Author Ольга Кияница
Unstable angina (HC) refers to acute coronary syndrome (ACS), which also includes myocardial infarction with an increase in the ST level and without an increase in the ST segment. Unstable angina is characterized by the formation of myocardial ischemia, which does not result in necrosis (ie cardiac biomarkers of myocardial necrosis, such as isozyme creatine kinase, isopropylene, troponin, myoglobin, absent in the bloodstream).
With unstable angina, emergency treatment is required, since the risk of myocardial infarction is high.
In the course of diagnosis, the NA first of all use an assessment of the clinical picture, after which they use instrumental and laboratory methods of investigation.During the treatment of NA, efforts are directed at restoring blood flow through the coronary vessels and preventing repeated cases of their blocking.
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Definition of unstable angina
The term "unstable angina" was first used in the early 1970s to determine the condition mentioned in earlier publications, such as pre-infarction angina, crescendo angina, acute coronary insufficiency, or an intermediate coronary syndrome. [1 - Fowler NO Preinfarction angina: a need for an objective definition and for a controlled clinical trial of its management]
There were several classifications of unstable angina. In the widely used classification of Braunwald, unstable angina was divided into three classes corresponding to the severity:
- Class I - includes primary cases of severe or accelerated angina less than 2 months without residual pain.
- Class II - includes painful conditions at rest during the previous month, but not during the last 48 hours.
- Class III - includes angina at rest for the last 48 hours.
For today, it is assumed that unstable angina is an intermediate state between stable angina and myocardial infarction (MI). Quite often unstable angina is the usual precursor of myocardial infarction; in some studies, patients reported that a week before the heart attack they had discomfort in the chest, corresponding to the clinic of the National Assembly.
Prevalence of unstable angina
Every year, about one million Americans are hospitalized because of the development of unstable angina. A similar number of patients does not enter the hospital due to the fact that they do not recognize themselves as sick or undergo treatment on an outpatient basis. Despite advances in medicine and increased survival after myocardial infarction (MI), the incidence of angina pectoris, as previously expected, is increasing, with various preventive measures being actively carried out.
According to the Global Registry and the evaluation of the treatment of unstable angina (GUARANTEE), the average age of patients with NS is 62 years, in 44% of these patients age over 65 is determined. Also in patients with unstable angina, hypertension (60%), hypercholesterolemia (43%), diabetes mellitus (26%) are determined.
On average, women develop NS five years later than men, with about half of all women diagnosed after 65 years of age.
It is believed that the formation of an intracoronary thrombus explains the pathogenesis in most patients with unstable angina. In contrast to myocardial infarction with an increase in the level of the ST segment, in which the thrombus was usually occlusive, a thrombus with unstable angina did not lead to complete occlusion of the coronary arteries, at least 80% -90% of the patients.
Formation of thrombi in unstable angina
The main mechanisms of development of unstable angina are intracoronary thrombus formation and complex lesions (ulcerated or destroyed plaque), which are found in 50% -80% of cases.
The results of angioscopic studies indicate that intracoronary thrombus or yellow plaque is found in most patients with unstable angina, whereas similar cases with stable angina are quite rare.
The thrombus with unstable angina is characterized by grayish-white color and is presumed to be saturated with platelets, whereas in MI it is more often red and red blood cells predominate in it. Also, the formation of thrombi on a fractured or eroded plaque is the most common pathophysiological mechanism in unstable angina, especially when it comes to acute pain. In the absence of pain, additional studies should be carried out to identify the true cause of development of the disease.
Other pathogenic mechanisms of development of unstable angina
Inflammation plays an important role in rupturing atherosclerotic plaques, and it contributes to the destabilization of the fibrous structure of so-called vulnerable plaques by secretion of matrix metalloproteinases. One of the difficulties with understanding the role of inflammation is the relationship between blood clot formation and inflammation. Tissue factor is more common in unstable versus stable plaques, and histological studies prove a strong connection between macrophage infiltration and tissue factor localization. Local expression of the tissue factor by macrophages can lead to activation of the coagulation cascade. In addition, platelet activation can lead to inflammatory reactions at the site of vascular lesions. [2 - Liuzzo GBiasucci LMGallimore JR et al. The prognostic value of C-reactive protein and serum amyloid. N Engl J Med. 1994; 331417-424.]
Another link between inflammation and thrombosis may be lipoprotein (a). Recent studies show that lipoprotein (a), which is considered an atherosclerotic and thrombogenic factor, is localized in macrophage-rich areas, as well as in unstable plaques.
In general, the pathogenesis of coronary disease is directly related to the slow or rapid progression of atherosclerosis.On the other hand, ischemic mechanisms reflect an imbalance between myocardial blood supply and oxygen consumption. With unstable angina, a short-term reduction in blood supply or even a slight increase in myocardial need in the presence of a new significant lesion can accelerate the ischemic manifestations of the disease, namely, the NA, by changing this balance. A transient reduction in diet associated with the formation of an intracoronary thrombus with spontaneous lysis or embolization can also lead to the development of retrosternal pain at rest. Activated platelets release several vasoactive substances that, in the presence of endothelial dysfunction (impaired vasodilation), can lead to vasoconstriction at the distal site and a short-term decrease in blood flow. Although a thrombus is usually present in such cases, any process (thrombotic or otherwise) that significantly disturbs this balance can lead to unstable angina.
Causes and risk factors
The main cause of unstable angina is ischemic heart disease caused by the accumulation of atherosclerotic deposits on the walls of the coronary arteries. As a result of such pathological changes, the arteries narrow and become more rigid.This reduces the flow of blood to the heart muscle, then the myocardium lacks nutrients and oxygen, which causes a pain in the chest.
