What is progressing angina?
Author Ольга Кияница
- 1 General characteristics of progressive angina of stress
- 2 Pathogenesis of progressive angina
- 3 Signs of progressive angina
- 4 Diagnosis of progressive angina
- 5 Clinical recommendations for progressive angina pectoris
- 6 Progressive angina: prognosis
Progressive angina (FS, frog) is one of the clinical forms of unstable angina. In addition to this, this group includes the first occurrence of angina, variant angina (or Printsmeta) and early postinfarction angina pectoris. This division (classification) was developed by Brownwald in the late 80's.
In angina pectoris, as in myocardial infarction, coronary blood supply is disturbed; only in the case of a thoracic toad there is no necrosis of the heart muscle.
In the diagnosis of patients with suspected progressive angina, electrocardiography is the first thing to do. Further, if necessary, ultrasound of the heart, radiography, and others can be prescribed. Much depends on the history of the disease and family predisposition to coronary heart disease.After the diagnosis is prescribed, treatment is prescribed, without which serious complications may occur.
Video: Acute Coronary Syndrome DETAILED Overview (MI, STEMI, NSTEMI)
General characteristics of progressive angina of stress
Unstable angina refers to a range of clinical manifestations commonly referred to as acute coronary syndrome (OCD), which also includes myocardial infarction with the ST segment elevation (STEMI) and without the rise of the indicated segment (NSTEMI English).
An unstable angina is considered as an OCD, as it develops myocardial ischemia during its development. But because there is no myocardial necrosis (i.e., cardiac necrosis biomarkers - such as creatine kinase, troponin, myoglobin - are not secreted into the bloodstream), they say just about angina pectoris or progressive angina.
Acute coronary syndrome
Progressive angina: ICD 10
According to the International Classification of Diseases (ICD-10), the code of unstable angina is I20.0. The refinement to this code is as follows:
- the tension that first appeared;
- tension progressive.
Also, this code refers to intermediate coronary syndrome and preinfarction syndrome.
Despite the fact that progressive angina is a separate form of unstable angina (according to Braunwald), yet it has not been assigned a code in ICD-10.
Progressive Angina: Functional Classes
To determine the severity of angina pectoris allow the functional classes (FCs) that correspond to the Braunwald classification. In particular, the following are singled out:
- IA FC - the external influence factor is determined, which contributes to the development of the coronary heart disease. Essentially, it is a secondary progressive angina.
- IB FC - it is impossible to determine the exact cause of IHD, so in this case speak of primary progressive angina.
- IC FC - is a consequence of myocardial infarction, after which occurs for two weeks. Defined as postinfarction angina pectoris.
Pathogenesis of progressive angina
Among the factors involved in the pathophysiology of unstable or progressive angina, one can distinguish the following:
- The mismatch of the body's demand and the possibilities of the heart muscle.
- Destruction or rupture of atherosclerotic plaque.
- Coronary artery thrombosis.
- Vasoconstriction, that is, spasm of blood vessels, blood supplying myocardium.
- Cyclic blood circulation.
Myocardial ischaemia with unstable angina, like any tissue ischemia, is the result of excessive intake or lack of oxygen supply, glucose, and free fatty acids.
The increased need for oxygen in the myocardium can cause the following conditions:
- Tachyarrhythmia (eg, atrial fibrillation or atrial fibrillation).
- Malignant hypertension.
- Drinking cocaine.
- The use of amphetamine.
- Aortic stenosis.
- Supravalvular aortic stenosis.
- Obstructive cardiomyopathy.
- Arteriovenous shunts.
- Congestive heart failure (CHF).
Reducing the supply of oxygen can be caused by various. reasons. In particular, such a violation often occurs on the background of anemia, hypoxia, polycythemia, hypotension.
The above reasons should be investigated, because some of them are reversible. For example, anemia due to chronic gastrointestinal bleeding is common in elderly patients. In such cases, it can coexist in an occult form with ischemic heart disease. Nevertheless, treatment with drugs from the group of anticoagulants and antiagregants can not only be ineffective, but even harmful.
It is important to know that the avoidance or treatment of the underlying disease causing progressive angina is of paramount importance.
Excessive myocardial loading due to increased stress (increased heart rate and systolic blood pressure) often leads to stable angina and possibly in one third of all cases contributes to the progression of angina pectoris.
The mechanism of formation and destruction of an atherosclerotic plaque, due to which progressive angina often develops:
- The deposition of lipid macrophages and smooth muscle cells, the so-called foam cells, occurs inside the atherosclerotic plaques.
