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Myocardial infarction: general information
Last reviewed: 12.07.2025
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Myocardial infarction is due to acute obstruction of a coronary artery. The outcome depends on the degree of obstruction and ranges from unstable angina to non-ST-segment elevation myocardial infarction (HSTHM), ST-segment elevation myocardial infarction (STHM), and sudden cardiac death. The presentation of each of these syndromes is similar (except sudden death) and includes chest discomfort with or without dyspnea, nausea, and diaphoresis. Diagnosis is by ECG and the presence or absence of serologic markers. Treatment of myocardial infarction involves antiplatelet agents, anticoagulants, nitrates, beta-blockers, and (in ST-segment elevation myocardial infarction) immediate restoration of myocardial perfusion by thrombolysis, NOVA, or CABG.
There are approximately 1.5 million myocardial infarctions per year in the United States. Myocardial infarctions result in death in 400,000 to 500,000 people, with about half dying before they reach the hospital.
There are two main types of myocardial infarction: “Q-wave myocardial infarction” (or “Q-infarction”) and “non-Q-wave myocardial infarction”.
Synonyms for Q-wave myocardial infarction include: large focal, transmural. Synonyms for non-Q-wave myocardial infarction include: small focal, subendocardial, non-transmural, intramural, or even "microinfarction" (these types of myocardial infarction are indistinguishable clinically and by ECG).
The precursor to the development of myocardial infarction with a Q wave is "acute coronary syndrome with ST segment elevation", and the precursor to myocardial infarction without a Q wave is "acute coronary syndrome without ST segment elevation" (some patients with ACS with ST segment elevation develop myocardial infarction without Q, and vice versa, some patients with ACS without ST segment elevation subsequently develop myocardial infarction with a Q wave).
Characteristic ECG changes over time (appearance of the 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 wave, changes in the ST segment and/or T wave are most often noted on the ECG; Changes in the ST segment and T wave are nonspecific and may be absent altogether. Therefore, to establish the diagnosis of myocardial infarction without a 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 CPK.
The clinical picture, nature and frequency of complications, treatment measures and prognosis differ significantly in Q-wave myocardial infarction and non-Q-wave myocardial infarction. The immediate cause of Q-wave myocardial infarction is thrombolytic occlusion of the coronary artery. In non-Q-wave myocardial infarction, the occlusion is incomplete, rapid reperfusion occurs (spontaneous thrombolysis or reduction of concomitant coronary artery spasm) or the cause of MI is microembolism of small coronary arteries by platelet aggregates. In ST-segment elevation ACS and Q-wave myocardial infarction, thrombolytic therapy should be administered as early as possible, while thrombolytics are not indicated in NSTE-ACS and non-Q-wave myocardial infarction.
The main features of non-Q-wave myocardial infarction include:
- ST segment depression and T wave inversion do not localize the area of infarction or ischemia (unlike ST segment elevation or Q wave).
- In non-Q-wave myocardial infarction, there may be no changes on the ECG.
- Less frequently than with Q-wave myocardial infarction, heart failure occurs and the mortality rate during hospital stay is 2-2.5 times lower.
- Recurrence of myocardial infarction is observed 2-3 times more often than in myocardial infarction with a Q wave.
- Patients with non-Q-wave myocardial infarction are more likely to have a history of angina and more severe coronary artery disease than patients with Q-wave myocardial infarction.
- In long-term follow-up, mortality in patients who have had a Q-wave myocardial infarction is approximately the same as in patients with a Q-wave myocardial infarction (according to some data, the long-term prognosis in patients with a non-Q-wave myocardial infarction is even worse than in patients with a Q-wave myocardial infarction).
The diagnosis and treatment of non-Q-wave myocardial infarction are discussed in detail in the section on acute coronary syndrome.
The identification of any intermediate forms of coronary heart disease (for example, “focal myocardial dystrophy”, “acute coronary insufficiency”, etc.) is meaningless from a clinical point of view, since there is neither a definition of these concepts nor criteria for their diagnosis.
After 2 months from the onset of myocardial infarction, the patient who has had a myocardial infarction is diagnosed with "post-infarction cardiosclerosis". The occurrence of a new myocardial infarction within 2 months from the onset of myocardial infarction is usually called a recurrence of myocardial infarction, and the occurrence of a new myocardial infarction after 2 months or more is called a repeated myocardial infarction.
