Unstable angina



OVERVIEW

Definition

It is a group of acute myocardial ischemia on the basis of coronary atherosclerosis, between stable angina and acute myocardial infarction clinical syndrome.

According to the clinical manifestations, it can be divided into resting angina pectoris, incipient angina pectoris, and worsening exertional angina pectoris.

Patients with chest pain, chest tightness, dyspnea as the main clinical manifestations, may be accompanied by sweating, cold and wet skin, palpitations, nausea, vomiting and other symptoms.

Types

According to clinical manifestations, unstable angina can be categorized into the following three types.

Resting angina

Angina that occurs in the resting state and lasts for more than 20 minutes.

Primary angina

Angina induced by very light physical activity within 1-2 months of the first symptoms of coronary artery disease.

Worsening exertional angina

The patient has a gradual worsening of symptoms on top of the original relatively stable exertional angina, which is characterized by more intense pain, longer duration, and more frequent episodes.

Morbidity

There are no definitive data on the epidemiology associated with unstable angina.

Etiology

Causes

On the basis of coronary atherosclerosis, unstable angina is caused by rupture or erosion of unstable plaque, resulting in thrombosis, vasospasm leading to increased coronary artery stenosis or transient occlusion, and myocardial ischemia, which then leads to unstable angina pectoris. Coronary artery dissection can also be caused.

Although unstable angina can also be triggered by exertional loading, chest pain is not relieved after the termination of exertional loading.

Predisposing Factors

The following factors can trigger an increase in cardiac oxygen consumption or myocardial ischemia, resulting in an attack or exacerbation of unstable angina.

Increased myocardial oxygen consumption

Infections, hyperthyroidism, arrhythmias and other diseases can lead to increased heart rate and increased myocardial oxygen consumption.

Decreased coronary blood flow

Decreased coronary blood flow in hypotensive and shock states can lead to unstable angina.

Decreased oxygen-carrying capacity of blood

Patients with anemia and hypoxemia are more likely to induce myocardial ischemia.

Hemodynamic changes

Increased myocardial oxygen consumption under emotional excitement, strenuous exercise or cold stimulation is prone to myocardial ischemia.

Risk factors

Unstable angina occurs on the basis of coronary atherosclerosis, so people with any one or more of the following risk factors for coronary atherosclerosis are at high risk for unstable angina.

Dyslipidemia

It is the main risk factor of coronary atherosclerosis and has the effect of promoting thrombosis.

Hypertension

60-70% of patients with coronary atherosclerosis suffer from hypertension.

Smoking

The incidence of coronary atherosclerosis is directly proportional to the number of cigarettes smoked per day.

Smokers are two to six times more likely to develop coronary atherosclerosis.

Diabetes mellitus, insulin resistance and metabolic syndrome

Coronary atherosclerosis is two times more common in people with diabetes than in those without diabetes.

People with impaired glucose tolerance are more common in patients with coronary atherosclerosis.

The risk of coronary atherosclerosis in patients with metabolic syndrome is twice as high as in those without metabolic syndrome.

Overweight and Obesity

Excessive accumulation of body fat in overweight and obese patients can lead to insulin resistance, hyperinsulinemia, hypertension, and dyslipidemia, which increase the risk of coronary atherosclerosis.

Excess adipose tissue can release pro-inflammatory cytokines, increasing the risk of coronary atherosclerosis.

Irrational diet

People who consume too many total calories and sodium, fats and oils, and too little vegetables and fruits are prone to coronary atherosclerosis, which can lead to unstable angina.

Lack of physical activity

Appropriate physical activity has the effect of reducing body weight, improving blood lipids, reducing insulin resistance and lowering blood pressure, as well as maintaining vascular endothelial function and antioxidant, thus helping to reduce the incidence of coronary atherosclerosis.

Age

Coronary atherosclerosis occurs in middle-aged and elderly people over 40 years old.

