Medical expert of the article
New publications
Early myocardial infarction
Last reviewed: 07.06.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Irreversible damage to part of the heart muscle as a result of the cessation of its blood supply - acute myocardial infarction - can occur not only in older people, but also in those under 45 years of age. And then it is defined as early myocardial infarction.
Epidemiology
Acute myocardial infarction and its mortality rates increase with age, with men of any age being affected much more often than women.
According to foreign cardiologists, the prevalence of acute myocardial infarction among men under 50 years of age is about 5%, and among women in this age category - no more than 2%. And the number of pre-hospital deaths reaches almost 16%.
However, cardiac vascular pathologies are often not detected by coronarography, and myocardial infarction without significant coronary artery changes has been reported to occur in 1-12% of patients. [1]
Patients <50 years of age had a lower prevalence of diabetes (19.4%) and stroke (1.8%), while they were more likely to be smokers (77.1%), obese (26%), dyslipidemic (74.7%), and with one vascular disease (16.2%). [2]
Data from a 10-year follow-up showed that the prevalence of AMI was higher in men than in women aged 30 to 55 years. [3]
Causes of the early myocardial infarction
If in people of older age category atherosclerotic lesion of coronary arteries feeding the heart - stenosing atherosclerosis [4] - is recognized as the main culprit of termination of normal blood supply to heart muscle cells, atherosclerosis of heart vessels and plaque instability in people under 45 years of age is quite rare.
Read more - Myocardial infarction: causes
Cardiologists attribute the key reasons for the development of early myocardial infarction (often called a heart attack) to non-atherosclerotic coronary artery disease or a state of hypercoagulability - thrombophilias, in which the propensity to clot formation is attributed to decreased levels of anticoagulant blood factors.
In addition, early infarction can result from the use of cardiotoxic medications and substance abuse.
Non-atherosclerosis-related coronary artery diseases and pathologies that can lead to heart attack at a young age include:
- congenital anomalies of the coronary arteries, for example, the so-called myocardial bridge - the passage of the artery deep in the myocardium (under the layer of muscle);
- spontaneous coronary artery dissection - separation of the arterial wall between any of its three layers when the vascular walls are weakened;
- arterial aneurysm of the coronary artery, which can form in Adamantiades-Behçet's disease, as well as a type of systemic vasculitis such as Kawasaki disease;
- systemic lupus erythematosus-associated coronary.
To the conditions of increased blood coagulability (violation of coagulation hemostasis), involved in the development of early infarcts, should be attributed: hypercoagulable syndrome, [5] as well as antiphospholipid syndrome - with the threat of blocking the lumen of the coronary arteries with thrombus.
Among the main medications that can cause early myocardial infarction by direct toxic effects on cardiomyocytes or through the development of vasospasm (narrowing of the lumen) of the coronary arteries, experts call: Chemotherapy drugs for cancer (Cisplatin, 5-fluorouracil), triptanate-containing migraine remedies, the dopamine receptor stimulating drug Bromocriptine, ephedrine adrenomimetics, certain steroidal and non-steroidal anti-inflammatory drugs, tricyclic antidepressants, and Methamphetamine and other psychostimulants with narcotic properties.
Risk factors
Significantly increase the risk of heart attack before age 45:
- Alcohol abuse [6] and sedentary lifestyle; frequent cigarette smoking can lead to endothelial dysfunction due to arterial cell damage, especially at an early age. [7]
- stresses; [8]
- high levels of trans fats and saturated fats in the diet;
- Disorder of fat metabolism and elevated blood cholesterol (LDL) levels; [9], [10]
- Metabolic syndrome with obesity (BMI >30), type 2 diabetes and arterial hypertension; [11], [12], [13]
- genetic predisposition (presence of vascular diseases, myocardial infarctions and premature CHD in the family history);
- Congenital anomalies of the cardiac septum. Specifically open oval window in the heart;
- angina pectoris (stable angina);
- infective endocarditis;
- frequent inflammatory diseases and/or the presence of foci of chronic bacterial infection;
- connective tissue pathology. [14]
In addition, in women under 40, taking combined oral contraceptives (because of their procoagulant activity) is a risk factor.
Pathogenesis
Regardless of the cause of impaired blood flow to the myocardium, the pathogenesis of its damage is due to the fact that in conditions of ischemia (blood supply interruption) - when blood does not reach one or another part of the heart muscle - its cells (cardiomyocytes) lack oxygen, which is required for the transformation of ADP (adenosine diphosphate) into ATP (adenosine triphosphate), necessary to maintain electrolyte balance and metabolism in living cells of all tissues.
Ischemia not only disturbs intracellular energy homeostasis, but also leads to the development of proinflammatory reactions (with infiltration of damaged tissue by neutrophils), activation of free-radical oxidation and irreversible changes in cells, resulting in their death - necrosis.
Further, anti-inflammatory and reparative reactions activate cardiac fibroblasts, which constitute the largest cell population in the heart. And due to their production of extracellular matrix, a scar is formed at the site of cardiomyocyte necrosis. Scarring or fibrosis begins in about two weeks, and full scar formation takes at least two months.
