Myocardial infarction: general information

Myocardial infarction develops because of acute obstruction of the coronary artery. The consequences depend on the degree of obstruction and range from unstable angina to myocardial infarction without ST- segment elevation (HSTHM), ST-ST elevation and sudden cardiac death. The manifestations of each of these syndromes are similar (except sudden death) and include discomfort in the chest with or without dyspnea, nausea and profuse sweating. The diagnosis is established with the help of ECG, and also on the basis of the presence or absence of serological markers. Treatment of myocardial infarction involves the appointment of antiplatelet drugs, anticoagulants, nitrates, b-adrenoblockers and (with myocardial infarction with ST-segment elevation) immediate restoration of blood supply to the myocardium by thrombolysis, NOVA or CABG.

In the United States, there are approximately 1.5 million myocardial infarctions per year. Myocardial infarction results in death in 400 000-500 000 people, with about half of them dying before they are taken to the hospital.

There are 2 main variants of myocardial infarction: "myocardial infarction with Q-wave" (or "Q-infarction") and "myocardial infarction without a Q wave".

Synonyms of the term myocardial infarction with a Q-wave: large-focal, transmural. Synonyms of the term myocardial infarction without a tooth Q: fine-focal, subendocardial, nontransmural, intramural or even "micro-infarction" (clinically and by ECG these variants of myocardial infarction are indistinguishable).

A precursor of myocardial infarction with Q wave is "acute coronary syndrome with ST segment elevation", and a precursor of myocardial infarction without a Q wave is "acute coronary syndrome without ST segment elevation" (in some patients with STS elevation, myocardial infarction without Q , and vice versa, in a number of patients with ACS without ST elevation, myocardial infarction with a Q-tooth subsequently develops).

Characteristic ECG changes in dynamics (appearance of Q wave) in comparison with the clinical picture are sufficient to establish the diagnosis of myocardial infarction with a Q wave. In myocardial infarction without a Q tooth, ECG and / or T wave changes are most often observed on the ECG; Changes in the ST segment and T wave are non-specific and may be absent altogether. Therefore, in order to establish a diagnosis of myocardial infarction without Q wave, it is necessary to identify biochemical markers of myocardial necrosis: an increase in the level of cardiac troponins T (or I) or an increase in MB CK.

The clinical picture, the nature and frequency of complications, treatment measures and prognosis differ markedly in myocardial infarction with a Q wave and in infarctectomy without a Q wave. The direct cause of a myocardial infarction with a Q-wave is thrombolytic occlusion of the coronary artery. With myocardial infarction without a Q wave, occlusion is incomplete, rapid reperfusion occurs (spontaneous lysis of the thrombus or a decrease in the concomitant spasm of the coronary artery) or the cause of myocardial infarction is the microembolia of the small coronary arteries by platelet aggregates. With ACS with ST segment elevation and myocardial infarction with Q wave, it is possible to perform thrombolytic therapy earlier, and with ACS without ST elevation and myocardial infarction without a Q wave, thrombolytic administration is not indicated.

The main features of myocardial infarction without a Q wave are:

• Depression of the ST segment and inversion of the T wave do not localize the zone of infarction or ischemia (in contrast to the ST segment or Q wave).
• With myocardial infarction without a Q wave, changes on the ECG may be absent.
• Less often than with myocardial infarction with a Q wave, there is a heart failure and 2-2.5 times lower than the mortality rate during inpatient stay.
• The recurrence of myocardial infarction is 2-3 times more frequent than in myocardial infarction with a Q wave.
• In patients with myocardial infarction without a Q wave, the angina is more frequent in the anamnesis and a more pronounced lesion of the coronary arteries is detected than in patients with a myocardial infarction with a Q wave.
• With prolonged follow-up in patients with myocardial infarction with Q-wave, mortality is approximately the same as in patients with myocardial infarction with Q-wave (according to some data, long-term prognosis in patients with myocardial infarction without Q wave is even worse than in myocardial infarction with tooth Q).

The issues of diagnosis and treatment of myocardial infarction without a Q wave are discussed in detail in the section "Acute Coronary Syndrome".

The isolation of any intermediate forms of IHD (for example, "focal dystrophy of the myocardium," "acute coronary insufficiency," etc.) from the clinical point of view is meaningless, since there is neither a definition of these concepts nor criteria for their diagnosis.

Two months after the onset of myocardial infarction, a patient who underwent myocardial infarction was diagnosed with postinfarction cardiosclerosis. The emergence of a new myocardial infarction within 2 months from the onset of myocardial infarction is commonly called recurrence of myocardial infarction, and the occurrence of a new myocardial infarction in 2 months or more by repeated myocardial infarction.