Causes of myocardial infarction
Acute coronary syndromes (ACS) typically occur when an atherosclerotic coronary artery becomes acutely thrombosed. The atherosclerotic plaque sometimes becomes unstable or inflamed, causing it to rupture. The plaque contents then activate platelets and the coagulation cascade, resulting in acute thrombosis. Platelet activation causes conformational changes in the IIb/IIIa glycoprotein receptors in the membrane, causing platelet aggregation (and thus clumping). Even atherosclerotic plaques that only minimally obstruct blood flow can rupture and cause thrombosis; in more than 50% of cases, the vessel is narrowed by less than 40%. The resulting thrombus severely restricts blood flow to areas of the myocardium.
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Symptoms of myocardial infarction
The main and most common clinical manifestation of myocardial infarction is pain, most often in the chest area behind the sternum. Painful sensations during myocardial infarction are usually more intense than during angina pectoris and usually last more than 30 minutes, often several hours or even days. Along with the pain, fear, profuse sweating, and a feeling of inevitable death occur. Patients are restless, constantly moving, trying to find a position that alleviates the pain. Some patients experience nausea, and vomiting may occur (more often during lower myocardial infarction).
Among the atypical variants of myocardial infarction, there are abdominal (abdominal pain, nausea, vomiting), asthmatic (cardiac asthma or pulmonary edema), arrhythmic, cerebral, painless or low-symptom (including completely asymptomatic - "silent", which, according to epidemiological data, accounts for about 20%).
During an objective examination of patients with "uncomplicated" myocardial infarction, tachycardia and increased respiratory rate due to anxiety are often observed (but these signs may also be a manifestation of heart failure). Blood pressure is usually within normal limits or slightly elevated. In myocardial infarction of the lower localization, sinus bradycardia with a tendency to decrease in blood pressure (especially in the first hours) is often observed. During examination and / or palpation, patients with anterior MI may note the so-called precordial (paradoxical) pulsation - the second systolic impulse inward from the apical impulse to the left of the sternum in the III-IV intercostal spaces (a manifestation of dyskinesia of the anterior wall of the left ventricle - bulging during systole). During auscultation, muffled tones and the appearance of the IV heart sound (atrial or presystolic gallop rhythm - reflects a decrease in the elasticity of the left ventricle) may be noted. Listening to the third tone is a sign of heart failure, i.e. complicated myocardial infarction. In some patients with myocardial infarction with a Q wave, pericardial friction noise is heard (usually on the 2nd day). This is a sign of transmural myocardial infarction with reactive inflammation of the pericardium - epistenocardic pericarditis.
Many patients have an increase in temperature, one of the early signs of myocardial infarction is neutrophilic leukocytosis, sometimes up to 12-15 thousand in μl (an increase in the number of leukocytes begins after 2 hours and reaches a maximum on days 2-4), from days 2-4 the ESR begins to accelerate, C-reactive protein is detected. Registration of the above changes (temperature, leukocytes, ESR, C-reactive protein) has a certain value in the diagnosis of myocardial infarction without a Q wave, if there is no possibility of determining the activity of troponins or MB CPK.
The mortality rate of patients with myocardial infarction is about 30%, with half of the fatal outcomes occurring in the first 1-2 hours at the pre-hospital stage. The main cause of death at the pre-hospital stage is ventricular fibrillation, 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 pathological examination. Hospital mortality is about 10%. After discharge from the hospital, mortality in the first year averages 4%, while in elderly people (over 65 years old) mortality is much higher: in the first month - up to 20%, in the first year - up to 35%.
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Complications of myocardial infarction
Electrical dysfunction occurs in more than 90% of patients with myocardial infarction. Electrical dysfunction that usually causes death within 72 hours includes tachycardia (from any source) with a heart rate high enough to decrease cardiac output and lower blood pressure, Mobitz type II (2nd degree) or complete (3rd degree) atrioventricular block, ventricular tachycardia (VT), and ventricular fibrillation (VF).
Myocardial infarction: complications
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Diagnosis of myocardial infarction
As noted, there are two main types of myocardial infarction: myocardial infarction with a Q wave and myocardial infarction without a Q wave. When pathological Q waves are recorded on the ECG in two or more adjacent leads, MI with a Q wave is diagnosed.
