Early post-infarction angina pectoris – Treatment of hypertension

With myocardial infarction, the muscle and nerve tissue of the heart muscle die in the area below the affected area of ​​the artery. But if living fibers remain in the necrosis zone, the patient develops a syndrome of early post-infarction angina pectoris.

The risk zone includes:

  • patients with coronary artery atherosclerosis, diseases that provoke hypertension and increased blood viscosity, diabetics and overweight people;
  • patients who do not comply with the load regime during the recovery period and / or experience constant stress.

The probability of the disease is increased by specific risk factors:

  • residual stenosis (narrowing) of the coronary arteries due to drug or spontaneous dissolution of a blood clot in an artery – thrombolysis;
  • multiple damage to the vessels of the heart;
  • post-infarction dilation (expansion) of the left ventricle, due to which it cannot fully contract;
  • diastolic pressure drops.

The cause of the development of post-infarction angina pectoris can also be acute myocardial infarction without raising the ST segment. Explaining to the patient his condition, the doctor in a conversation can say about “microinfarction.”

In the development of post-infarction angina pectoris, both common causes for any other types of angina pectoris and specific factors play a role. Common causes include coronary atherosclerosis, hyperlipidemia, obesity, hypertension, diabetes mellitus, an increased tendency to thrombosis, and stress.

Specific factors of post-infarction angina are: the presence of residual stenosis of the coronary arteries after spontaneous or drug thrombolysis; multiple damage to the vessels of the heart; post-infarction dilatation of the cavity of the left ventricle, its systolic dysfunction; increased diastolic pressure.

Post-infarction angina often occurs after heart attacks without raising the ST segment. The pathogenetic mechanisms of early post-infarction angina include severe atherosclerotic lesions of the coronary arteries, impaired integrity (stratification, hemorrhages) of atherosclerotic plaques, progressive vascular stenosis, which are accompanied by functional changes – coronary spasm, impaired and fibrinolysis and hemocoagulation, damage.

In the development of post-infarction angina pectoris, both common causes for any other types of angina pectoris and specific factors play a role. Common causes include coronary atherosclerosis, hyperlipidemia, obesity, hypertension, diabetes mellitus, an increased tendency to thrombosis, and stress.

Specific factors of post-infarction angina are: the presence of residual stenosis of the coronary arteries after spontaneous or drug thrombolysis; multiple damage to the vessels of the heart; post-infarction dilatation of the cavity of the left ventricle, its systolic dysfunction; increased diastolic pressure. Post-infarction angina often occurs after heart attacks without raising the ST segment.

The pathogenetic mechanisms of early post-infarction angina include severe atherosclerotic lesions of the coronary arteries, impaired integrity (stratification, hemorrhages) of atherosclerotic plaques, progressive vascular stenosis, which are accompanied by functional changes – coronary spasm, impaired and fibrinolysis and hemocoagulation, damage.

Post-infarction angina can develop for general reasons, characteristic of all types of pathology, or specific. One of the most common causes is atherosclerosis, whose plaques constrict blood vessels. Common causes include:

  1. hyperlipidemia;
  2. obesity;
  3. hypertension;
  4. stressful situations;
  5. cardiomyopathy;

The most common cause among the specific causes is stenosis in residual form, which appears after thrombolysis. Specific reasons include the following:

  • extensive damage to the heart vessels;
  • dilation of the cavity of the left ventricle arising from a heart attack;
  • systolic dysfunction of the left ventricle;
  • increased diastolic pressure;

Most often, post-infarction angina pectoris manifests itself against a background of a heart attack without raising the ST segment.

The clinical picture of re-im

1)
high frequency among men;

2)
the onset of an acute period with collapse and
dynamic cerebral impairment
blood circulation;

3)
frequent development of thromboembolic
complications and hypostatic pneumonia;

4)
predominance in the clinical picture
heart failure phenomena
cardiogenic shock, cardiac arrhythmias;

5)
lingering or relapsing course,
prolonged preservation of elevated
indicators of resorption-necrotic
syndrome.

ECG symptoms
re MI can be distinct and
characteristic, while maintaining
signs of previous cicatricial
changes in the myocardium, however sometimes
ECG signs of recurrent heart attack
unconvincing, in this case special
diagnostic role
dynamic analysis of ECG, echocardiography,
determination of blood indicators
biomarkers of myocardial necrosis.

Classification and Forms

According to the development mechanism and flow characteristics, RPS syndrome is referred to as variants of unstable angina pectoris. Post-infarction angina is considered one of the most severe forms of the disease and is divided into three varieties:

  1. Early (in the first two weeks). A sudden attack during the first two days after a heart attack speaks of an acute manifestation, the chronic one gradually grows.
  2. Late (in the third or fourth week after a heart attack).
  3. Painless or atypical (can occur in the early and late).

An early manifestation of the syndrome indicates a serious condition of the heart and increases the risk of death of the patient within a year after a heart attack to 20 – 50%. The atypical form is dangerous because, due to the absence of pain, it is difficult to understand how serious damage to the heart muscle is and to prescribe adequate treatment.

Generally accepted
IM classification does not exist. Proceeding
for clinical reasons before
total in terms of volume needed
drug therapy as well as evaluations
forecast, it is advisable to classify
IM in depth (vastness) of necrosis,
localization, clinical features
currents (complicated, uncomplicated),
and also highlight periods of MI.