Gender

Coronary atherosclerosis affects more men than women, with a male to female ratio of about 2:1.

The incidence of atherosclerosis in women increases rapidly after menopause.

Heredity

Coronary atherosclerosis has a certain family aggregation.

Psychosocial factors

Psychological stresses such as depression, anxiety, and type A personality can cause neuroendocrine dysfunction, leading to elevated blood pressure and platelet reactive activation in affected individuals, thus promoting the development of coronary atherosclerosis.

Pro-thrombotic state

Increased concentrations of fibrinogen and plasminogen activator inhibitor-1 (PAI-1) may promote thrombosis.

Increased high-sensitivity C-reactive protein (hsCRP)

Increased hsCRP suggests the presence of a persistent inflammatory response and indicates an increased risk of developing coronary atherosclerosis.

Renal Insufficiency

Renal insufficiency can contribute to the development of coronary atherosclerosis in a number of ways, including elevated blood pressure, insulin resistance, elevated homocysteine, and increased levels of fibrinogen and hsCRP.

Hyperhomocysteinemia

Studies have shown that hyperhomocysteinemia is one of the most important risk factors for cardiovascular and cerebrovascular diseases.

Pathogenesis

Rupture or erosion of unstable plaque

Weakening of plaque structure

Unstable plaques contain a large number of T-lymphocytes, which can cause the plaque structure to weaken by synthesizing and releasing cytokines.

Plaque becomes more vulnerable to damage

The large number of macrophages and mast cells in unstable plaques can secrete matrix metalloproteinases, making the plaque more vulnerable to damage.

Plaque rupture or erosion

Under the effect of the above factors, the structure of atherosclerotic plaque becomes weak and vulnerable to damage.

Atherosclerotic plaques may rupture or erode as a result of increased pressure in the lumen of the coronary arteries, increased vascular tone or spasm in the coronary arteries, and excessive contraction or dilation of the ventricles during tachycardia.

Thrombosis

After rupture of an unstable plaque, the lipid core and matrix within the plaque are exposed, and adhesion and aggregation of platelets and subendothelial adhesion factors occur, leading to thrombus formation, complete or incomplete obstruction of the coronary artery lumen, resulting in a sudden decrease or intermittent interruption of coronary blood flow.

Vasospasm

The thrombus is rich in platelets, which can release a large number of vasoactive substances, causing increased vasoconstriction, resulting in spasm of the coronary arteries, leading to a reduction in blood flow and varying degrees of ischemia in the myocardium.

Coronary artery sandwich formation

Coronary artery sandwich lining itself back to block blood flow, in addition to platelet adhesion and activation of the coagulation waterfall to produce thrombus, resulting in acute occlusion of coronary arteries or on the verge of occlusion, triggering unstable angina pectoris.

Symptoms

Main Symptoms

The main symptoms of unstable angina are chest pain, chest tightness and dyspnea at rest or at night, which can only be relieved temporarily or even not completely after rest or the use of nitrate drugs such as nitroglycerin.

Chest pain

Chest pain is mainly located after the sternum body, can also be located in the pre-cardiac area of the palm size range, or even can be manifested as unclear boundaries, transverse anterior chest pain.

Chest pain can radiate to the left upper arm and ring finger and little finger, or radiate to the neck, pharynx and jaw, and some patients may manifest toothache or epigastric pain.

It is usually a compressive boring or tightening pain, and some patients may present with a burning sensation, but usually not a sharp pain like a pinprick or knife stab.

Chest pain can occur at rest and lasts for a long time, usually up to tens of minutes.

Chest pain is usually not relieved significantly by rest or vasodilator medications such as nitroglycerin.

Chest tightness and dyspnea

Chest tightness and dyspnea may occur at rest and worsen with activity.

Some patients only experience chest tightness without chest pain.

Other symptoms

Some patients may experience sweating, cold clammy skin, palpitations, abdominal pain, nausea, vomiting, and a sense of dying during the attack.