The registration of pathological Q waves is called macrofocal ECG changes. In myocardial infarction without a Q wave, in most cases, changes in the ST segment and T wave are observed. These changes can be of any duration or even absent. Sometimes, as a result of early thrombolysis, myocardial infarction with a Q wave does not develop in patients with ACS with ST segment elevation.
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Treatment of myocardial infarction
The general plan for managing patients with myocardial infarction can be presented as follows:
- Relieve pain, calm the patient, give aspirin.
- Hospitalize (deliver to the intensive care unit).
- An attempt to restore coronary blood flow (myocardial reperfusion), especially within 6-12 hours from the onset of myocardial infarction.
- Measures aimed at reducing the size of necrosis, reducing the degree of left ventricular dysfunction, preventing recurrence and repeated myocardial infarction, reducing the incidence of complications and mortality.
Pain relief
The cause of pain in myocardial infarction is ischemia of viable myocardium. Therefore, to reduce and stop pain, all therapeutic measures aimed at reducing ischemia (reducing the need for oxygen and improving oxygen delivery to the myocardium) are used: oxygen inhalation, nitroglycerin, beta-blockers. First, if there is no hypotension, nitroglycerin is taken sublingually (if necessary, repeated at 5-minute intervals). If nitroglycerin is ineffective, morphine is considered the drug of choice for pain relief - 2-5 mg intravenously every 5-30 minutes until pain is relieved. Respiratory depression from morphine in patients with severe pain in myocardial infarction is very rare (in these cases, intravenous administration of nalorphine or naloxone is used). Morphine has its own anti-ischemic effect, causing vein dilation, reduces preload and reduces the myocardial need for oxygen. In addition to morphine, promedol is most often used - intravenously at 10 mg or fentanyl - intravenously at 0.05-0.1 mg. In most cases, relanium (5-10 mg) or droperidol (5-10 mg under blood pressure control) are added to narcotic analgesics.
A common mistake is to prescribe non-narcotic analgesics, such as analgin, baralgin, tramal. Non-narcotic analgesics do not have an anti-ischemic effect. The only justification for using these drugs is the lack of narcotic analgesics. In most countries, these drugs are not even mentioned in myocardial infarction treatment guidelines.
In cases of pain syndrome that is difficult to relieve, repeated administration of narcotic analgesics, nitroglycerin infusion, and beta-blockers are used.
Intravenous nitroglycerin infusion is prescribed for intractable pain syndrome, signs of persistent myocardial ischemia or pulmonary congestion. Nitroglycerin infusion is started at a rate of 5-20 mcg/min, increasing the rate of administration to 200 mcg/min if necessary, while monitoring blood pressure and heart rate (blood pressure should be at least 100 mm Hg, and heart rate no more than 100 per minute). Increased caution should be exercised when prescribing nitroglycerin to patients with myocardial infarction of the lower localization (or not prescribing it at all) - a sharp drop in blood pressure is possible, especially with concomitant myocardial infarction of the right ventricle. A common mistake is to prescribe nitroglycerin to all patients with myocardial infarction.
In the absence of contraindications, beta-blockers are prescribed as soon as possible: propranolol (obzidan) intravenously at 1-5 mg, then orally at 20-40 mg 4 times a day; metoprolol - intravenously at 5-15 mg, then metoprolol orally at 50 mg 3-4 times a day. You can switch to taking atenolol - 50 mg 1-2 times a day.
All patients with the first suspicion of myocardial infarction are recommended to receive aspirin earlier (the first dose of aspirin 300-500 mg should be chewed and washed down 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 decrease 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%. By optimizing treatment measures, using nitroglycerin, beta-blockers, and aspirin, a further reduction in myocardial infarction mortality was achieved - to 8-12%. With the use of thrombolytic therapy, mortality in a number of studies was 5% and lower. Most studies with the use of thrombolytics noted a decrease in mortality by about 25% (on average from 10-12% to 7-8%, i.e. in absolute figures by about 2-4%). This is comparable to the effect of prescribing beta-blockers, aspirin, heparin, indirect anticoagulants, ACE inhibitors. Under the influence of each of these drugs, a decrease in mortality by 15-25% is also observed. The use of thrombolytics allows preventing from 3 to 6 deaths per 200 treated patients, the prescription of aspirin - the prevention of about 5 deaths, the use of beta-blockers - the prevention of about 1-2 deaths per 200 treated patients. It is possible that the simultaneous use of all these drugs will further improve the treatment results and prognosis in myocardial infarction. For example, in one study, the introduction of streptokinase led to a decrease in mortality by 25%, the prescription of aspirin - by 23%, and their combined use allowed to reduce mortality by 42%.