1.
Depth and extent of necrosis (according to
ECG)


large focal transmural (with
pathological tooth QS)


large focal not transmural (with
pathological Q wave)


posterior (posterior diaphragmatic or lower;
backbasal)

2.2.
Right ventricular myocardial infarction

2.3.
Atrial myocardial infarction

4.
Features of the clinical course

4.1.
Protracted, recurrent, repeated

4.3.
Typical, atypical

RPS itself is not subdivided into other forms, however, it can be acute, occurring suddenly within 48 hours after a heart attack, and chronic, lasting for a long time.

It is also customary to distinguish several functional classes.

  • I – arising for the first time or intensified within a month.
  • II – angina pectoris, developing in the previous month.
  • II – angina pectoris that occurred in the last 48 hours.

About the causes of an attack of such angina pectoris below.

2. The development of thrombosis in the coronary artery

On
angiographic and
pathological studies,
coronary infarction-related thrombosis
arteries are observed with MI in 80-90% of cases,
especially with myocardial infarction
ST and the presence of Q wave.


atherosclerotic hemorrhage
plaque;


the formation of an intracoronary thrombus,
initially unblocking;


thrombus lengthwise
total into the lumen of the coronary artery with
its complete occlusion.

Symptoms

The main symptom of RPS syndrome is painful angina attacks (from Latin ango “squeeze, squeeze”). They have much in common with the typical manifestation of angina pectoris: pain occurs behind the sternum, gives to the left hand, lower jaw, neck, under the shoulder blade, the patient complains of heaviness, burning in the chest. The attack is accompanied by nausea and vomiting, fluctuations in blood pressure, inexplicable fear, anxiety.

Unlike other types of angina pectoris, the pain is accompanied by low and high pressure and is not relieved by Nitroglycerin: discomfort has to be stopped by an intravenous injection of analgesics, including narcotic drugs. Attacks occur at rest or under mild exertion, when a person sits down in bed, they may alternate in one patient.

A sign of post-infarction angina is the resumption of attacks of anginal pain in the period from 1-3 days to 2-4 weeks after the development of acute myocardial infarction. The pain has a localization (behind the sternum) typical of angina pectoris and irradiation (in the neck, left arm, shoulder blade, and lower jaw); poorly stopped with nitroglycerin, often for its removal, the introduction of analgesics is required, in t.

Narcotic. Pain attacks with post-infarction angina can occur both in conditions of absolute rest, and with minor psycho-emotional and physical exertion. Post-infarction angina pectoris is characterized by a low threshold of loads provoking an attack. Sometimes attacks of angina pectoris of rest and tension alternate in the same patient. Angina pectoris may be accompanied by increased blood pressure or hypotension.

A sign of post-infarction angina is the resumption of attacks of anginal pain in the period from 1-3 days to 2-4 weeks after the development of acute myocardial infarction.

The pain has a localization (behind the sternum) typical of angina pectoris and irradiation (in the neck, left arm, shoulder blade, and lower jaw); it is poorly stopped by nitroglycerin, often for its removal, the introduction of analgesics, including narcotic, is required. Pain attacks with post-infarction angina can occur both in conditions of absolute rest, and with minor psycho-emotional and physical exertion.

Post-infarction angina pectoris is characterized by a low threshold of loads provoking an attack. Sometimes attacks of angina pectoris of rest and tension alternate in the same patient. Angina pectoris may be accompanied by increased blood pressure or hypotension.

Atypical cases of post-infarction angina occur with mild pain or a complete absence thereof. In this case, myocardial ischemia is usually accompanied by arrhythmias and heart failure, which are unfavorable prognostic signs. Post-infarction angina pectoris may be complicated by recurrence of myocardial infarction.

A symptom of RPS is pain. Pain fetters a person; he seeks to sit or stop. Patients claim that the pain is stitching and pressing, intense. Often pain can be given to the shoulders, shoulder blades, jaw and very rarely to the lower abdomen. Usually, a pain attack lasts no more than 10 minutes.

A pain attack can be accompanied by other symptoms, for example:

  1. vomiting;
  2. fear of death;
  3. nausea;
  4. increased blood pressure;
  5. heart palpitations;

Diagnosis of post-infarction angina

Anamnestic data are important for making a diagnosis: cardiac pathologies, heart attack, and concomitant diseases. After examination, the patient is given a referral for further examinations:

  1. An ECG at rest reveals RPS in 75% of cases. Daily Holter monitoring gives a more accurate result – continuous recording of an electrocardiogram by a portable device for a day or more.
  2. Coronary angiography (coronarography) visualizes the area of ​​muscle necrosis, narrowing of the arteries, the presence of blood clots. It is carried out on CT or MRI devices.
  3. Ultrasound (Echocardiography) is preferable to prescribe to patients who have preserved the results of an ultrasound scan of the heart before a heart attack.

Instrumental examinations are supplemented by stress tests (with hyperventilation, on simulators) and pharmacological tests with dipyridamole, dobutamine, ergometrine. These examination methods most accurately suggest a recent heart attack and post-infarction angina pectoris. Tests are contraindicated for people who are having a hard time recovering from a heart attack.