Complications

Unstable angina may lead to the following complications.

Acute myocardial infarction

Unstable angina may lead to acute myocardial infarction if the coronary artery stenosis is not improved or driven by certain triggering factors, resulting in aggravation of coronary artery stenosis or even complete occlusion, with severe reduction or even complete interruption of coronary artery blood flow.

Patients may experience symptoms such as irritability, persistent and severe chest pain, significant dyspnea, and impaired consciousness.

Acute myocardial infarction may further induce acute heart failure, malignant arrhythmia, cardiac arrest, etc. leading to the death of the patient.

Heart Failure

Unstable angina may lead to reduced coronary blood flow, and may even induce acute myocardial infarction, causing a serious reduction or even complete interruption of coronary blood flow, so that the myocardium appears ischemia, hypoxia, affecting the normal pumping function of the heart, inducing cardiac insufficiency, or even heart failure.

Patients may have symptoms such as dyspnea, sedentary breathing, and pink foamy sputum.

If not treated in time, circulatory failure may lead to death.

Malignant arrhythmia

On the basis of reduced coronary blood flow caused by unstable angina, myocardial ischemia and hypoxia can affect its normal conduction, inducing severe conduction block, ventricular fibrillation and other malignant arrhythmias, and in severe cases, cardiac arrest can occur, causing sudden cardiac death.

Patients may experience palpitations, dyspnea, blackout, syncope, convulsions and other symptoms.

Consultation

Department of Medicine

Cardiovascular Medicine

If the patient has chest pain, chest tightness, dyspnea, palpitations, etc., it is recommended to consult a doctor promptly.

Patients with coronary atherosclerosis or coronary heart disease are advised to seek timely medical treatment if chest pain worsens and the duration and frequency of attacks increase.

If coronary artery disease or myocardial ischemia is detected during physical examination, it is recommended to consult a doctor in time.

Emergency Department

If the patient develops symptoms such as persistent unrelieved chest pain, irritability, severe dyspnea, or impaired consciousness, it is recommended to consult the Emergency Department or call 120 emergency for emergency services immediately.

Preparation for medical treatment

Preparation for medical consultation: registration, preparation of documents, common problems

Tips for seeking medical treatment

Before seeking medical treatment, patients should rest in bed and minimize activities and lifting.

For patients with a clear diagnosis of coronary artery disease, sublingual nitroglycerin or fast-acting heart-saving pills can be taken.

Preparation List

Symptom list

Especially need to pay attention to the time of symptom onset, special performance, etc.

Are there symptoms such as chest pain, chest tightness, dyspnea, palpitations, etc.?

How long have these symptoms been present?

What is the nature of the chest pain (e.g., cutting, squeezing, boring, etc.)?

What is the frequency and duration of these symptoms?

Do these symptoms get better on their own? Do they improve with sublingual nitroglycerin?

Medical History Checklist

Do you have regular medical checkups? Are there any abnormalities in the physical examination results?

Is there any history of cardiovascular disease such as hypertension, coronary atherosclerotic heart pump? Do you take medication regularly?

Is there any family history of cardiovascular disease in the immediate family?

Is there any underlying disease such as diabetes, dyslipidemia, renal insufficiency, etc.?

Is there a history of long-term smoking?

Checklist

Test results in the past six months, which can be brought to the doctor’s office.

Blood biochemistry

Blood test

Urine routine

24-hour urine protein quantification

Echocardiogram

Head CT and/or head magnetic resonance imaging (MRI)

Adrenal gland and renal artery ultrasound

Ambulatory blood pressure monitoring

Electrocardiogram

List of medications used

Medication use in the last 3 months, if available in boxes or packages, carry to doctor’s appointment

Diuretics: hydrochlorothiazide, furosemide, spironolactone

Beta-blockers: metoprolol, bisoprolol, carvedilol, propranolol

Calcium channel antagonists (CCB): nifedipine, verapamil, diltiazem

Angiotensin II receptor antagonists (ARBs): chlosartan, valsartan, irbesartan

Lipid regulating drugs: simvastatin, atorvastatin

Diagnosis

Diagnosis is based on

Medical history

History of coronary atherosclerosis.