[1], [2], [3], [4], [5],

Causes of myocardial infarction

Acute coronary syndromes (ACS) usually develop in cases when there is an acute thrombosis of an atherosclerotic coronary artery. Atherosclerotic plaque sometimes becomes unstable or inflames, which leads to its rupture. In this case, the contents of the plaque activate platelets and a cascade of coagulation, resulting in acute thrombosis. Activation of platelets leads to conformational changes in the IIb / IIIa glycoprotein receptors of the membrane, which leads to gluing (and, thus, accumulation) of platelets. Even an atherosclerotic plaque, which blocks the blood flow to a minimum, can tear and lead to thrombosis; more than 50% of cases the vessel is narrowed by less than 40%. As a result, the thrombus sharply limits the flow of blood to the sites of the myocardium.

Myocardial infarction: causes

[6], [7], [8], [9], [10], [11], [12], [13], [14]

Symptoms of myocardial infarction

The main and most frequent clinical manifestation of myocardial infarction is pain, most often in the chest area behind the sternum. Pain sensations with myocardial infarction are usually more intense than with angina pectoris, and usually last more than 30 minutes, often several hours or even days. Simultaneously with pain, fear arises, profuse sweat, a sense of imminent death. Patients are restless, constantly moving, seeking to find a position that alleviates pain. Some patients experience nausea, there may be vomiting (more often with lower myocardial infarction).

Among abnormal variants of myocardial infarction, abdominal pain (abdominal pain, nausea, vomiting), asthmatic (cardiac asthma or pulmonary edema), arrhythmic, cerebral, painless or low-symptomatic (including completely asymptomatic - "mute" which, according to epidemiological data, accounts for about 20%).

In an objective examination, patients with "uncomplicated" myocardial infarction often have tachycardia and an increased respiratory rate due to anxiety (but these signs may be a manifestation of heart failure). The blood pressure is usually normal or slightly increased. With myocardial infarction of the lower location, sinus bradycardia is often observed with a tendency to lower blood pressure (especially in the first hours). When viewed and / or palpated in patients with anterior MI, the so-called precardial (paradoxical) pulsation may be noted - the second systolic impulse to the inside of the apical impulse to the left of the sternum in III-IV intercostal spaces (manifestation of the dyskinesia of the anterior wall of the left ventricle - swelling during systole). At auscultation, muffling of tones and appearance of IV heart tone may be noted (atrial or presystolic gallop rhythm - reflects a decrease in left ventricular dilatation). Listening to III tone is a sign of heart failure, i.e. Complicated myocardial infarction. In some patients with a myocardial infarction with a Q wave, the pericardial friction noise is heard (usually on the 2nd day). This is a sign of transmural myocardial infarction with reactive inflammation of the pericardium - episthenocardial pericarditis.

Many patients have a fever, one of the early signs of myocardial infarction is neutrophilic leukocytosis, sometimes up to 12-15 thousand in μl (the increase in the number of white blood cells begins after 2 hours and reaches a maximum of 2-4 days), from 2-4 days begins acceleration of ESR, C-reactive protein is detected. The registration of these changes (temperature, leukocytes, ESR, C-reactive protein) has definite value in the diagnosis of myocardial infarction without a Q wave, if there is no possibility of determining the activity of troponins or MB CK.

Mortality of patients with myocardial infarction is about 30%, with half the deaths occurring in the first 1-2 hours in the prehospital stage. The main cause of death at the prehospital stage is fibrillation of the ventricles, half of the patients die within the first hour of myocardial infarction. It should be noted that in cases of death of patients within 2-2.5 hours from the onset of myocardial infarction, standard histological methods do not allow detecting signs of myocardial infarction (and even special histochemical methods are not accurate enough). This may be one of the reasons for the discrepancy between the clinical diagnosis and the results of the pathoanatomical study. Hospital mortality is about 10%. After discharge from the hospital, the death rate in the first year is 4% on average, while in elderly people (over 65 years) the death rate is much higher: in the first month - up to 20%, in the first year - up to 35%.

Myocardial infarction: symptoms

Complications of myocardial infarction

Electrical dysfunction occurs in more than 90% of patients with myocardial infarction. Electrical dysfunction, which usually leads to death in the first 72 hours, includes tachycardia (from any source) with a sufficiently high heart rate, capable of reducing cardiac output and lowering blood pressure, an atrioventricular block of the Mobitz II type (2 degrees) or complete (grade 3), ventricular tachycardia (VT) and ventricular fibrillation (VF).