The patient is prescribed general and specific laboratory tests. General ones allow revealing concomitant diseases, while specific ones, for troponin and creatine phosphokinase, indicate repeated circulatory disorders and allow us to make a differential diagnosis.

Anamnesis plays a large role in the diagnosis of angina pectoris. When making a preliminary diagnosis, doctors take into account the localization of pain, the duration and causes of its appearance. If you suspect angina, the patient is sent for a hardware examination and asked to take a blood test. The following types of diagnostics are used:

  1. ECG. It is considered a relatively accurate way to diagnose angina pectoris. The disease is detected in 75% of patients. More accurate is daily monitoring using electrocardiography. It allows you to diagnose angina pectoris before a repeated attack of a heart attack.
  2. Ultrasound It is carried out in order to detect changes in the heart muscle.
  3. Coronary angiography of blood vessels. Helps identify lesions in arteries and blood vessels.
  4. Stress tests. They can cause an attack of angina pectoris, which plays a significant role in its diagnosis.

A general blood and urine test is taken in order to identify other diseases that are present in the human body and can affect the heart muscle. Stress tests are carried out extremely carefully. The general condition of the patient is taken into account. If a person is hard to recover from a heart attack, they are not carried out.

The diagnosis of post-infarction angina is confirmed by clinical laboratory and instrumental methods: ECG, ultrasound of the heart, 1-hour ECG monitoring, coronarography, etc. Depression of the ST segment by mm or more, T wave inversion during a pain attack can be recorded on the electrocardiogram.

The differential diagnostic sign of recurrence of myocardial infarction can be an increase in the activity of the myocardial fraction of creatine kinase and troponin. With varying degrees of sensitivity, post-infarction angina can be detected using stress tests (58%), Holter monitoring (27%), and hyperventilation tests (11%).

To assess the general and regional contractile function of the left ventricular myocardium, echocardiography and left ventriculography are performed. When conducting coronarography (CT-coronarography, MSCT-coronarography) in most cases, stenosis of the interventricular (anterior descending) coronary artery is detected; in 8-12% damage to the trunk of the left coronary artery.

The diagnosis of post-infarction angina is confirmed by clinical laboratory and instrumental methods: ECG, ultrasound of the heart, 1-hour ECG monitoring, coronarography, etc. Depression of the ST segment by mm or more, T wave inversion during a pain attack can be recorded on the electrocardiogram.

However, elevation of the ST segment may indicate both acute ischemia and changes associated with a recent heart attack, which reduces the sensitivity of the electrocardiographic diagnosis of post-infarction angina pectoris. The differential diagnostic sign of recurrence of myocardial infarction can be an increase in the activity of the myocardial fraction of creatine kinase and troponin.

With varying degrees of sensitivity, post-infarction angina can be detected using stress tests (58%), Holter monitoring (27%), and hyperventilation tests (11%). To assess the general and regional contractile function of the left ventricular myocardium, echocardiography and left ventriculography are performed.

When conducting coronarography (CT-coronarography, MSCT-coronarography) in most cases, stenosis of the interventricular (anterior descending) coronary artery is detected; in 8-12% damage to the trunk of the left coronary artery. With post-infarction angina, the envelope and diagonal branches of the left coronary artery, the right coronary artery can also be affected; multivascular lesions are common.

Often, angina pectoris can be detected at the first appointment with a cardiologist if the doctor can relate anginal attacks with a previous heart attack. The main diagnosis is made on the basis of hardware research:

  • ECG for the detection of post-infarction angina pectoris. The main diagnostic method, which reveals the displacement of the ST segment, as well as the inversion of the T wave.
  • Load tests. Angina pectoris is detected in about 60% of cases, showing a connection between seizures and stress.
  • Ultrasound of the heart, revealing changes in the heart muscle.
  • Coronary angiography, revealing stenosis of the coronary artery, lesions of the coronary left artery, other signs.
  • Daily ECG monitoring. The study allows you to determine the occurrence of anginal attacks.

Also, the patient is shown general studies, for example, blood and urine tests, which determine the concomitant diseases and the condition of the patient’s body.

Read about how to treat patients diagnosed with early post-infarction angina pectoris.

Pericarditis treatment

The goal of therapeutic and surgical treatment of RPS syndrome is to reduce the risk of re-infarction, and to prevent and stop attacks. At high risk of complications, surgical treatment is recommended.

Depending on the general condition of the patient, the doctor recommends limiting physical activity or staying in bed for at least a month.

The list of medicines used includes:

  • β-adrenergic blockers (Propranolol, Bisoprolol) – reduce the pulse rate, reducing the tension and duration of the attack;
  • calcium antagonists (Cordaflex, Nifedipine) – prevent coronary artery spasm;
  • ACE inhibitors (Captopril, Enalapril, Fosinopril) – reduce blood pressure with hypertension and diabetes;
  • nitrates (Nitroglycerin, Nitrosorbide and preparations based on them: Nitroject, Isoket, Cardiket) – relax the heart muscle, preventing and stopping attacks, with severe pain Nitroglycerin is administered dropwise;
  • direct anticoagulants (Heparin) and antithrombotic drugs (Aspirin, Ticlopidine, Clopidogrel) – prevention of thrombosis.

Patients who have used certain medications before a heart attack are prescribed in large doses. During the treatment course, regular monitoring of the state of the heart and blood vessels is carried out.

