Unstable angina pectoris in the elderly
Introduction
Introduction to unstable angina in the elderly Refers to an unstable myocardial ischemic syndrome between stable angina and acute myocardial infarction. Because it is easy to develop acute myocardial infarction or sudden death, timely diagnosis and correct treatment are essential. Mainly including initial angina pectoris, worsening angina pectoris, spontaneous angina pectoris, syndrome X, angina pectoris, and postprandial angina are also areas of unstable angina. Variant angina is also an unstable angina. basic knowledge The proportion of illness: 80% of the probability of being over 50 years old Susceptible people: the elderly Mode of infection: non-infectious Complications: acute myocardial infarction
Cause
The cause of unstable angina in the elderly
(1) Causes of the disease
1. Smoking, dramatic changes in mood, cold stimulation, etc.
2. Anemia, thyroid disease, hypertension, arrhythmia, infection, polycythemia and hypoxemia.
3. Antihistamines and adrenergic drugs, cocaine, amphetamine, etc., in addition to short-acting dihydropyridines, high doses of dipyridamole, etc. can induce UA attacks.
4. Sudden withdrawal of anti-ischemic drugs (including nitrates, beta blockers, calcium antagonists).
(two) pathogenesis
Pathogenesis
The pathogenesis of unstable angina may be based on coronary atherosclerosis, combined with certain acute factors such as plaque rupture, thrombosis, platelet aggregation, inflammation triggering and development, coronary artery spasm, intra-plaque hemorrhage, etc. Rapid development in a short period of time, but not completely occluded, leading to unstable myocardial ischemia, endothelial functional status and platelets play an important role in these factors.
(1) plaque rupture: plaque surface suddenly rupture, thrombosis is the main cause of UA, the main factor determining plaque rupture is the composition and fragility of plaque, rather than the degree of stenosis, clinical studies show that:
1 small, early moderately narrow plaque is more likely to rupture than late severe stenosis.
2 formed by crescent-shaped lipid accumulation, the eccentric plaque separated by the fibrous cap and the vascular cavity contains high cholesterol ester, and the content of crystals higher than free cholesterol is easily broken.
3 macrophages rich in extracellular matrix and visceral caps reduce extracellular matrix by phagocytosis, secrete proteases, weaken fibrous caps, and make plaques easy to rupture.
4 Macrophages in the fibrous cap reduce the extracellular matrix by phagocytosis, secrete proteases, weaken the fibrous cap, and make the plaque easy to rupture.
5 Under the action of many trigger factors, such as heart rate, blood pressure, myocardial contractility, coronary flow and tension increase, plaque load increases, vulnerable plaque can rupture, but most UA patients are without any obvious Under the triggering factor, the increase of plaque lesion activity and plaque fatigue play a major role.
(2) Platelet aggregation: There is sufficient evidence to date that platelet aggregation is the original finding of ischemic attack or continuation of plaque rupture in patients with UA and AMI, and other factors also play a role, such as increased sympathetic vascular tone. Increased levels of catecholamines in the blood, hypercholesterolemia, leukocyte activation, and abnormal fibrinolysis may be manifested by increased serum concentrations of plasminogen activator inhibitor type I (PaI-I), alpha 2 adrenergic And activation of serotoninergic platelet receptors, which can promote platelet aggregation.
(3) Acute thrombosis: rapid changes in fragile plaque rupture or unstable plaque geometry. Subsequent thrombosis leads to near complete occlusion of the blood vessels, causing clinical manifestations of UA. When plaque ruptures, some local and systemic The factors affect the extent and timing of thrombosis. Local factors include hemorheological properties and tissue characteristics at the arterial lesion. Platelet deposition is also proportional to blood shear force. Various plaques are often exposed to high shear. The blood flow site of the force, their thrombogenicity increases, about 2 / 3 of UA patients, cholesteryl plaque ulcer surface is the strongest tissue factor, the tissue characteristics of the blood vessel wall including the depth of the injury site , area, shape, collagen fiber type, tissue thromboplastin, prostacyclin production, coagulation
Enzyme content, etc., systemic factors such as infection, hypercholesterolemia, etc. may be related to thrombosis.