Myocardial infarction: complications

[15], [16], [17], [18], [19], [20], [21], [22], [23]

Diagnosis of myocardial infarction

As noted, two main variants of myocardial infarction are distinguished: myocardial infarction with Q-wave and myocardial infarction without Q-wave. When an abnormal Q-wave is recorded on two or more adjacent leads, MI with a Q-wave is diagnosed on the ECG.

Registration of pathological Q waves is called large-scale ECG changes. With myocardial infarction without a Q wave, in most cases, changes in the ST segment and T wave are noted. These changes can be of any duration or even absent. Sometimes, as a result of early thrombolysis, myocardial infarction with Q-wave does not develop in STS patients with ST-segment elevation.

Myocardial infarction: diagnosis

[24], [25], [26], [27], [28], [29], [30],

Treatment of myocardial infarction

The general plan of management of patients with myocardial infarction can be presented in the following form:

1. To stop the pain syndrome, calm the patient, give aspirin.
2. Hospitalize (to deliver to BIT).
3. Attempt to restore coronary blood flow (reperfusion of the myocardium), especially within 6-12 hours from the onset of myocardial infarction.
4. Measures aimed at reducing the size of necrosis, reducing the degree of violation of the function of the left ventricle, preventing recurrence and repeated myocardial infarction, reducing the incidence of complications and mortality.

Pain relief syndrome

The cause of pain in myocardial infarction is ischemia of the viable myocardium. Therefore, all therapeutic measures aimed at reducing ischemia (reduction of oxygen demand and improvement of oxygen delivery to the myocardium) are used to reduce and stop pain: inhalation of oxygen, nitroglycerin, beta-blockers. First, if there is no hypotension, take nitroglycerin under the tongue (if necessary, again at intervals of 5 minutes). In the absence of the effect of nitroglycerin, the drug of choice for the management of the pain syndrome is morphine-IV 2-5 mg every 5-30 minutes before the pain is relieved. Inhibition of respiration from morphine in patients with severe pain syndrome with myocardial infarction is very rare (in these cases, iv injection of nalorphine or naloxone is used). Morphine has its own anti-ischemic action, causing dilatation of veins, reduces preload and reduces the need for myocardium in oxygen. In addition to morphine, the most commonly used promedol - iv in 10 mg or fentanyl - iv in the 0,05-0,1 mg. In most cases, to the narcotic analgesics add Relanium (5-10 mg) or droperidol (5-10 mg under the control of blood pressure).

A common mistake is the appointment of non-narcotic analgesics, for example, analgin, baralgin, tramal. Non-narcotic analgesics do not possess anti-ischemic action. The only excuse for using these drugs is the lack of narcotic analgesics. In the guidelines for the treatment of myocardial infarction in most countries, these drugs are not even mentioned.

In case of hard-to-stop painful pain, re-introduction of narcotic analgesics, the use of nitroglycerin infusion, the appointment of beta-blockers are used.

Intravenous infusion of nitroglycerin is prescribed for non-occlusive pain syndrome, signs of persistent myocardial ischemia, or stagnation in the lungs. Infusion of nitroglycerin begins at a rate of 5-20 μg / min, if necessary, increasing the rate of administration to 200 μg / min under the control of blood pressure and heart rate (blood pressure should be not less than 100 mm Hg, and heart rate not more than 100 per min). Caution should be exercised when prescribing nitroglycerin to patients with myocardial infarction of the lower location (or not to prescribe at all) - possibly a sharp drop in blood pressure, especially with concomitant myocardial infarction of the right ventricle. A common mistake is the appointment of nitroglycerin to all patients with myocardial infarction.

In the absence of contraindications, beta-blockers are prescribed as early as possible: propranolol (obzidan) iv 1-5 mg, then inside 20-40 mg 4 times a day; metoprolol - in / in 5-15 mg, then metoprolol orally 50 mg 3-4 times a day. You can go to take atenolol - 50 mg 1-2 times a day.

All patients with the first suspicion of myocardial infarction showed an earlier appointment of aspirin (the first dose of aspirin 300-500 mg must be chewed and washed with water).

Thrombolytic therapy

Coronary thrombosis plays a major role in the occurrence of myocardial infarction. Therefore, thrombolytic therapy is pathogenetic in myocardial infarction. Numerous studies have shown a reduction in mortality with thrombolytic treatment.