With frequent seizures and a high risk of recurrent heart attack, the patient is recommended a planned surgical intervention:

  • coronary artery bypass grafting (operative formation of a “workaround” for blood flow, which goes around the damaged part of the vessel);
  • balloon angioplasty (a catheter with a balloon is inserted into the lumen of the vessel, which is inflated and deflated several times to stretch the vascular walls, and then removed);
  • artery stenting (installation of a mesh frame in the narrowed part of the vessel to restore patency).

The operation is performed no earlier than 3 to 4 weeks after a cardiovascular accident. At the same time, symptomatic and supportive therapy is continued and physical activity is limited.

Treatment can be medical and surgical. Particular attention is paid to bed rest. For a full recovery, the patient will have to completely abandon bad habits. Do not smoke or drink alcohol. Medicines are selected individually.

If repeated seizures occur, doctors are considering surgical treatment. The operation can not be performed earlier than 21 days after a heart attack. The essence of all operations is to normalize the work of the coronary vessels. For this, shunts, stents are installed or cholesterol plaques are directly removed.

About
in 10-20% of patients with an acute period of heart attack
signs of myocardium
pericarditis. Most often, pericarditis
develops with transmural infarction
myocardium. The course of pericarditis in
in most cases favorable
usually pericarditis is dry (fibrinous).

Treatment
measures for pericarditis is
in the following.

Assigned
NSAIDs – indomethacin (75-100 mg per day),
voltaren or orthophene (75-100 mg per day),
ibuprofen (0.6-1.2 g per day). NSAID treatment
conducted within 6-7 days against
taking antacids (to avoid
damage to the gastric mucosa).

RџSЂRё
severe pain and insufficient
NSAIDs may be administered
treatment with glucocorticoid drugs.
Prescribing prednisone in the initial
daily dose of 20-40 mg with its quick
reduction, the course of treatment is usually not
exceeds 7-10 days. Long-term therapy
glucocorticoids are contraindicated.

Autoimmune
Dressler’s post-infarction syndrome –
this is an autoimmune syndrome,
developing a heart attack in a patient
myocardium at the 2-6th week of the disease and
manifested by the clinic of pericarditis,
pleurisy, joint damage (synovitis,
polyarthralgia), sterno-costal
articulations (anterior thoracic syndrome
walls), leukocytosis, eosinophilia,
an increase in ESR, an increase in temperature
body.

It should be noted that far from
always at the dressler syndrome clinic
all of the above is present
symptomatology can only occur
symptoms of pericarditis, pleurisy,
polyarthralgia, laboratory signs
inflammatory process. Pericarditis
and pleurisy may be fibrinous or
exudative.

Typical
Dressler autoimmune syndrome
observed in 3.5-5.8% of patients with heart attack
myocardium, the frequency of autoimmune syndrome
taking into account typical, atypical and
malosymptomatic forms is 15-23%.

В
association with the autoimmune genesis of the syndrome
Prednisone is prescribed in the initial
dose of 20-40 mg per day, in the absence of effect
after 2-3 days, this dose increases in
1.5-2 times. After receiving therapeutic
the effect of the daily dose of prednisolone
reduced by 2.5 mg every 5-7 days. At
mild postinfarction
treatment duration syndrome
prednisone is 2-4 weeks. At
recurrent course of the syndrome
minimum maintenance dose
prednisone (usually 2.5-5 mg) is taken
for months.

NSAIDs
(indomethacin, voltaren, ibuprofen and
etc.) are assigned only with severe
pain syndrome as analgesics
for several days.

Conservative therapy for post-infarction angina pectoris is aimed at stopping and preventing angina attacks, and preventing reoccurrence of myocardial infarction and its complications. Patients are assigned a bed or half-bed regimen, complete physical and mental rest, hypocaloric nutrition, monitor control.

Medication for post-infarction angina includes the use of beta-blockers (metoprolol, propranolol, atenolol), nitrates (nitrosorbide) and calcium antagonists (nifedipine). Some cardiologists with severe combat syndrome simultaneously prescribe intravenous drip of nitroglycerin.

In the complex treatment of post-infarction angina pectoris, antithrombotic drugs (acetylsalicylic acid, ticlopidine), direct anticoagulants (heparin subcutaneously) are used. Since post-infarction angina pectoris significantly increases the risk of re-catastrophe, with repeated attacks after coronary angiography, the issue of aorto-coronary artery bypass grafting, percutaneous trinsluminal coronary angioplasty and stenting of the affected coronary artery is resolved.

Conservative therapy for post-infarction angina pectoris is aimed at stopping and preventing angina attacks, and preventing reoccurrence of myocardial infarction and its complications. Patients are assigned a bed or half-bed regimen, complete physical and mental rest, hypocaloric nutrition, monitor control.

Medication for post-infarction angina includes the use of beta-blockers (metoprolol, propranolol, atenolol), nitrates (nitrosorbide) and calcium antagonists (nifedipine). Some cardiologists with severe combat syndrome simultaneously prescribe intravenous drip of nitroglycerin.

Since post-infarction angina pectoris significantly increases the risk of re-catastrophe, with repeated attacks after coronary angiography, the issue of aorto-coronary artery bypass grafting, percutaneous trinsluminal coronary angioplasty and stenting of the affected coronary artery is resolved.