Men over 40 years of age or postmenopausal women.

History of obesity, smoking, hyperlipidemia, diabetes mellitus, hypertension and other risk factors for coronary atherosclerosis.

Clinical manifestations

Symptoms

Patients often present with chest pain, chest tightness, dyspnea, which is not significantly relieved after rest and sublingual nitroglycerin.

Some patients may experience sweating, clammy skin, palpitations, nausea, vomiting, and a sense of impending death during the attack.

Physical signs

Cardiac auscultation may show a transient third or fourth heart sound.

In some patients, a transient systolic murmur may be heard in the mitral valve area (the strongest point of the apical beat).

Laboratory Tests

Myocardial necrosis markers

These are used to characterize myocardial metabolism and to assess the condition.

They include serum troponin and cardiac enzymes.

Generally not elevated or only mildly elevated, if significantly elevated suggests the possibility of complication of acute myocardial infarction.

Serum troponin is important for risk stratification and assessment of myocardial ischemia, and the higher the troponin level at the time of consultation, the higher the risk of death.

Heart failure markers

Including blood B-type natriuretic peptide (BNP) or N-terminal B-type natriuretic peptide proteins (NT-ProBNP).

It can assess the presence of cardiac insufficiency and determine the prognosis and treatment effect.

It may be elevated in the presence of cardiac insufficiency.

Lipids

Lipid profile can be obtained to assess the presence or absence of hyperlipidemia.

Patients with decreased HDL and elevated total cholesterol, LDL, triglycerides, etc. suggest combined hyperlipidemia.

Blood Glucose

Blood glucose can be obtained to assess the presence or absence of diabetes mellitus.

The presence of fasting blood glucose ≥ 7 mmol/L and/or random blood glucose ≥ 11.1 mmol/L suggests possible diabetes mellitus.

Coagulation

Coagulation was assessed.

Increased concentrations of fibrinogen and plasminogen activator inhibitor-1 (PAI-1) suggest a high risk of thrombosis.

Renal Function

To assess renal function.

Calculation of the glomerular filtration rate allows assessment of the severity of the disease and guides treatment.

Blood homocysteine measurement

To find out if there is hyperhomocysteinemia.

High Sensitivity C-Reactive Protein (hsCRP)

To assess the inflammatory response in the body.

An increase in hsCRP indicates an increased risk of coronary atherosclerosis.

Electrocardiogram (ECG)

Provides a quick look at the patient’s cardiac activity. Assesses the presence of myocardial ischemia.

Important in the diagnosis of unstable angina.

Myocardial ischemia manifestations such as ST-segment elevation or depression, T-wave flattening or inversion may be present.

If the dynamic change of ST segment elevation or depression of ≥0.1mV occurs, it suggests the manifestation of severe coronary artery ischemia, and the patient may have acute myocardial infarction or sudden cardiac death at any time.

If ECG changes persist for more than 12 hours, it suggests the possibility of non-ST-segment elevation myocardial infarction.

Continuous electrocardiographic monitoring

Some patients with unstable angina may not present with chest pain.

Continuous electrocardiographic monitoring can capture ST-segment changes in patients with episodes of myocardial ischemia.

Imaging

Echocardiography

Echocardiography is valuable in the diagnosis of unstable angina pectoris because it provides information about the dynamics of the patient’s heart.

Abnormal ventricular wall motion in the ischemic area may be seen.

Left and right ventricular function can be assessed.

Can be used to identify lesions such as valvular stenosis and hypertrophic cardiomyopathy.

CT Coronary Artery Imaging (CTA)

Provides insight into the degree of coronary artery lumen stenosis and wall calcium.