Forty years ago, hospital mortality in myocardial infarction was about 30%. The creation of intensive care units in the 1960s made it possible to reduce hospital mortality to 15-20%. With the optimization of medical measures, the use of nitroglycerin, beta-blockers, aspirin, a further reduction in mortality was observed with myocardial infarction - up to 8-12%. Against the background of the use of thrombolytic therapy, mortality in a number of studies was 5% or lower. In most studies with the appointment of thrombolytics, there was a decrease in mortality by about 25% (on average from 10-12% to 7-8%, ie in absolute figures by about 2-4%). This is comparable to the effect of the appointment of beta-blockers, aspirin, heparin, indirect anticoagulants, ACE inhibitors. Under the influence of each of these drugs, there is also a decrease in mortality by 15-25%. The use of thrombolytics can prevent 3 to 6 deaths in 200 treated patients, the appointment of aspirin - the prevention of about 5 deaths, the use of beta-blockers - the prevention of approximately 1-2 deaths in 200 treated patients. Perhaps the simultaneous use of all these drugs will further improve the results of treatment and prognosis for myocardial infarction. For example, in one study, the administration of streptokinase led to a 25% reduction in mortality, aspirin use by 23%, and their joint appointment reduced the lethality by 42%.

The main complication of thrombolytics are bleeding. Expressed bleeding is relatively rare - from 0.3 to 10%, including cerebral hemorrhages in 0.4-0.8% of patients, an average of 0.6% (ie 6 cases per 1000 patients treated - 2-3 times more often than without the use of thrombolytics). The frequency of strokes with the use of preparations of the tissue activator plasminogen is greater than against the background of streptokinase (0.8% and 0.5%). When using streptokinase, allergic reactions - less than 2% and a decrease in blood pressure - in about 10% of patients are possible.

Ideally, the time from the onset of myocardial infarction symptoms to the onset of thrombolytic therapy ("call-to-needle" time) should not exceed 1.5 hours, and the time from admission to the hospital before the start of thrombolytics (time from door to needle) - not more than 20-30 minutes.

The question of the introduction of thrombolytics at the prehospital stage is decided individually. In the recommendations for management of patients with myocardial infarction in the US and Europe, it is considered more appropriate to conduct thrombolytic therapy in a hospital. The reservation is made that if the time of transportation of the patient to the hospital is more than 30 minutes or the time to the expected thrombolysis exceeds 1-1.5 hours, it is permissible to conduct thrombolytic therapy at the prehospital stage, i.e. In the conditions of first aid. Calculations show that the implementation of thrombolytic therapy in the prehospital stage allows to reduce mortality in myocardial infarction by approximately 20%.

With iv injection of streptokinase, reperfusion begins in about 45 minutes. Recovery of coronary blood flow occurs in 60-70% of patients. Signs of successful thrombolysis include cessation of pain, rapid ECG dynamics (return of the ST segment to the isoline or a decrease in the height of the ST segment by 50%), and a second increase in the activity of CKK (and MB CK) approximately 1.5 hours after streptokinase administration. At this time, the occurrence of reperfusion arrhythmias - most often, ventricular extrasystoles or an accelerated idioventricular rhythm, but also increases the incidence of ventricular tachycardia and ventricular fibrillation. If necessary, standard medical measures are taken. Unfortunately, early reocclusion occurs in 10-30% of patients.

The main indication for the appointment of thrombolytic therapy is considered to be ACS with ST segment elevation in 2 or more adjacent leads or the appearance of left bundle branch blockade in the first 6 hours from the onset of symptoms. The best results were found in patients with anterior myocardial infarction, with the registration of ST rise in 4 or more leads and at the beginning of the drug administration during the first 4 hours. During thrombolysis during the first hour of myocardial infarction, there was a decrease in hospital mortality in more than 2 times (there are reports of a decrease in mortality with successful thrombolysis during the first 70 minutes from 8.7% to 1.2%, ie 7 times (!) - "golden" hour). However, the inflow of patients during the first hour is extremely rare. Decrease in mortality is noted with thrombolytic therapy within 12 hours from the onset of myocardial infarction. With the preservation of the pain syndrome and the recurrence of ischemia, thrombolytics are used within 24 hours of the onset of symptoms of MI.

In patients with ACS without ST segment elevation and with myocardial infarction without a Q wave, the use of thrombolytics was not indicated; on the contrary, deterioration (increase in mortality) was noted.

The main absolute contraindications to the use of thrombolytic therapy are: active or recent internal bleeding, a hemorrhagic stroke in the anamnesis, other disorders of cerebral circulation for 1 year, signs of possible aortic dissection. The main relative contraindications: surgical operations for 2 weeks, prolonged resuscitation (more than 10 min), severe arterial hypertension with blood pressure above 200/120 mm Hg. St., hemorrhagic diathesis, exacerbation of peptic ulcer.

Currently, streptokinase is the most accessible and the most studied drug. Streptokinase does not have an affinity for fibrin. Streptokinase is administered as an intravenous infusion of 1.5 million units for 60 minutes. Some authors recommend to enter streptokinase more quickly - for 20-30 minutes.