The treatment of angina pectoris is aimed at the prevention of pain attacks, complications of the pathology and prevention of recurrent heart attack. The basis of treatment is the therapeutic and drug methods. Treatment is carried out in a hospital, which allows you to fully control the patient’s condition.

The basis of therapy is the restriction of motor activity and smoking cessation. The patient should remain calm and quit smoking. It is also necessary:

  1. observe a hospital diet;
  2. observe the regime of work and rest;

After discharge from the hospital, the patient must be observed by a cardiologist, follow all recommendations of the attending doctor.

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Medicated

Drug therapy includes such drugs:

  • Antithrombolic, for example, aspirin, which prevents the formation of blood clots.
  • Nitroglycerin to relieve heart pain.
  • Direct anticoagulants, for example, heparin.
  • Beta blockers, such as atenolol or propranolol, which eliminate ischemic manifestations and reduce vascular damage.
  • Calcium antagonists, if there are contraindications for taking beta-blockers.

Additional medications, such as laxatives, may also be prescribed.

Operation

Post-infarction angina pectoris many times increases the risk of recurrence of a heart attack. And if medication does not give results, it is necessary to resort to surgical intervention. The main types of operations include:

  • Coronary artery bypass grafting, in which a workaround is created for the bloodstream.
  • Stening of the affected artery, in which a stent is placed in it to maintain a normal state.

Very rarely, a heart after a myocardial infarction is affected so badly that an organ transplant is required.

Dosing and Administration

CHD: angina pectoris (treatment. Prevention). Vasospastic angina pectoris (Prinzmetal). Unstable angina pectoris. Coronary artery spasm during coronary angiography. Acute coronary syndrome. Acute myocardial infarction. Acute left ventricular failure (cardiac asthma. Interstitial and alveolar pulmonary edema).

Chronic heart failure. Controlled arterial hypotension during surgical procedures. Prevention of hypertensive reactions with endotracheal intubation. Skin cuts. Sternotomy. Occlusion of the central retinal artery. Esophageal dyskinesia. Functional cholecystopathy. Acute pancreatitis. Biliary colic. Spastic intestinal dyskinesia.

In / in, sublingual, transdermal, inward, subbuccally.

In the acute period of myocardial infarction and with the development of acute heart failure, it is prescribed under strict control of hemodynamics. It is used with caution in case of aortic and mitral stenosis, in patients with hypovolemia and low blood pressure (less than 90 mmHg). With hypertrophic cardiomyopathy, it can cause an increase and / or aggravation of angina attacks.

With prolonged uncontrolled administration of nitroglycerin, the administration of high doses to patients with liver failure and children, the risk of methemoglobinemia, manifested by cyanosis and the appearance of a brown tint in the blood, increases. In cases of the development of methemoglobinemia, the drug must be urgently canceled and an antidote is introduced – methylthioninium chloride (methylene blue).

If it is necessary to continue using nitrates, it is mandatory to control the content of methemoglobin in the blood or replace nitrates with sydnonimines. To reduce the risk of side effects, caution should be exercised while taking with drugs with pronounced hypotensive and vasodilating properties;

taking the drug against the background of alcohol consumption is not recommended in rooms with a high ambient temperature (bath, sauna, hot shower), as well as taking several tablets at the same time or sequentially for a short period of time at the first dose. You can not chew tablets and capsules in order to stop an attack of angina pectoris, because an excess amount of the drug from the destroyed microcapsules through the mucous membrane of the oral cavity can enter the systemic circulation.

With the appearance of a headache and other unpleasant sensations in the head area, improvement is achieved by the administration of validol or drops of menthol sublingually. Often only the first doses are poorly tolerated, then the side effects subside. With simultaneous use with heparin, it is necessary to increase the dose of heparin and strictly control the partially activated thromboplastin time.

Use with caution in elderly patients. The appointment of buccal forms is not recommended for patients with aphthous stomatitis, gingivitis, periodontal and root system diseases, removable upper dentures. Uncontrolled intake can lead to the development of tolerance, expressed in a decrease in the duration and severity of the effect with regular use or the need to increase the dose to achieve the same effect.

With the regular use of prolonged forms of nitroglycerin, especially plasters and ointments, the drug is almost always present in the blood, so the risk of tolerance increases significantly. To prevent the occurrence of resistance, intermittent administration during the day is necessary, or co-administration of calcium antagonists, ACE inhibitors, or diuretics.

Transdermal forms of nitroglycerin are recommended to be removed from the body at night, thus leaving a period free from the action of the drug. In this case, one should beware of the development of withdrawal syndrome associated with a sharp cessation of nitroglycerin intake in the body and manifested by the sudden development of angina attacks.

With the on / in the introduction, the development of tachyphylaxis is possible, which requires a change in dosage in the direction of increase. The degree of tolerance can be judged by the dynamics of pressure in the right atrium. Approaching a tolerance index of 25% requires stopping the introduction of the solution. To imitate the development of tolerance during intravenous administration, a decrease in the content of nitroglycerin in the solution can occur due to a violation of the administration technique, destruction of nitroglycerin by direct exposure to light rays or its absorption on the walls of the plastic infusion system (20-80% when using systems of polyvinyl chloride, polystyrene butadiene, propionate cellulose, latex or polyurethane).