Important in the diagnosis of unstable angina.

Has a high negative predictive value, and coronary angiography is usually not necessary if no significant coronary stenosis is seen on CT coronary imaging.

Factors such as coronary artery spasm may lead to false positives, so if coronary artery stenosis is seen on CT coronary imaging, further coronary angiography is recommended.

Bedside chest X-ray

Mostly used in critically ill patients, it can assess the heart size and find out whether the patient has pulmonary stasis, pulmonary edema, pleural effusion, secondary lung infection, etc. It can be used to evaluate the treatment effect.

Radionuclide examination

It can understand myocardial metabolism, exercise and perfusion, and is of significance in the diagnosis of unstable angina.

Invasive examination

Coronary angiography (CAG)

Coronary angiography (CAG) can detect the location of stenotic lesions in the coronary arteries and estimate their extent.

Coronary angiography can be used to clarify the diagnosis, guide treatment, and evaluate the efficacy of treatment.

It is important for the development of treatment strategies.

Coronary ultrasonography and intracoronary optical coherence tomography.

Can understand the distribution, nature and size of plaque, as well as the existence of rupture and thrombosis, etc., which can help to guide the interventional therapy.

Diagnostic criteria

The diagnosis of unstable angina can be made on the basis of typical angina symptoms and ischemic electrocardiographic changes (new or transient ST-segment depression ≥0.1 mV or T-wave inversion ≥0.2 mV), as well as the measurement of myocardial injury markers, such as serum troponin and cardiac enzymes.

In atypical patients with unclear diagnosis, if the condition is stable, load electrocardiogram or load echocardiogram, myocardial radionuclide examination, coronary arteriography and other investigations can be performed to clarify the diagnosis before discharge from the hospital.

Differential diagnosis

Unstable angina should be differentiated from the following diseases.

Acute pericarditis

Similarities: both can lead to chest pain.

Differences:

Chest pain due to acute pericarditis is characterized by irritating pain that radiates to the shoulders and is relieved by forward sitting, pericardial friction is audible on cardiac auscultation, and the electrocardiogram is characterized by a bow-back-down type of elevation of the T-segment in all leads except the aVR lead.

Chest pain due to unstable angina manifests as oppressive boring pain or constrictive pain, and some patients may manifest burning sensation, but usually there is no sharp pain like pins and needles or knives, and the electrocardiogram manifests myocardial ischemia manifestations such as ST-segment elevation or depression, and T-wave flattening or inversion.

Acute pulmonary embolism

Similarity: Both can cause chest pain and dyspnea.

Differences

Acute pulmonary embolism occurs after surgery and long-term bed-ridden people, in addition to chest pain, dyspnea, hemoptysis, D-dimer is often elevated, and pulmonary angiography can see pulmonary embolism foci.

Unstable angina occurs in men over 40 years of age or postmenopausal women, with the basis of coronary atherosclerosis, as well as obesity, smoking, hyperlipidemia, diabetes mellitus, hypertension and other risk factors for coronary atherosclerosis in the population, check the electrocardiogram has ST-segment elevation or depression, T-wave flattening or inversion and other manifestations of ischemia in the myocardium, and D-dimer is usually not high.

Acute abdomen

Similarity: Acute pancreatitis, perforated peptic ulcer, acute cholecystitis, cholelithiasis and unstable angina may present with epigastric pain.

Differences:

Patients with acute abdomen often have sharp pain, abdominal pressure, rebound pain and abdominal muscle tension and other peritonitis manifestations, blood routine, CRP often suggests elevated inflammatory indicators, acute pancreatitis can be seen in the blood and urine amylase elevation, abdominal imaging manifestations can be seen in pancreatitis, cholecystitis, subdiaphragmatic free gas and other corresponding manifestations, and check the electrocardiogram, myocardial necrosis markers are mostly normal.