In case of unstable angina, the risk factors that are common to all cardiovascular diseases are taken into account:
- Increased body weight
- Family history of heart disease
- High blood pressure
- High cholesterol and low-density lipoprotein
- Low level of high density lipoprotein
- Keeping a sedentary lifestyle
- The presence of bad habits
- Excessive physical activity
- Chronic lack of sleep
If the patient is determined by stable angina, then under the influence of the above factors of influence, she can go into an unstable form.
Men over 45 and women over 55 are more likely to develop unstable angina.
Signs and Symptoms
With unstable angina, symptoms can occur at rest; then become more pronounced, severe and prolonged than the usual picture of angina pectoris. There may also be a change in the usual pattern of angina pectoris; or lack of improvement after resting or taking nitroglycerin.
Symptoms of unstable angina are similar to those of myocardial infarction (MI) and include the following:
- Chest pain
- Feeling of pressure in the heart
- Pain or pressure in the back, neck, jaw, abdomen, shoulders or arms
- Reinforced sweating
- Shortness of breath
- Nausea, vomiting
- Dizziness or sudden weakness
Of great importance is the medical history and diagnostic examination of the patient, which are usually more sensitive and specific for unstable angina than a physiological examination, which may not give significant information.
An objective examination of a patient with unstable angina may lead to the following results:
- Increased sweating
- Tachycardia or bradycardia
- Unstable myocardial dysfunction (eg, systolic blood pressure
Various laboratory studies are conducted, among which the following are most commonly used to determine unstable angina:
- Standard 12-lead electrocardiography
- Serial analysis of cardiac biomarkers (eg, creatine kinase, troponin, myoglobin, etc.)
- Complete blood count with determination of hemoglobin level
- Biochemical analysis of blood serum (including magnesium and potassium)
- Lipid panel
Coronary angiography helps visualize narrowed arteries or places of obstruction. This is one of the most common tests that are used to diagnose unstable angina.
Other methods that may be useful in assessing patients with suspected HC include:
- Level of creatinine
- Physical testing of the patient in a stable state
- Chest X-ray
- Computed tomography angiography
- Magnetic resonance angiography
- Single photon emission computed tomography
- Magnetic resonance imaging
- Perfusion imaging of the myocardium
Treatment of unstable angina depends on the severity of the condition. Most often in the therapy of NA, the tactics of exposure are selected with the aim of:
- Decreased myocardial oxygen demand
- Improve myocardial blood supply
- Evaluation of the risk of progression of myocardial disease or complications associated with treatment.
Patients with unstable angina should undergo treatment in a hospital with continuous monitoring of telemetry.Intravenous access is provided and additional oxygen supply is provided, especially if signs of desaturation are noted.
In critical cases, when the clinical symptoms of NA are extremely pronounced, the primary treatment method is invasive (surgical) or conservative (medical).
In the treatment of unstable angina, the following drugs are used:
- Antiaggregants (aspirin, clopidogrel)
- Lipidosnizhayuschie statinovye drugs (simvastatin, atorvastatin, Pitavastatin and pravastatin)
- Cardiovascular antiplatelet agents (tirofiban, eptifibatid and abciximab)
- Beta-blockers (atenolol, metoprolol, esmolol, nadolol and propranolol)
- Anticoagulants (heparin, low molecular weight heparin or enoxaparin, dalteparin and tinzaparin)
- Thrombin inhibitors (bivalirudin, lepiridin, desyrudin and argatroban)
- Nitrates (nitroglycerin IV)
- Calcium channel blockers (diltiazem, verapamil or nifedipine)
- Angiotensin-converting enzyme inhibitors (captopril, lisinopril, enalapril and ramipril)
In addition, a diet with low cholesterol and saturated fat is recommended. Limitation of sodium is prescribed for patients with heart failure or hypertension.
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Surgical treatment for unstable angina may include the following:
- Setting the shunt into the coronary artery - part of the blood vessel is taken from another part of the body and used to redirect the blood bypassing the blocked or narrowed part of the artery.
- Percutaneous coronary intervention - a narrowed section of the artery is dilated with a tiny device called a stent.
Both these operations are equally effective. The most optimal method of treatment is selected by the doctor taking into account individual circumstances. Sometimes even after the operation, you have to continue taking medication.
Regardless of the severity of the condition, the patient may need to change his lifestyle, and with a long-term focus, which is also the prevention of repeated attacks of unstable angina. The main recommendations from this area of improving heart health are:
- Practice healthy eating
- Reduction of stressful situations
- Weight reduction, especially if its excess is noted
- Refusal to smoke, if there is this habit
Correction of a way of life in most cases allows to reduce risk of development of a stenocardia and a heart attack. If necessary, you can discuss with your doctor appropriate options for exercise to avoid hypodynamia.
The course of the disease largely depends on the severity of the disease. The stronger the pathological manifestations, the higher the risk of developing various complications that worsen the prognostic conclusion. If in addition the patient is diagnosed with concomitant diseases like arterial hypertension or diabetes, then an unfavorable prognosis is also given.
Studies have shown that there are the following significant prognostic factors for poor outcome in patients with unstable angina:
- The presence in the history of the disease of a bad fraction of the ejection of the left ventricle
- Hemodynamic instability
- Recurrent angina, despite intense anti-ischemic therapy
- The first occurrence or repeated mitral regurgitation
- Stable ventricular tachycardia
With timely treatment started, the forecast is often improved, especially against the background of successfully performed revascularization or catheterization of the coronary arteries.
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