(4) Coronary artery spasm: may play an important role in the pathogenesis of unstable angina pectoris, unstable angina coronary artery lesions are more common in eccentric stenosis, and the curved normal wall remains in the coronary artery diameter of the lesion. This provides conditions for coronary spasm. In severe coronary stenosis, mild changes in coronary tension can cause angina pectoris. Coronary lesions of partially unstable angina are not serious, and 10% to 20% of patients may not have Significantly narrow, in these patients, coronary vasospasm may be the main pathogenesis of unstable angina, coronary vasospasm can rupture the softer atheromatous plaque, on the one hand can cause bleeding under the plaque, on the other hand can lead to platelets Aggregation, platelet rupture, release of thromboxane A2 and other vasoactive substances lead to vasospasm, thrombosis, and induction of unstable angina.
(5) Endothelial function: vascular endothelium is the most active part of protein synthesis, is a very important secretory organ, endothelial cells synthesize various connective tissue components, vasoconstrictor (endothelin, angiotensin factor, endothelial contraction factor EDCF), vasodilation Substance (endothelium relaxing factor EDRF), calmodulin gene-related peptide (CGRP) and anticoagulant (heparin analogue), fibrinolytic tissue plasminogen activator (tPA), these endocrine factors regulate coronary artery Reduces the reaction and maintains the fluidity of the blood. The function of endothelial cells can be impaired by ischemia, lipid deposition, and mechanical damage of hemodynamics. Therefore, abnormal endothelial function plays an important role in vasospasm and thrombosis in unstable angina pectoris. .
2. Pathophysiology
The cause of coronary blood flow reduction in UA patients can be attributed to two aspects: vascular morphological changes and vascular functional changes. The instability of angina depends largely on the ischemia-related coronary atherosclerotic plaque in the near future. Progressive changes within the atherosclerotic plaque and/or atheromatous plaque hemorrhage and wall thrombosis, and vasospasm also play an important role in UA, and heart rate or blood pressure is elevated There are few factors (Table 1).
In short, the pathological basis of UA is unstable plaque, which is due to the fissure or rupture of the fibrous cap of the atherosclerotic plaque in the coronary artery, causing the lipid nucleus of collagen fibers and plaques to be exposed, triggering platelets and promoting Coagulation factors and other activation, and a series of waterfall-like reactions, eventually leading to coronary artery (coronary) thrombosis; angiotensin II (ATII), endothelin-1 (ET-1) and thromboxane A2 (TXA2) The release of endothelium-derived contractile factor can cause coronary spasm. UA patients undergo coronary angiography (CAG), intravascular ultrasound, and post-mortem examinations. Atherosclerosis (AS) plaque rupture with local platelet thrombosis Formation plays an affirmative role in the pathogenesis of UA, unless UA further develops into acute myocardial infarction (AMI), coronary thrombosis often only causes incomplete occlusion of the lumen, UA is a non-occlusive thrombus (ie unstable thrombus) The incidence can be as high as 80% to 85%, and the total occlusive thrombosis is usually only 15% to 20%. The components of UA and AMI coronary thrombosis are significantly different. The AMI coronary occlusion is mainly caused by red blood cells and fibers. Protein composed of red thrombus; Most of the non-occlusive thrombus in the UA coronary artery is superficial, composed of platelets and white blood clots with less fibrin. The latter can cause transient complete occlusion of the coronary arteries, and then partially dissolve or fall off and recanalize. Coronary blood flow is periodically reduced.
ST segment elevation in the onset of angina pectoris, the main cause of which is local occlusive stenosis of the coronary arteries. The sacral site often occurs in CAG-displayed non-occlusive atherosclerotic lesions with irregular vascular margins.
Injury or activation of coronary endothelial cells plays an important role in UA. The former can lead to the weakening or loss of a variety of endogenous vascular physiological protective factors, which can lead to increased production of vasoconstrictors such as ATII and ET-1.
Prevention
Unstable angina prevention in the elderly
1. Appropriate physical exercise to improve the function of the myocardium and promote the formation of coronary collateral circulation.
2. Try to avoid factors that induce angina attacks, such as smoking, drinking, and emotional agitation.
3. Work and rest.
4. Reasonable nutrition, less use of high-fat foods.
5. Prevention and active treatment of diseases that cause angina, such as hypertension, obesity, diabetes, etc.
Complication
Complications of unstable angina in the elderly Complications, acute myocardial infarction, sudden death
Older unstable angina can evolve into acute myocardial infarction, and a small number can sudden sudden cardiac death.