It is recommended to use systems of chemically pure glass, polyethylene, nylon, teflon, silicone. It is not recommended to use too long hydraulic lines. With the on / in the introduction of nitroglycerin, it is necessary to take into account that after the termination of infusion and when the patient is transferred to tabletted (even long-acting) nitrates, withdrawal syndrome or insufficient dose may occur, while it is possible to increase the frequency of complications in the acute period of myocardial infarction – increased angina attacks, increase phenomena of circulatory failure, recurrence of myocardial infarction, the formation of acute cardiac aneurysm, an increase in the frequency of myocardial ruptures. 42a96bb5c8a2acfb07fc866444b97bf1

First aid

First aid during an attack of RPS does not differ from that which must be provided with typical angina pectoris. However, it cannot be removed with the usual medications, so you must immediately call an ambulance. Before doctors:

  • comfortably seat the patient – if the attack began while lying down, help the person sit down and hang his legs from the bed;
  • unfasten his collar, and clothes with a narrow neck should be removed;
  • ventilate the room;
  • give the victim a tablet of Nitroglycerin, and after five minutes – one more.

People with low blood pressure are not recommended to take Nitroglycerin, and Aspirin helps to relieve the condition. Those patients who have recently suffered a heart attack should not refuse hospitalization and examination, even if the pain in the heart was short-lived.

Indications for use

Hypersensitivity, pronounced hypotension, collapse, myocardial infarction with low final diastolic pressure in the left ventricle and / or severe hypotension (with arterial pressure below 90 mmHg) or collapse, right ventricular infarction, bradycardia less than 50 beats. / min Primary pulmonary hypertension. Brain hemorrhage.

Head injury. Increased intracranial pressure. Cerebral ischemia. Heart tamponade. Toxic pulmonary edema. Severe aortic stenosis. States. Accompanied by a decrease in the final diastolic pressure in the left ventricle (isolated mitral stenosis. Constrictive pericarditis). Angle-closure glaucoma. Pregnancy. Lactation.

Possible complications after myocardial infarction

RPS syndrome suggests that functional cells remained in the area of ​​cardiac muscle necrosis: if they die, the heart attack will recur. One of the possible complications of RPS is coronary artery thrombosis.

The general prognosis of the disease depends on whether the heart attack was primary or recurrent. Other factors:

  • age of the patient;
  • severity and degree of damage to the heart;
  • timeliness of thrombolytic therapy;
  • the presence / absence of attacks before a heart attack.

The early and atypical forms of the syndrome have a less favorable prognosis: the first indicates significant myocardial damage, and the atypical forms are difficult to diagnose – against the background of the absence of pain, arrhythmias progress, heart failure develops and becomes chronic.

Most often, RPS is complicated by the transition to another form of angina pectoris, which can lead to a recurrence of a heart attack. In turn, a heart attack is the most common complication.

RPS can also be complicated by heart rhythm disturbances, thrombosis, and chronic heart failure.

Myocardial infarction is an insidious disease that takes the lives of many people. Death does not always occur, but even a surviving patient may face serious complications, the likelihood of which is very high. Complications of myocardial infarction manifest themselves in different ways, a lot depends on the time that has passed after the attack, the patient’s condition and other factors.

  • Classification of complications
  • Acute complications
  • Late consequences
  • Other complications
  • Treatment of complications
  • Prevention

disease prevention

During treatment and after completing a course of therapy, the patient must carefully follow the doctor’s recommendations, which are developed for a particular patient, but always include:

  • complete cessation of smoking (a bad habit by half increases mortality from cardiovascular disease) and alcohol;
  • diet
  • adequate loads – physiotherapy exercises, swimming;
  • treatment of concomitant diseases;
  • normalization of weight;
  • supportive drug therapy.

RPS syndrome is a serious complication of a heart attack. To minimize the risk of relapse, you need to undergo a timely medical examination. Noticing signs of deterioration, the doctor will adjust the treatment and prescribe additional measures to restore the body.

Secondary
prevention after MI
aims to prevent
death, development re
MI and chronic heart failure


indirect anticoagulants (warfarin,
Sincumar and others.);


ACE inhibitors (in patients with symptoms
heart failure in acute
MI period);


amiodarone (cordaron) (in patients with dangerous
ventricular arrhythmias);


hypocholesterolemic drugs from
Vastatin groups

Application
indirect anticoagulants for secondary
prevention after myocardial infarction

Extremely
effective for secondary
prophylaxis after myocardial infarction are indirect
anticoagulants. However, due to the large
the risk of hemorrhage these drugs have
patients with myocardial infarction are prescribed
only at high risk of development
systemic thromboembolism (atrial
arrhythmia, congestive heart
insufficiency, parietal thrombosis
left ventricle). While reducing risk
development of systemic thromboembolism
indirect anticoagulants cancel and
prescribe aspirin

Application
aspirin for secondary prevention
after
myocardial infarction

Aspirin
during secondary prevention
after MI less effective than indirect
anticoagulants (reduces mortality by
15%, the frequency of repeated MI – by 31%), but
much less likely to cause side effects
effects. Aspirin is prescribed in a dose.
160-325 mg / day, however prophylactic
the effect is achieved when using
doses of 75-150 mg / day.