- Oxidative low density lipoprotein cholesterol (LDL-X) in foam cells is cytotoxic, procoagulant, and chemotactic, that is, it acts on the vascular wall destructively.
- As the atherosclerotic plaque grows, the production of macrophageal proteases and neutrophilic elastase in the plaque can cause thinning of the fibro-muscular cap, which covers the lipid core.
- Strengthening the plate instability, combined with changes in the intensity of blood flow and the voltage of the circumferential wall, results in the formation of cracks or rupture of the plaque, especially in the place where the lid and vessel wall is connected.
Mechanism of formation and destruction of atherosclerotic plaque
Signs of progressive angina
In unstable angina pectoris, symptoms may occur in a state of rest. They also often become more frequent, severe or prolonged in comparison with the usual picture of stable angina pectoris. Thus, the main distinguishing feature of progressive angina is the lack of a reaction to rest or reception of nitroglycerin.
Symptoms of unstable (progressive) angina are similar to clinical signs of myocardial infarction (MI). Most often, the following is determined:
- Chest pain or pressure sensation.
- Pain or feeling of pressure in the back, neck, jaw, abdomen, shoulders or hands (most often in the left one).
- Enhanced sweating.
- Odd (most often on a background of physical activity or after plentiful food).
- Nausea, vomiting.
- Dizziness or loss of consciousness.
- Sudden weakness.
- Pronounced weakness.
Clinical picture of the disease and diagnostic testing are usually more pronounced and specific to unstable (progressive) angina. At the same time, the physical state is practically intact, therefore it is often considered to be insignificant. During the examination of a patient with unstable angina, the doctor may indicate the following changes:
- Tachycardia (palpitations) or bradycardia (weakened palpitation).
- Temporary myocardial dysfunction.
In the latter variant, systolic arterial pressure may be determined to be less than 100 mm Hg. Art., which indicates an obvious hypotension. Sometimes jugular venous pressure also increases, there is dyskinesia of the vertices of the heart, reverse splitting of S2, the presence of S3 or S4. In some cases, new or deteriorating apical-systolic noise or wheezing is detected.
In some patients, the occlusive disease of the peripheral arteries is further determined. In particular, the carotid artery, supraclavicular or femoral arteries can be involved in the pathological process, as a result of which there is a decrease in peripheral impulses or arterial pressure.
Diagnosis of progressive angina
The following laboratory and instrumental studies are recommended for assessing the patient's condition with suspected progressive angina:
- ECG in 12 standard leads.
- Serial studies of cardiac biomarkers (e.g., MB (KK-MB) creatin kinase isoenzymes, troponin I or T).
- General blood test (OAA) with hemoglobin level determination.
- Biochemical analysis (including magnesium and potassium).
- Lipid profile.
Other tests that can be used to evaluate patients suspected of having FP are:
- Analysis of creatinine levels.
- Testing the patient in a stable condition.
Visual diagnostic methods may also be useful in assessing the patient's condition with suspected progressive angina:
- Roentgenography of the chest.
- Computer tomography with angiography.
- Single-photon emission computer tomography.
- Magnetic resonance angiography.
- Magnetic resonance imaging.
- Myocardial perfusion tomography.
Video: ECG-NSTEMI & Unstable Angina
Clinical recommendations for progressive angina pectoris
When confirming the diagnosis of progressive angina, proper medical supervision should be provided. The medical management of the patient's condition mainly focuses on:
- Reducing the need for oxygen in the myocardium.
- Improvement of supply of oxygen to the heart muscle.
- Assessing the risk of progression of the disease to myocardial infarction or the risk of complications associated with treatment.
Patients with unstable progressive angina require hospitalization, which will allow them to adhere to bed rest with continuous telemetry monitoring. Intravenous access is made and a way to receive additional oxygen is provided, which is especially important in the presence of signs of desaturization.
The course of unstable progressive angina is very variable and may be potentially dangerous to the patient's life, therefore, in a critical situation, the physician will give advice for treatment using invasive (surgical) therapy or conservative (medical) management strategy.
In the treatment of unstable angina, the following drugs are used:
- Antiagregants (for example, aspirin, clopidogrel), which prevent platelet cuffs and, thus, do not allow thrombosis to develop.