Unstable angina usually does not show sharp pain, no peritoneal irritation, ST-segment elevation or depression, T-wave flattening or inversion and other manifestations of myocardial ischemia on electrocardiogram, and myocardial necrosis markers may be elevated on electrocardiogram.

Aortic dissection

Similarity: Both can cause chest pain, dyspnea and other symptoms.

Differences:

Chest pain due to aortic coarctation is often severe tearing pain that radiates to the back, and in addition to chest pain, there may be a difference in blood pressure in the extremities, etc. Aortic CTA or magnetic resonance imaging of the aorta can make a clear diagnosis.

Chest pain caused by unstable angina manifests as oppressive boring pain or tightening pain, some patients may manifest burning sensation, ECG manifests ST-segment elevation or depression, T-wave flattening or inversion and other manifestations of myocardial ischemia, and myocardial necrosis markers may be elevated.

Spontaneous pneumothorax

Similarity: Both can lead to chest pain, dyspnea and other symptoms.

Differences:

Spontaneous pneumothorax occurs in long and thin young people and middle-aged and old people with underlying lung diseases. Chest pain is often characterized by pins and needles or knife-like pain of short duration; myocardial necrosis markers and electrocardiograms are normal, and pneumothorax lines can be seen on chest imaging.

Chest pain caused by unstable angina manifests as oppressive boring pain or constrictive pain, mostly without pinprick or knife-like sharp pain, some patients may manifest burning sensation, ECG manifests ST-segment elevation or depression, T-wave flattening or inversion and other manifestations of myocardial ischemia, and myocardial necrosis markers may be elevated.

Treatment

The purpose of treatment: to improve myocardial ischemia, prevent further development of myocardial infarction, and at the same time, carry out long-term secondary prevention to delay the onset of the disease.

Treatment principle: general treatment and drug treatment, and surgery if necessary.

General treatment

Rest

Bed rest, keep the environment quiet, eliminate the patient’s tension and anxiety.

If necessary, small doses of sedatives or anti-anxiety drugs can be used.

Oxygenation

For patients with cyanosis, dyspnea, left heart insufficiency and arterial oxygen saturation less than 90%, oxygen should be given to maintain arterial oxygen saturation above 90%.

Patients with severe hypoxia or respiratory failure may be given mechanical ventilation.

Removal of triggers

Promptly remove infections, fever, hyperthyroidism, anemia, hypotension, arrhythmia and other triggers that can lead to increased myocardial oxygen consumption.

Drug therapy

Anti-myocardial ischemic drugs

Nitrate drugs

Nitrate drugs can dilate veins, reduce cardiac preload, reduce myocardial oxygen consumption, and at the same time can dilate coronary arteries, increase coronary artery blood flow, improve myocardial ischemia, and alleviate patients’ chest pain symptoms.

Commonly used drugs are nitroglycerin, isosorbide nitrate and so on.

β-receptor antagonist

They can act on myocardial receptors, slow down the heart rate, reduce myocardial oxygen consumption, relieve myocardial ischemia, and improve the near and long-term prognosis of patients.

Commonly used drugs include metoprolol, bisoprolol, esmolol and so on.

Calcium channel blockers

It has the effect of effectively improving myocardial ischemia and reducing angina pectoris.

Commonly used drugs are nifedipine, amlodipine, felodipine and so on.

Anti-platelet drugs

Cyclooxygenase (COX) inhibitors

Can inhibit the activity of cyclooxygenase, thus blocking the synthesis of thromboxane A2 (TXA2), and achieve the purpose of anti-platelet aggregation.

Commonly used drugs include aspirin, the cornerstone of antiplatelet therapy.

Indobufen is an option for those who are intolerant to aspirin.

Receptor antagonists

Receptor antagonists can block the receptors on platelets and inhibit platelet activation to achieve the purpose of anti-platelet aggregation.

Commonly used drugs include clopidogrel.

Platelet glycoprotein IIb/IIIa (GPIIb/IIIa) receptor antagonist (GPI)

It can competitively bind to the GPIIb/IIIa receptor on the platelet surface to achieve the purpose of anti-platelet aggregation.