Application
β-blockers for secondary
prevention after myocardial infarction

β-blockers
it is advisable to appoint all patients
undergoing MI, in the absence of
contraindications. Should combine them
with hypocholesterolemic drugs
from the group of vastatin (simvastatin,
pravastatin, lovastatin, fluvastatin
and etc.). These prepartes neutralize the negative
effect of β-blockers on lipid
exchange and, in addition, significantly reduce
mortality and recurrence rate
myocardium.

RџSЂRё
life-threatening ventricular
treatment refractory arrhythmias
β-blockers, used
amiodarone (cordaron).

Application
sulodexide for secondary prevention
after myocardial infarction

D.M.
Aronov et al. (1995) suggest using
for secondary prevention after
myocardial infarction, as well as with unstable
low-molecular-weight angina pectoris
heparin sulodexide (Wessel).

Sulodexide
by the strength of antithrombotic action
not inferior to heparin, but compared
with it very rarely causes hemorrhagic
complications and thrombocytopenia. A drug
initially assigned 600 units intramuscularly
2 times a day for 15 days; further on
500 PIECES inside (in capsules) 2 times a day in
for three months or more.

Application
ACE inhibitors for secondary prevention
after myocardial infarction

2)
treatment with ACE inhibitors can begin
on the first day of acute myocardial infarction
after assessing the clinical condition and
hemodynamic parameters (decrease
diastolic blood pressure below 100 mm Hg. Art.
is a contraindication) and purpose
other conventional means (thrombolytics,
aspirin, β-blockers);

3)
treatment with ACE inhibitors should not be
delay due to high mortality
in the acute phase of MI;

4)
ACE inhibitors prescribed in acute
MI period, can be canceled after 4-6
weeks in the absence of left dysfunction
ventricle;

5)
ACE inhibitor dose should be selected
individually.

Inhibitors
ACEs reduce the frequency of repeated MI,
mortality from myocardial infarction and prevent development
or reduce the severity of failure
blood circulation. Positive action
ACE inhibitors explained by the warning
progressive dilation of the left
ventricle, decreased activity
renin-angiotensin system.

Application
hypocholesterolemic agents for
secondary prevention after heart attack
myocardium

1)
statins are effective secondary
prophylaxis in patients with clinical
manifestations of coronary heart disease;

2)
long-term statin therapy increases
survival not only in patients with
angina pectoris or myocardial infarction, but also
patients with hypercholesterolemia without
clinical manifestations of ischemic heart disease.

Preventive measures are aimed at improving the patient’s lifestyle. So, it is recommended:

  • Create a balanced diet for yourself, for example, limit the consumption of fatty and sweet, alcohol, lean on vegetables, cereals, lean meat and fish.
  • Stop tobacco completely. It is proved that smoking by about 40% increases the likelihood of myocardial infarction.
  • Exercise regularly. These should be moderate and constant loads: at least 20 minutes per day. Particular attention should be paid to cardio exercises, for example, squats that develop the heart muscle.

Next, we will tell you about the emergency care algorithm for the symptoms and signs of an attack of early post-infarction angina pectoris in women and men.

Possible complications and prognosis

Early post-infarction angina is an unfavorable prognostic sign, several times increasing the risk of recurring heart attack and sudden death. Post-infarction angina does not respond well to drug therapy, so about 60% of patients are candidates for myocardial revascularization operations.

Surgical intervention allows to improve the clinical condition in 80-90% and the disappearance of postinfarction angina syndrome in 60% of patients. Perioperative myocardial infarction develops in 5-7% of cases, mortality is about 1%. In the pre- and postoperative period, patients need dynamic monitoring by a cardiac surgeon. 42a96bb5c8a2acfb07fc866444b97bf1

Early post-infarction angina is an unfavorable prognostic sign, several times increasing the risk of recurring heart attack and sudden death. Post-infarction angina does not respond well to drug therapy, so about 60% of patients are candidates for myocardial revascularization operations.

Surgical intervention allows to improve the clinical condition in 80-90% and the disappearance of postinfarction angina syndrome in 60% of patients. Perioperative myocardial infarction develops in 5-7% of cases, mortality is about 1%. In the pre- and postoperative period, patients need dynamic monitoring by a cardiac surgeon.

The prediction problem is that post-infarction angina does not respond well to drug therapy and increases the risk of re-development of a heart attack (7% of relapses among patients). Therefore, approximately 60% of patients require myocardial revascularization subsequently.

If we talk about surgical treatment, then about 90% of patients have a significant improvement, and full recovery occurs in about 60% of patients. Mortality from angina pectoris is extremely low – 1%.

For many years, diseases of the cardiovascular system have confidently led the way in the sad list of mortality, but so far not a single, even the best, specialist will take the responsibility to say how much they live with coronary heart disease. The disease does not spare either old or young, we are talking about a real epidemic.

The first group includes:

  • heart disease (defects, cardiac conduction disturbance, myocardial disease);
  • internal organs or systems (lungs, thyroid gland, blood);
  • hypertonic disease.

The second group includes:

  • bad habits (alcohol, smoking, drugs);
  • irrational nutrition (overeating, inclusion in the diet of fatty, salty, rich in preservatives food);
  • chronic stress;
  • sedentary lifestyle;
  • excessive physical activity (especially in untrained people).