Symptoms of the early myocardial infarction
The first signs of a heart attack are discomfort and chest pain (left or center) that can go to the shoulder, arm, back, neck, or lower jaw.
The most common symptoms are a feeling of weakness, dizziness, shortness of breath, fainting, nausea, increased sweating and increased heart rate (tachycardia). In inferior wall myocardial infarction, there may be bradycardia - a decrease in HR due to vagus nerve stimulation.
At the same time, early myocardial infarctions can be symptomless (22-64% of all cases), so they are called "silent" or "mute".
More information in the article - Symptoms of myocardial infarction
The development of myocardial infarction includes stages: the ischemia stage, the stage of myocardial reperfusion injury and subsequent inflammatory response, and the remodeling stage (which begins one to three weeks after the onset of a heart attack).
Also distinguish periods of the course of infarction: acute, acute, subacute and postinfarction.
According to ECG results, the main types are divided into myocardial infarction with ST-segment elevation (STEMI) and myocardial infarction without ST-segment elevation (NSTEMI), with the formation of pathologic Q tooth and without Q tooth formation.
And according to the depth of damage to the heart muscle and its localization, such morphological types as subepicardial, subendocardial (small-focal), intramural and transmural myocardial infarction; myocardial infarction of the left or right ventricle are defined.
Complications and consequences
Complications and consequences of any myocardial infarction are divided into early and late.
In the first hours or days of acute myocardial ischemia, early complications of myocardial infarction develop: Heart rhythm disturbance; primary ventricular fibrillation and sustained ventricular tachycardia; disappearance of myocardial electrical activity - asystole; pulmonary edema; fibrinous pericarditis; [15] ventricular extrinsic thrombosis; mitral valve insufficiency of the heart - mitral regurgitation; rupture of the interventricular septum, [16] myocardium, or papillary (papillary) muscle of the heart. [17]
Late complications of myocardial infarction are manifested by heart failure with atrial fibrillation, inflammation of cardiac muscle tissue, conduction disturbance with heart block, postinfarction Dressler syndrome, myocardial aneurysm, [18] cardiogenic shock with cardiac arrest.
A repeat infarction may develop that localizes to the area of another coronary artery or to the area of the primary heart attack.
Also read - Myocardial infarction: complications
Diagnostics of the early myocardial infarction
More information in the article - Myocardial infarction: diagnosis
Instrumental diagnostics are used to detect myocardial damage:
ECG in myocardial infarction, [19] Cardiac ultrasound, left ventricular echocardiography, chest X-ray or CT scan, coronary angiography, etc. For more information see - Instrumental methods of cardiac examination
Experts note the leading role of cardiac markers in the early diagnosis of myocardial infarction. Elevated concentrations of the globular heart muscle proteins troponin I (TnI) and troponin T (TnT), [20], [21] which are released into the bloodstream after myocardial cell necrosis, are now accepted as a standard biochemical marker for the diagnosis of myocardial infarction. For details see:
But an earlier marker of myocardial infarction is the free oxygen-binding protein myoglobin, as well as the myocardial (MB) fraction of creatine kinase.
For more information, see:
In addition, blood tests are taken for the level of C-reactive protein, for the activity of LDH1 isoenzyme (lactate dehydrogenase 1), for the content of anticardiolipin antibodies (to detect antiphospholipid syndrome), for blood coagulation factors, etc.
A differential diagnosis is necessary, including: musculoskeletal chest pain, myocarditis, pericarditis (primarily constrictive), dilated and restrictive cardiomyopathy, cardiac conduction system dysfunction, stress cardiomyopathy (Takotsubo syndrome), acute aortic insufficiency, pulmonary embolism, lung tumors, pneumonia, tension pneumothorax, pericardial effusion.
Who to contact?
Treatment of the early myocardial infarction
In the treatment of early myocardial infarction drugs of different pharmacological groups are used: antiaggregants and anticoagulants preventing thrombus formation [22] (Aspirin and Clopidogrel), antianginal agents (Nitroglycerin, beta-adrenoreceptor blockers) - to counteract coronary spasm.
To restore blood flow in the coronary arteries, reperfusion therapy (intracoronary fibrinolytic therapy) with the administration of thrombolytic drugs is performed. All details in the publication - Myocardial infarction: treatment
Also read - First aid for an attack of acute myocardial infarction
Stages of rehabilitation after a heart attack are discussed in detail in the material - Myocardial infarction: prognosis and rehabilitation
Prevention
Lifestyle changes - smoking cessation, healthy diet, sufficient physical activity, normalization of body weight - play an important role in the prevention of myocardial infarction in people under 45 years of age.
Although in the presence of some n atherosclerotic coronary artery disease, hypercoagulable states and certain risk factors, it is not possible to prevent the development of a heart attack with irreversible myocardial ischemic damage.
Forecast
Early myocardial infarction has a better prognosis with appropriate treatment. [23], [24] On the other hand, poor control of risk factors leads to significant morbidity and mortality.
Due to coronary circulatory arrest in the first hours of acute myocardial infarction sudden cardiac death is observed in almost 30% of all fatal cases. Patients die as a result of ventricular fibrillation and ventricular arrhythmias, as well as variously localized ruptures of cardiac muscle tissue, which occur with extensive areas of myocardial necrosis.