Commonly used drugs include tirofiban.

Cyclic nucleotide phosphodiesterase inhibitors

As an alternative drug for aspirin intolerant patients.

Commonly used drugs are cilostazol.

Anticoagulants

In the absence of absolute contraindications, all patients with intermediate- to high-risk unstable angina should routinely receive anticoagulation in addition to antiplatelet therapy.

Normal heparin

Monitor platelet changes during use.

Low molecular weight heparin

The efficacy of low molecular weight heparin is superior or equal to that of normal heparin, and the incidence of thrombocytopenia is lower.

Commonly used are enoxaparin and naltrexone heparin.

Fondaparinux sodium

Effective in reducing cardiovascular events and lowering the risk of bleeding.

It is the anticoagulant of choice for conservatively treated patients, especially those at risk of bleeding.

Bivalirudin

A direct antithrombin agent that prevents contact thrombosis.

The bleeding incidence ratio is significantly lower than that of heparin.

Mainly used for intraoperative anticoagulation in interventional patients.

Lipid regulating and stabilizing drugs

Can stabilize coronary plaque.

Commonly used drugs are statins such as atorvastatin and resuvastatin.

Pay attention to monitor the changes of liver function and muscle enzymes during use.

Drugs to improve ventricular remodeling

They mainly include angiotensin receptor enkephalinase inhibitors (ARNI), angiotensin converting enzyme inhibitors or (ACEI), angiotensin II receptor blockers (ARB).

They may improve ventricular remodeling and reduce the incidence of cardiovascular events.

Commonly used drugs include sacubitril valsartan, benazepril, enalapril, and irbesartan.

Surgical treatment

Percutaneous coronary intervention (PCI)

Indications

Emergency PCI within 2 hours is recommended for patients with any of the following very high-risk criteria

Unstable flow dynamics or cardiogenic shock.

Recurrent or persistent episodes of chest pain not responding to pharmacologic therapy.

Fatal arrhythmia or cardiac arrest.

Myocardial infarction combined with mechanical complications such as ventricular septal defect, papillary muscle dysfunction or rupture.

Acute heart failure.

Repeated dynamic evolution of ST-T waves on the ECG, especially with intermittent ST-segment elevation.

Early PCI within 24 hours is recommended for patients with any of the following high-risk criteria

Elevated or decreased troponin associated with myocardial infarction.

Dynamic changes in ST-segment or T-wave on ECG.

Global Registry of Acute Coronary Events Risk Score (GRACE score) >140 (parameters for this risk calculation include age, systolic blood pressure, pulse rate, serum creatinine, Killip classification at presentation, cardiac arrest on admission, elevated cardiac biomarkers, and ST-segment changes).

PCI within 72 hours is recommended for patients with any of the following intermediate-risk criteria

Diabetes mellitus.

Glomerular filtration rate below 60 ml/(min-1.73m²).

Ejection fraction less than 40%.

Congestive heart failure.

Early post-infarction angina.

History of percutaneous coronary intervention.

History of coronary artery bypass grafting.

GRACE score >109 but <140.

Contraindications

Presence of severe bleeding disorders.

Hypersensitivity to contrast agents.

Hypersensitivity to antiplatelet agents and/or stent materials.

Target vessel less than 2.25 mm.

Presence of other conditions that make it impossible to tolerate the procedure.

Coronary artery bypass grafting (CABG)

Indications

Patients with severe vascular lesions, multiple vascular lesions, or severe left heart insufficiency who are not suitable for PCI.

Contraindication

Diffuse coronary artery lesions.

Left ventricular ejection fraction less than 25%.

Extensive myocardial cell necrosis.

Other conditions that make it impossible to tolerate the procedure or anesthesia.

Intra-aortic balloon counterpulsation (IABP)

Indications

Repeated episodes of ischemia or persistent ischemia after pharmacologic treatment.