In addition to streptokinase, the action of the recombinant tissue plasminogen activator (TAP, alteplase) has been studied quite well. TAP is a fibrin-specific thrombolytic. The introduction of alteplase is somewhat more effective than streptokinase, and allows the additional saving of one patient in the treatment of 100 patients. Reteplase is also a recombinant form of TAP, with slightly less fibrin specificity. The reteplase can be injected intravenously. The third drug, tenecteplase, is also a TAP derivative.

Less studied the effect of drugs APCAK (anestreplase, eminase), urokinase, prourokinase and other thrombolytics.

In Russia, streptokinase is most commonly used because it is 10 times cheaper and in general it's not much inferior to tissue activators of plasminogen for its effectiveness.

Surgical methods of coronary blood flow restoration

Approximately 30% of patients with myocardial infarction have contraindications for the appointment of thrombolytics and 30-40% have no effect on thrombolytic therapy. In specialized departments, some patients on the first 6 hours after the onset of symptoms receive urgent balloon coronaroangioplasty (CAP). In addition, even after successful thrombolysis, the overwhelming majority of patients have residual coronary artery stenosis, so attempts have been made to perform KAP immediately after thrombolytic therapy. However, in the randomized trials, the advantages of this approach are not revealed. The same can be said for urgent aortocoronary shunting (CABG). The main indications for KAP or CABG in the acute period of myocardial infarction are complications of myocardial infarction, primarily postinfarction angina and heart failure, including cardiogenic shock.

Additional assignments

In addition to relief of pain syndrome, inhalation of oxygen and attempts to restore coronary blood flow, all patients with the first suspicion of the possibility of myocardial infarction prescribe aspirin in a loading dose of 300-500 mg. Further, aspirin is taken at 100 mg per day.

Opinions about the need to prescribe heparin in uncomplicated myocardial infarction against the background of thrombolytics are quite contradictory. Intravenous administration of heparin is recommended for patients who do not undergo thrombolytic therapy. After 2-3 days pass to the SC administration of heparin at 7.5-12.5 thousand units ED 2 times a day subcutaneously. Intravenous infusion of heparin has been shown in patients with advanced anterior myocardial infarction, with atrial fibrillation, with a clot in the left ventricle (under the control of coagulation rates). Instead of conventional heparin, subcutaneous administration of low molecular weight heparins can be used. Indirect anticoagulants are prescribed only in the presence of indications - an episode of thromboembolism or an increased risk of thromboembolism.

All patients, in the absence of contraindications, are prescribed beta-blockers as early as possible. With myocardial infarction, the use of ACE inhibitors has also been shown, especially in the detection of left ventricular dysfunction (ejection fraction less than 40%) or signs of circulatory insufficiency. With myocardial infarction, there is a decrease in total cholesterol and LDL cholesterol ("reverse phase reactant"). Therefore, normal indices indicate an increased level of lipids. Most patients with myocardial infarction should be prescribed statins.

In some studies, a positive effect of the use of cordarone, verapamil, magnesium sulfate and a polarizing mixture in myocardial infarction was revealed. Against the background of taking these medications, there was a decrease in the frequency of ventricular arrhythmias, recurrent and repeated myocardial infarctions, as well as a reduction in the mortality of patients with myocardial infarction (with a follow-up of up to 1 year or more). However, there are not enough reasons for recommending the routine use of these drugs in clinical practice.

Management of patients with MI without a Q wave is almost identical to the management of patients with unstable angina (acute coronary syndrome without ST segment elevation). The main drugs are aspirin, clopidogrel, heparin and beta-blockers. In the presence of signs of an increased risk of complications and death or the absence of the effect of intensive drug therapy, a coronagraphography is shown to assess the possibility of surgical treatment.

Myocardial infarction: treatment

[31], [32], [33], [34],

Prognosis and rehabilitation of myocardial infarction

Physical activity gradually increases during the first 3-6 weeks after discharge. The resumption of sexual activity, which often worries the patient, and other moderate physical activities are encouraged. If good cardiac function persists for 6 weeks after an acute myocardial infarction, most patients can return to normal activity. A rational program of physical activity, taking into account the lifestyle, age and condition of the heart, reduces the risk of ischemic events and increases overall well-being.

Acute period of the disease and treatment of ACS should be used to develop a patient's persistent motivation to modify risk factors. When assessing the patient's physical and emotional status and discussing them with the patient, it is necessary to talk about lifestyle (including smoking, diet, work and rest, exercise), since eliminating risk factors can improve the prognosis.

Myocardial infarction: prognosis and rehabilitation