The main complication of thrombolytics is bleeding. Severe bleeding is observed relatively rarely - from 0.3 to 10%, including cerebral hemorrhage in 0.4-0.8% of patients, on average 0.6% (i.e. 6 cases per 1000 treated patients - 2-3 times more often than without the use of thrombolytics). The frequency of strokes when using tissue plasminogen activator drugs is higher than with streptokinase (0.8% and 0.5%). When using streptokinase, allergic reactions may occur - less than 2% and a decrease in blood pressure - in about 10% of patients.
Ideally, the time from the onset of myocardial infarction symptoms to the start of thrombolytic therapy (the time “from bell to needle”) should not exceed 1.5 hours, and the time from admission to hospital to the start of thrombolytic administration (the time “from door to needle”) should not exceed 20-30 minutes.
The question of administering thrombolytics at the pre-hospital stage is decided individually. In the recommendations for the management of patients with myocardial infarction in the USA and Europe, it is considered more appropriate to administer thrombolytic therapy in a hospital setting. It is stipulated that if the time of patient transportation to the hospital is more than 30 minutes or the time before the expected thrombolysis exceeds 1-1.5 hours, it is permissible to administer thrombolytic therapy at the pre-hospital stage, i.e. in an emergency room. Calculations show that administering thrombolytic therapy at the pre-hospital stage reduces mortality in myocardial infarction by approximately 20%.
With intravenous administration of streptokinase, reperfusion begins in about 45 minutes. Restoration of coronary blood flow occurs in 60-70% of patients. Signs of successful thrombolysis are cessation of pain, rapid ECG dynamics (return of the ST segment to the isoline or a decrease in the height of the ST segment elevation by 50%) and a repeated increase in the activity of CPK (and MB CPK) approximately 1.5 hours after the administration of streptokinase. At this time, reperfusion arrhythmias may occur - most often, these are ventricular extrasystoles or accelerated idioventricular rhythm, but the incidence of ventricular tachycardia and ventricular fibrillation also increases. Standard treatment measures are carried out if necessary. Unfortunately, early reocclusion is observed in 10-30% of patients.
The main indication for thrombolytic therapy is considered to be ACS with ST segment elevation in 2 or more adjacent leads or the appearance of left bundle branch block in the first 6 hours from the onset of symptoms. The best results were found in patients with anterior myocardial infarction, with ST segment elevation registered in 4 or more leads and with the start of drug administration within the first 4 hours. When thrombolysis is performed within the first hour of myocardial infarction, a more than 2-fold decrease in hospital mortality is observed (there are reports of a decrease in mortality with successful thrombolysis within the first 70 minutes from 8.7% to 1.2%, i.e. 7 times (!) - the "golden" hour). However, admission of patients within 1 hour is extremely rare. A decrease in mortality is noted when thrombolytic therapy is performed within 12 hours from the onset of myocardial infarction. If pain syndrome persists and ischemia recurs, thrombolytics are used within 24 hours from the onset of MI symptoms.
In patients with ACS without ST segment elevation and non-Q-wave myocardial infarction, no benefit from the use of thrombolytics was found; on the contrary, deterioration (increased mortality) was noted.
The main absolute contraindications to thrombolytic therapy are: active or recent internal bleeding, history of hemorrhagic stroke, other cerebrovascular accidents within 1 year, signs of possible aortic dissection. The main relative contraindications are: surgery within 2 weeks, prolonged resuscitation (more than 10 minutes), severe arterial hypertension with BP above 200/120 mm Hg, hemorrhagic diathesis, exacerbation of peptic ulcer disease.
Currently, the most accessible and most studied drug is streptokinase. Streptokinase has no affinity for fibrin. Streptokinase is administered as an intravenous infusion of 1.5 million units over 60 minutes. Some authors recommend administering streptokinase more quickly - 20-30 minutes.