Patients who are hemodynamically unstable before or after coronary angiography or in the presence of cardiogenic shock.

Patients with mechanical complications of myocardial infarction.

Contraindications

Severe aortic valve lesions.

Aortic aneurysm.

Cerebral hemorrhage.

Severe bleeding tendency.

Peripheral arterial disease.

Presence of other conditions that make it impossible to tolerate surgery and anesthesia.

Prognosis

Cure

Myocardial infarction occurs in about 30% of patients with unstable angina within 3 months of the onset of the disease, but sudden death is less common.

The near-term mortality rate of unstable angina is lower than that of acute non-ST-segment elevation myocardial infarction and acute ST-segment elevation myocardial infarction.

The long-term mortality rate of unstable angina is comparable to that of acute non-ST-segment elevation myocardial infarction and higher than that of acute ST-segment elevation myocardial infarction.

Prognostic factors

The prognosis of unstable angina is influenced by a number of factors, and the following factors often lead to a poor prognosis.

Advanced age.

Failure to receive timely treatment or poor patient compliance.

Involvement of acute myocardial infarction, especially large infarctions or anterior myocardial infarctions.

Involvement of serious complications such as heart failure and malignant arrhythmias.

Combination of other serious underlying diseases.

Daily management

Daily management

Dietary management

Maintain a low-salt and low-fat diet, and try to avoid high-fat and high-cholesterol foods such as animal oil, fatty meats, animal offal and fried foods.

Eat more fresh fruits and vegetables rich in vitamins and fiber.

Life management

Quit smoking and drinking.

Regular work and rest, avoid overwork and staying up late.

After the disease is stabilized, you can carry out low and medium intensity aerobic exercise, such as jogging, tai chi, etc., for 30 minutes three or more times a week after the physician refers to the assessment of exercise tolerance and exercise risk, and should not do strenuous exercise.

Strict blood pressure control is recommended when hypertension is present: diastolic blood pressure target <90 mmHg (<85 mmHg in diabetic patients); systolic blood pressure target <140 mmHg.

In the presence of diabetes mellitus, strict control of blood glucose should be achieved: glycosylated hemoglobin <7%.

Strict adherence to medication and regular follow-up.

Psychological support

Relaxed mood, avoiding blood pressure fluctuation due to excessive emotional fluctuation, causing myocardial ischemia aggravation.

Disease monitoring

Pay attention to the changes of symptoms related to cardiovascular disease, such as chest pain worsening, profuse sweating, dyspnea, impaired consciousness and other symptoms are often indicative of deterioration of the condition, and need to return to the hospital for follow-up.

Patients with hypertension or diabetes should monitor and record changes in blood pressure and blood glucose every day.

Follow-up review

Patients with unstable angina should have regular follow-up examinations so that the doctor can assess the changes in the patient’s condition and adjust the treatment plan accordingly.

The schedule of follow-up examinations should be set by the specialist according to the patient’s specific condition.

The main review items include cardiac enzymology, troponin, BNP, blood lipids, blood glucose, blood homocysteine and other laboratory indicators, as well as electrocardiogram, cardiac ultrasound and other examinations, and CT coronary artery imaging and coronary angiography may be required if necessary.

Prevention

Avoid risk factors for cardiovascular disease

Control body weight within a reasonable range, it is recommended to keep the body mass index (BMI) below 24.

Eat a sensible diet, low-salt and low-fat diet, and stop smoking and drinking.

Regular work and rest, avoid overwork and late nights.

Exercise properly: aim for moderate exercise of 30 minutes or more each time, at least 5 days a week.

Emphasize the management of underlying diseases

Regular medical checkups and timely treatment for detected diseases.

Actively intervene and treat underlying diseases such as hyperlipidemia, diabetes mellitus, hypertension, coronary heart disease, etc., and strengthen daily management to control the disease and slow down and curb its progress.