- Hypolipidemic drugs of the type statins (for example, simvastatin, atorvastatin, pivastatin and pravastatin), slowing the development of atherosclerosis, and thus impede the development of IHD,
- Cardiovascular antiplatelet agents (eg, tirofiban, eptifibatide and abciximab), which improve blood circulation in the coronary arteries.
- Beta-blockers (for example, atenolol, metoprolol, esmolol, nadolol, and propranolol), which normalize the heart rhythm.
- Anticoagulants (for example, heparin or low molecular weight heparins such as enoxaparin, dalteparin and tinzaparin), dilute blood that eliminates already formed blood clots in vessels.
- Thrombin inhibitors (for example, bivalirudin, lepirudin, desirudin and argatroban), slowing the formation of thrombotic clots.
- Nitrates (eg, nitroglycerin IV), improving the supply of oxygen to the heart muscle.
- Blockers of calcium channels (diltiazem, verapamil or nifedipine), which are also antiarrhythmic drugs.
- Angiotensin converting enzyme (ACE inhibitors) (eg captopril, lysinopril, enalapril, and ramipril), which help to normalize cardiac activity.
Surgical intervention with unstable progressive angina, depending on the indications, may be represented by one of the following procedures:
- Catheterization of the heart.
Whichever method of exposure is not given preference, patients after surgical treatment should continue to be observed by their district physician so that it is possible to spot the precursors to the exacerbation of the disease in a timely manner.
Progressive angina: prognosis
Unstable angina is characterized by high risk of myocardial infarction, complications and death. The therapeutic approach is most often co-ordinated with an individualized assessment risk. As a rule, the following predictive conclusions are defined:
- Patients with a new deviation of the ST segment (greater than 1 mm) are at a 11% risk of death or myocardial infarction during the first year after the onset of an attack. With isolated inversion of the tooth T, the risk is 6.8%.
- The rates of 30-day myocardial infarction and mortality are currently about 8.5% and 3.5%, respectively, despite the increase in the severity of the course of the disease in patients of different ages.
It should be noted that there are important prognostic factors of poor outcome in patients with unstable angina pectoris.In particular, we are talking about the following diseases:
- Congestive heart failure.
- Presence (in the past or at the time of illness) of a bad fraction of left ventricular ejection.
- Hemodynamic instability.
- Recurrent angina, despite intensive anti-ischemic therapy.
- New or worsening of already existing mitral regurgitation.
- Persistent ventricular tachycardia.
These factors are not always evaluated during a physical examination, but nevertheless they should be taken into account when determining the range of medical care.
Other predictors of adverse long-term outcomes in progressive angina include the underlying systolic dysfunction of the left ventricle and more common cardiomyopathy.
Some studies show that the thickness of epicardial adipose tissue (EHT) can also be used to predict serious adverse cardiac events. In a study of 200 patients who were hospitalized with stable angina, unstable angina or acute myocardial infarction who had coronary angiography, in patients with a baseline ECG of over 7 mm, significant revascularization, nonfatal myocardial infarction and a low risk of cardiovascular death were detected.
Progressive angina can occur either because of a clearly defined cause, or without it. It is a precursor to myocardial infarction and often its complication becomes. Diagnosed by symptoms (prolonged pain, even in a calm condition) and by means of instrumental research methods. For treatment, drugs from different pharmacological groups are used, depending on the indications. In the prognostic conclusion an important role is played by the dynamics of the disease and its response to the use of medicines.
Video: Unstable Angina ¦ Treatment and Symptoms
1. Нестабильная стенокардия - Википедия - свободная энциклопедия 2. Unstable Angina (англ.) - статья Уолтера Тана на портале eMedicine (https://emedicine.medscape.com/article/159383-overview) от Дек. 26, 2017. 3. Lee HJ, Berman GM, Bassett J. Atypical progressive angina pectoris caused by a congenital coronary-pulmonary shunt and coronary atherosclerosis. Angiology. 1977 Jan;28(1):15-8.
A pronounced clinic and a long process of development is characterized by angina, formerly known as "chest frog". The disease has specific symptoms that allow faster and accurate diagnosis of the pathology. When performing the patient's medical recommendations, stable angina is characterized by a favorable flow.
Angina is most often manifested by pain in the heart or behind the sternum. At the same time there are additional symptoms indicating a violation of the coronary circulation. When identifying them, it is important to know what to do.
When there is a pain behind the sternum, many immediately think about angina pectoris and it is not justified. This disease occurs more often after 50 years, but may develop even younger ones. The greatest risk is associated with angina pectoris, which is rather difficult and can have an unfavorable prognosis.