Symptom
Symptoms of unstable angina in the elderly Common symptoms Sudden angina pectoris postprandial syndrome myocardial oxygen consumption increased abdominal discomfort breathing difficulties gastrointestinal symptoms dull pain vagus nerve excited lungs voice
Clinical manifestation
(1) Symptoms and clinical features: The clinical symptoms of UA in the elderly are:
1 Typical angina is a heavy squeezing sensation behind the sternum, radiating from the forearm, especially to the inside of the left forearm, the lower jaw and the teeth.
2 Although some patients have denied chest pain, they may have other symptoms such as tightness, clogging, crushing, burning and pressure.
3 with dull pain, tearing pain, knife-like pain, tingling, etc., which are characterized by ischemic atypical chest pain.
4 dyspnea in the middle chest may indicate angina pectoris.
5 Typical symptoms include left and right forearms with finger pain, pain between shoulders or shoulder blades, and even gastrointestinal symptoms such as abdominal discomfort.
6 chest pain time is more than 5 ~ 15min, a few can last 30min to several hours.
7 nitroglycerin to relieve chest pain may not be effective, suggesting that there are fewer components of vasospasm in the mechanism of UA attack.
8 UA can be excluded only for chest pain that lasts only a few seconds.
9 Other conditions that need to be differentiated from UA include esophageal lesions, digestive ulcers, skeletal muscle diseases, anxiety, hyperventilation, pericarditis, aortic dissection, intercostal neuralgia, psychosis, mitral sag and biliary tract disease, etc. .
(2) Clinical features of various types of unstable angina:
1 First-time exertion of angina pectoris: refers to the occurrence of exertional angina pectoris within 1 month, can be used in mild exertion, or at rest, or at night and early morning, the patient is younger, male is more, this type of coronary artery disease is more Light, more common with single-vessel disease, involving the most anterior descending (43%), 3 lesions and left main lesions (23%, 5%, respectively), but progressed faster, lacking enough time to form collateral circulation, Therefore, once UA pathological changes occur, the possibility of AMI or sudden death within 1 year is greater. The clinical symptoms are similar to those of general stable labor angina. The signs of increased myocardial oxygen consumption, such as increased heart rate and elevated blood pressure, are caused by the symptoms. Attack, clinical often misdiagnosed as stable labor angina, the main point of identification is to ask in detail the time of onset of angina pectoris is critical, this type of angina can not be timely and correct treatment, eventually AMI and sudden death.
2 worsening angina pectoris: a history of stable labor angina pectoris, decreased exercise tolerance in the past month, often in mild exertion, or at rest, manifested under the same conditions and the same level of labor, induced The number of chest pain episodes, severity and duration suddenly increased, and the amount of nitroglycerin increased, the efficacy decreased, and occasionally at rest, this type of angina should be distinguished from myocardial infarction.
3 angina pectoris: patients with severe angina pectoris on the basis of severe angina pectoris in the supine position, angina pectoris is severe angina pectoris, patients are prone to myocardial infarction.
It is currently believed that its pathogenesis is related to the following factors: the first coronary artery multi-vessel disease with severe stenosis, leading to a significant decrease in coronary circulatory reserve function, is the main pathological basis of supine angina pectoris, and second, due to varying degrees of left ventricular diastolic dysfunction In addition, after the supine position, the amount of blood returned to the heart and the heart is increased. Therefore, the myocardial oxygen consumption is significantly increased after the supine position, resulting in myocardial ischemia.
Clinical features of supine angina:
A. There is a long history of SA. The patient has more seizures during supine nighttime. It can also occur during the daytime after a meal or during a lunch break. In severe cases, it cannot be supine during the day and night. The patient must sit up or stand immediately during the attack. Even getting out of bed, in order to reduce chest pain, chest pain is more intense than SA, lasting for a long time.
B. Electrocardiogram (ECG): The ST segment is significantly depressed when it occurs.
C. Hemodynamic monitoring: Continuous monitoring of hemodynamic parameters before and after the onset of angina pectoris through the Seangana floating balloon catheter can be divided into the following three types:
a. normal heart function: angina pectoris has little relationship with left heart function. The heart rate, blood pressure product and stroke volume increase after supine to angina pectoris, suggesting that angina pectoris is mainly due to the increase of oxygen consumption and exceeds the fixation. Due to the narrow coronary reserve capacity.
b. Left ventricular diastolic dysfunction: There are different degrees of pulmonary diastolic blood pressure (PADP) increase before angina pectoris, and left ventricular ejection fraction (LVEF) is normal, suggesting that angina pectoris has an increase in myocardial oxygen consumption and has left ventricle. Diastolic dysfunction, which further increases myocardial oxygen consumption.