In addition to streptokinase, the action of recombinant tissue plasminogen activator (TPA, "alteplase") has been studied quite well. TPA is a fibrin-specific thrombolytic. The introduction of alteplase is somewhat more effective than streptokinase, and allows for an additional saving of one patient when treating 100 patients. Reteplase is also a recombinant form of TPA, with somewhat less fibrin specificity. Reteplase can be administered intravenously by jet stream. The third drug, tenecteplase, is also a derivative of TPA.
The effect of APSAC drugs (anistreplase, eminase), urokinase, prourokinase and other thrombolytics has been less studied.
In Russia, streptokinase is most often used, since it is 10 times cheaper and, in general, is not much inferior in effectiveness to tissue plasminogen activators.
Surgical methods for restoring coronary blood flow
Approximately 30% of patients with myocardial infarction have contraindications for thrombolytics, and 30-40% do not respond to thrombolytic therapy. In specialized departments, some patients undergo emergency balloon coronary angioplasty (CAP) upon admission within 6 hours of the onset of symptoms. In addition, even after successful thrombolysis, the vast majority of patients have residual coronary artery stenosis, so attempts have been made to perform CAP immediately after thrombolytic therapy. However, randomized trials have not shown any advantages of this approach. The same can be said about emergency coronary artery bypass grafting (CABG). The main indications for CAP or CABG in the acute period of myocardial infarction are complications of myocardial infarction, primarily postinfarction angina and heart failure, including cardiogenic shock.
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In addition to pain relief, oxygen inhalation and attempts to restore coronary blood flow, all patients are prescribed aspirin at a loading dose of 300-500 mg at the first suspicion of a possible myocardial infarction. Then aspirin is taken at 100 mg per day.
Opinions on the need to prescribe heparin for uncomplicated myocardial infarction against the background of thrombolytics are quite contradictory. Intravenous heparin is recommended for patients who do not undergo thrombolytic therapy. After 2-3 days, switch to subcutaneous heparin administration of 7.5-12.5 thousand U 2 times a day subcutaneously. Intravenous heparin infusion is indicated for patients with widespread anterior myocardial infarction, atrial fibrillation, detection of a thrombus in the left ventricle (under control of blood clotting parameters). Subcutaneous administration of low molecular weight heparins can be used instead of conventional heparin. Indirect anticoagulants are prescribed only if indicated - an episode of thromboembolism or an increased risk of thromboembolism.
All patients, unless contraindicated, are prescribed beta-blockers as soon as possible. In myocardial infarction, ACE inhibitors are also indicated, especially if left ventricular dysfunction (ejection fraction less than 40%) or signs of circulatory failure are detected. In myocardial infarction, total cholesterol and LDL cholesterol (the "reverse acute phase reactant") decrease. Therefore, normal values indicate elevated lipid levels. Statins are appropriate for most patients with myocardial infarction.
Some studies have shown a positive effect of cordarone, verapamil, magnesium sulfate, and polarizing mixture in myocardial infarction. These drugs were used to reduce the incidence of ventricular arrhythmias, recurrent and repeated myocardial infarctions, and to reduce mortality in patients with myocardial infarction (with observation periods of up to 1 year or more). However, there are still insufficient grounds to recommend routine use of these drugs in clinical practice.
Management of patients with non-Q-wave MI is virtually identical to that of patients with unstable angina (non-ST-segment elevation acute coronary syndrome). The main drugs are aspirin, clopidogrel, heparin, and beta-blockers. If there is evidence of an increased risk of complications and death or if intensive drug therapy is ineffective, coronary angiography is indicated to assess the possibility of surgical treatment.
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Prognosis and rehabilitation of myocardial infarction
Physical activity is gradually increased during the first 3 to 6 weeks after discharge. Resumption of sexual activity, which is often a concern for the patient, and other moderate physical activity are encouraged. If good cardiac function is maintained for 6 weeks after acute myocardial infarction, most patients can resume normal activity. A rational physical activity program, taking into account lifestyle, age, and cardiac condition, reduces the risk of ischemic events and increases overall well-being.
The acute period of the disease and treatment of ACS should be used to develop a strong motivation for risk factor modification in the patient. 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 regimen, the need for physical exercise), since eliminating risk factors can improve the prognosis.