cardiac output

No signs of cardiogenic shock

No signs and symptoms of congestive heart failure (CHF) or minimal use of pressor agents to control initial symptoms

No fluid retention

Good renal function

The natural history of the disease is such that few patients present with these signs and symptoms. In most patients, rupture of the interventricular septum after a heart attack quickly leads to a deterioration in the hemodynamic state, with cardiogenic shock, severe and intractable symptoms of CHF and fluid retention. Urgent surgery is usually needed. High surgical risk early recovery accepted due to more high risk death without surgery under such circumstances.

In some cases, there is a delay in the diagnosis and appointment of surgical intervention. Although most patients with postinfarction rupture of the IVS require emergency surgery, the occasional patient, due to a delay in diagnosis or referral, may be in a state of multiple organ failure and may not be a candidate for surgery. The chances of such a patient surviving the operation are minimal; in these circumstances, supportive medical therapy may be adequate. Patients who are in a coma and have cardiogenic shock have a particularly poor prognosis after surgery, and surgery is best avoided in such circumstances.

Forecast

Operative mortality is directly related to the interval between MI and surgery. In retrospective clinical analysis 41 patients treated for postinfarction ventricular septal defect confirmed that while female gender, older age, hypertension, acute anterior wall myocardial infarction, no previous acute myocardial infarction, and late arrival at hospital were associated with a higher risk of mortality from acute rupture of the IVS, the time from the onset of acute myocardial infarction to surgery was the most an important factor determining operative mortality and in-hospital survival.

If repair of a ruptured interventricular septum after a heart attack is performed 3 weeks or more after a heart attack, the mortality rate is approximately 20%; if it is performed before this time, the mortality approaches 50%. Most obvious reason This is that the higher the degree of myocardial damage and hemodynamic disturbances, the more urgent the need for early surgical intervention.

When using the early operative approach, most studies show an overall mortality rate of less than 25%. Mortality is generally lower in patients with anterior IVS rupture and lowest in patients with apical IVS ruptures. For anterior defects, mortality ranges from 10% to 15%; for posterior defects, mortality ranges from 30% to 35%.

In the first week of infarction, the scar is not yet fully formed, and in the presence of risk factors ( high pressure, extensive damage, physical activity) wall rupture may occur. This complication is most often poor prognosis for the life of the patient. For treatment can only be used surgical intervention- Stitching of the wall or septum between the ventricles.

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Causes of a heart rupture

Myocardial infarction is the most probable cause heart rupture, but it can also occur with tumor destruction of myocardiocytes, endocrine diseases. The immediate cause of the rupture of the muscle layer during necrosis of the heart muscle is the weakness and softening of the wall to the formation of dense connective tissue. Therefore, the most likely time of development is the first week from the onset of a heart attack.

Factors that increase the risk of this complication:

• age of patients - in older people, the duration of damage recovery is longer;
• female;
• extensive, penetrating through the entire thickness of the myocardium () necrosis;
• high degree of arterial hypertension;
• severe coughing or vomiting;
• motor excitation;
• primary heart attack (there were no previous angina attacks);
• bouts of chest pain in early period infarction as evidence of the spread of the lesion;
• untimely diagnosis and treatment (more than a day from the beginning);
• early physical activity(violation of bed rest);
• taking corticosteroids and nonsteroidal drugs to relieve inflammation, they prevent the formation of a scar in the area of ​​necrosis;
• the beginning of thrombolytic therapy later than 12 hours from the onset of a heart attack.

Types of rupture of the myocardial wall

Depending on the place of violation of the integrity of the muscular layer of the heart, the following types of pathology are distinguished:

• external - blood flows from the chambers of the heart to the pericardium with the development of tamponade,
• internal - a partition between the ventricles or internal (papillary) muscles.

Left ventricular ruptures are the most common; the atria and right ventricle are rarely injured.

By development time:

• early - up to 72 hours from the onset (more often with extensive and deep infarction),
• late - after 3 days, provoke their hypertension, stress on the heart.

Depending on the breaking speed:

• simultaneous - a sharp gap with pericardial tamponade,
• long - slow flowing with a gradual increase in symptoms.

When examining the structure of the myocardium, damage may affect the entire thickness (complete rupture) or be incomplete. In the latter case, an aneurysmal protrusion of the muscle layer is formed.

Signs of complications of myocardial infarction

The harbingers of the emerging gap are:

• increasing, not decreasing from the use of analgesics and nitrates;
• sticky and cold sweat;
• weak pulse.

With a sudden rupture of the wall, blood from the chambers of the heart enters the pericardial sac, which leads to tamponade, compression of the myocardium from the outside and cardiac arrest.

Patients are in an unconscious state, there is intense cyanosis of the skin of the face, hands, chest, neck veins filled with blood, pulse and pressure are difficult to determine. The cessation of breathing and heart work occurs in a matter of minutes. Therefore, most often it is impossible to save the sick.

The slow development of the gap can be for several hours and even up to 2 - 3 days. Clinical manifestations in such cases are as follows:

• intermittent severe heart pain - undulating and increasing, not amenable to treatment;
• progressive hypotension;
• difficulty breathing;
• increase in cyanosis of the skin.

Prognosis for myocardial rupture

This complication of a heart attack is an extremely adverse effect, since when it occurs, an operation is required within a few minutes, which is usually difficult to perform even in a hospital. Therefore, most often myocardial rupture is considered fatal, but if the area of ​​damage is insignificant, then a blood clot forms at the site of the tear, there are isolated cases of patients surviving, even without surgery.

With timely treatment, the chances of recovery increase, but such patients must observe a sparing regimen for a long time and be under the supervision of doctors, since the sutures on the myocardium must heal under conditions of complete unloading of the heart.

Prevention of heart attack and its complications

In order to reduce the risk of coronary heart disease and all its consequences, it is necessary:

• control blood cholesterol levels, avoid animal fats, take lipid-lowering drugs;
• support arterial pressure in the range of 120 - 140/80 - 90 mm Hg. Art.;
• completely give up smoking, alcohol and self-medication;
• in case of pain in the heart, undergo a complete cardiological examination;
• if an angina attack lasts more than 15 minutes, you need to call an ambulance.

Rupture of the heart muscle is an extremely severe complication of myocardial infarction, its development is usually sudden. Pathology can be provoked by early motor activity, extensive and penetrating into all layers, the affected area. A chance to save a life can only be a timely operation.

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Depending on the time of onset, as well as the complexity, such complications of myocardial infarction are distinguished: early, late, acute period, frequent. Their treatment is not easy. To avoid them, prevention of complications will help.