c. Left ventricular dysfunction: Pulmonary systolic pressure (PASP) and pulmonary diastolic blood pressure (PADP) have increased significantly before angina pectoris. After the patient is supine, the heart rate and sudden increase in blood pressure increase the myocardial oxygen consumption and lead to angina, but the heart No increase in stroke volume; due to the decrease of myocardial contractility, it can not compensate for the increase of blood volume after supine supine, leading to the gradual enlargement of the heart chamber, resulting in left ventricular dysfunction, cardiac B-ultrasound and radionuclide examination showing left ventricular function and LVEF reduce.
D. Coronary angiography (CAG): often showed multiple severe occlusive lesions, and most of them were severe coronary stenosis. The left main coronary artery lesions or 3 lesions accounted for the majority, and left ventricular angiography showed a significant decrease in LVEF.
4 post-infarction (early) angina pectoris: refers to the recurrence of angina pectoris in the acute phase (1 day to 4 weeks after onset) after the onset of AMI onset of chest pain disappears, most of the episodes are at rest, but also when slightly stressed, Can be accompanied by or without new infarct ECG changes and elevated serum enzymes, 80% of post-infarction angina occurs within 10 days after the onset of AMI, CAG is mostly multi-vessel disease, clinically prone to myocardial infarction area expansion, myocardial infarction Post-angina has the following pathological features:
A. Severe residual stenosis of infarct-related vessels: reversal of infarct-related blood vessels by thrombolytic therapy or spontaneous thrombolysis, but severe residual stenosis in the coronary arteries, resulting in angina pectoris due to insufficient blood supply to the reperfusion site, this type More common in non-Q-wave myocardial infarction, ECG showed ischemic (ST-segment level depression, T-wave inversion) lead and the same as the original myocardial infarction pattern lead, suggesting ischemia around the infarction.
B. Severe residual stenosis of non-infarct-related vessels: In addition to infarct-related angiogenic occlusive lesions, there are still 1 or 2 coronary artery main branches with severe stenosis, which makes the myocardial ischemia away from the infarction site, due to non-infarction Related coronary artery spasm, platelet aggregation or increased myocardial oxygen consumption induced angina pectoris, may also be caused by a sudden interruption of the collateral circulation established by the original infarct-related blood vessels, this type is more common in Q-wave myocardial infarction, ECG shows myocardial ischemic lead Unlike the infarct lead, it suggests ischemia away from the infarct.
5 acute coronary insufficiency (intermediate syndrome): also known as rest angina pectoris, intermediate syndrome, premature myocardial infarction state, near infarction, etc., there are many labor angina, recent aggravation, chest pain symptoms can be similar to acute myocardial infarction, that is, at rest In the state, there is no obvious cause of angina pectoris, such angina is more serious, lasting longer, can be more than half an hour, often accompanied by sweating, blood pressure can be reduced, nitroglycerin efficacy is poor, should be differentiated from acute myocardial infarction.
6 postprandial syndrome: angina pectoris often occurs after a meal break, most of which occurs 20 to 30 minutes after a meal, the mechanism of action is not clear, the author believes that may be the filling of the stomach after a meal, reflexively causing coronary spasm Leading to the onset of angina pectoris, it is suggested that after the meal, the heart rate is accelerated, the blood pressure is increased, and the blood output of the heart is increased. Therefore, the myocardial oxygen consumption after the meal increases, which is the predisposing factor of angina pectoris, but careful observation, the angina pectoris is more than 25 minutes after the meal. At this time, the heart rate and blood pressure have dropped to the pre-prandial level, so it is difficult to explain the increase in myocardial oxygen consumption. Figueras et al. performed continuous hemodynamics and electrocardiogram observation on postprandial angina pectoris, and found that pulmonary arterioles were embedded before angina pectoris. Pressure rise and myocardial ischemia changes, and then angina pectoris, there is no increase in heart rate-blood pressure double product, so it is considered that the increase in myocardial oxygen consumption is not the main reason, in addition to eating high-fat foods, post-prandial angina, the onset time is 3 to 5 minutes after a meal, when triacylglycerol rises, blood viscosity increases, coronary blood flow decreases (hyperlipidemia can reduce coronary blood flow by 20%) and cause angina Painful attack.
7 variant angina.
8X syndrome.