Exposure to both internal and external factors gradually leads to atherosclerosis of the coronary arteries. The disease is characterized by deposition of cholesterol plaques on the vascular walls. As they grow, the lumen of the vessel narrows more and more, the amount of oxygen supplied by the blood decreases, and ischemia develops. With complete closure of the lumen of the vessel, necrosis occurs, in which necrosis of the heart muscle tissue occurs.

Classical coronary heart disease in most cases occurs gradually and develops over many years.

During this time, it goes through several stages:

  • Asymptomatic.
  • Stable angina.
  • Unstable angina.
  • Myocardial infarction.

There are such forms of the disease as sudden coronary death, cardiac arrhythmias, microvascular ischemia.

Angina pectoris manifests itself in the form of periodic seizures lasting no more than 5 minutes, during which a person is disturbed by uncomfortable sensations behind the sternum with radiation to the left shoulder blade, shoulder or arm. The patient does not experience pain as such, but there is burning or squeezing, the exact location of which is difficult to determine, so the person continues to live with this disease.

With an unstable form of angina pectoris:

  • attacks worry more and more;
  • their duration increases;
  • lowering the threshold of physical activity;
  • decrease in the effectiveness of drugs taken.

Depending on the ability to tolerate physical activity, angina pectoris is divided into four functional classes (I, II, III, IV).

With myocardial infarction, the influx to the heart muscle abruptly stops, due to which the nutrition in the myocardium is interrupted, and the tissues begin to die. Sudden coronary death occurs due to a sharp spasm of the coronary arteries.

A heart attack is accompanied by:

  • Unconsciousness.
  • Cardiac arrest and breathing.

In this case, it is necessary to immediately provide assistance, because the life of the patient will depend on the timeliness of resuscitation.

Patients with coronary artery disease may develop complications:

  • postinfarction cardiosclerosis;
  • arrhythmia;
  • cardiogenic shock;
  • acute and chronic heart failure.

In the initial stages of the disease, a good effect is given by drug therapy aimed at eliminating or attenuating the factors that cause coronary heart disease. In the absence of an effect or threat of complications, surgery is performed.

Modern methods of restoring blood flow in the arteries:

  • stening (a thin mesh tube inserted into the vessel prevents the walls from falling off);
  • aterectomy (thrombus dissection);
  • brachytherapy (radiation therapy inside a diseased organ);
  • coronary artery bypass grafting (insertion into the bloodstream of the internal thoracic artery instead of the affected part of the vessel);
  • Indirect laser revascularization of the heart muscle (laser pinpoint on the myocardium to form a new vascular network).

The effectiveness of treatment and patient survival depends on many factors, including:

  • IHD stage.
  • Location and degree of vascular damage.
  • The condition of the heart muscle.
  • The severity of atherosclerosis of the coronary arteries.
  • The presence of heart rhythm disturbance.
  • The number of affected arteries.
  • Functional class of coronary disease.
  • The age of the patient.
  • The presence of concomitant diseases or complications.

A patient with ischemic heart disease is recommended to adhere to simple rules so that the disease from a sentence is transformed into a special lifestyle.

  • regularly take medications prescribed by a specialist;
  • control blood pressure;
  • periodically take a blood test to determine the level of sugar and cholesterol;
  • using an ECG and other research methods to determine the performance of the heart muscle;
  • periodically visit specialists (cardiologist, therapist);
  • undergo specialized spa treatment.

The main emphasis is on the patient’s desire to maintain physical, psychoemotional and social well-being at an acceptable level. In the power of each person to learn to control the manifestations of the disease, cope with them in time and maintain a satisfactory quality of life.

Since time immemorial, it is known that many diseases are easier to prevent than to treat. Coronary heart disease is no exception.

The following rules can significantly reduce the risk of developing coronary heart disease:

  • To give up smoking.
  • Maintaining optimal weight.
  • Regular physical activity.
  • Preventive medical examinations.
  • Compliance with the regime of work and rest.
  • The principles of proper nutrition.

9. Therapeutic nutrition

Food
patients in the intensive care unit do not
should be burdensome for
of cardio-vascular system. Daily allowance
energy value of the diet
makes 1000-1500 kcal.

В
in order to reduce the load on
cardiovascular system recommended
fractional (5-6 times) small meals
in portions. Easily digestible,
rough foods poor in cholesterol and
animal fats, not causing
increased gas formation. Food
should contain enough
potassium, plant fiber and not more
4-5 g of table salt.

В
diet must include foods
bowel movements
(prunes, dried apricots, beets, vinaigrette,
vegetable oil, etc.). Normalization
stool is extremely important as constipation
and straining worsen coronary
blood circulation and promote development
arrhythmias of the heart.

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Svetlana Borszavich

General practitioner, cardiologist, with active work in therapy, gastroenterology, cardiology, rheumatology, immunology with allergology.
Fluent in general clinical methods for the diagnosis and treatment of heart disease, as well as electrocardiography, echocardiography, monitoring of cholera on an ECG and daily monitoring of blood pressure.
The treatment complex developed by the author significantly helps with cerebrovascular injuries and metabolic disorders in the brain and vascular diseases: hypertension and complications caused by diabetes.
The author is a member of the European Society of Therapists, a regular participant in scientific conferences and congresses in the field of cardiology and general medicine. She has repeatedly participated in a research program at a private university in Japan in the field of reconstructive medicine.

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