9 mixed angina: the pathological basis of mixed angina has two: First, single or multiple coronary arteries on the basis of critical fixed stenosis, due to increased myocardial oxygen consumption induced angina, second, coronary artery spasm caused by myocardial blood supply Sudden reduction of angina pectoris, this type of angina can be caused by the above factors alone or both.
A. Clinical type:
a. Labor-type angina with spontaneous angina pectoris: including worsening angina pectoris, b. labor angina with variant angina pectoris.
B. Clinical features: a. Labor-type angina pectoris during the day, spontaneous angina pectoris at night, b. angina pectoris induced by morning activities (such as dressing, washing, urination and walking), mostly mixed angina pectoris, c. Anyone who induces labor-type angina due to emotions, cold and other factors may increase the myocardial oxygen consumption due to excitatory sympathetic nerves, and reduce the oxygen supply caused by coronary artery contraction. d. Labor-type angina pectoris induces angina after a meal. It is due to an increase in blood flow in the gastrointestinal tract, an increase in vagal excitability, and a decrease in coronary blood flow reflexivity.
(3) Signs: Palpation of apex during angina pectoris may have double pulsation and abnormal pulsation in the anterior region, suggesting left ventricular dysfunction or abnormal left ventricular wall motion, auscultation can hear the fourth heart sound, third heart sound, or Acute papillary dysfunction, such as transient apical systolic murmur, "ka La" sound, severe breathing can have difficulty breathing, lung voice, blood pressure and heart rate generally increase, blood pressure can be reduced in severe attacks.
2. Unstable angina classification
(1) First-time exertional angina.
(2) Deteriorating angina pectoris.
(3) Spontaneous angina:
1 collateral angina;
2 early post-infarction angina;
3 variant angina;
4 acute coronary insufficiency (intermediate syndrome).
(4) Postprandial angina.
(5) Syndrome X.
(6) Coronary artery bypass grafting, coronary stenting, angina after postoperative angioplasty.
Examine
Examination of unstable angina in the elderly
1. Serum cholesterol and triglyceride are elevated or normal.
2. Systemic response indicators of tissue necrosis such as white blood cells and erythrocyte sedimentation rate are normal.
3. Myocardial enzymes CPK (creatine kinase), CK-MB, troponin, myosin are generally normal, but also slightly elevated, but did not reach the level required for the diagnosis of acute myocardial infarction.
4. Video room inspection
(1) X-ray chest radiograph: showing normal or slightly enlarged heart, or aortic ball protrusion, with enhanced lung texture during heart failure.
(2) two-dimensional echocardiography: transient ventricular wall motion abnormality or reverse pulsation can be observed in the onset of angina pectoris, such as long-term failure to recover the stunned myocardium caused by severe ischemia, so-called myocardial stun When myocardial ischemia is short-lived and myocardial cells have not undergone necrosis, coronary blood flow can be restored, which can save ischemic myocardium, but may cause reperfusion injury and temporary, recoverable left ventricular dysfunction. The mechanism of its formation includes oxygen free. Basal production, temporary calcium overload leads to calcium abnormalities; excitatory contraction uncoupling or simultaneous myocardial fiber is less sensitive to calcium, persistent or worsening left ventricular wall segmental motion abnormalities suggest poor prognosis.
(3) Electrocardiogram (ECG) examination: When the angina is not attacked, the resting ECG is mostly normal. For example, if there is hypertension, the history of old myocardial infarction has left ventricular strain, hypertrophy or abnormal Q wave.
The most common electrocardiogram changes in the onset of angina pectoris are ST-segment or down-slope type, suggesting subendocardial ischemia, and horizontal ST-segment depression suggesting that the lesion is left main lesion, and the ST-segment depression and prognosis on conventional electrocardiogram Inversely, sometimes only the upright T wave becomes inverted, or the resting ECG if there is a T wave inversion, can become erect in the onset of angina pectoris (T wave pseudo-improvement), and then return to the original state after the episode, such as ST segment horizontal down At the same time, the presence of coronary T waves is a manifestation of severe myocardial ischemia. ST-T changes usually return to normal within a few minutes or hours after the termination of the seizure. If the recovery is not more than 6 to 12 hours, non-Q-wave myocardial infarction should be considered. The possibility, a small number of patients with severe angina, manifested as ST-segment elevation, suggesting myocardial full-thickness ischemia, may cause complete occlusion of the lumen due to unstable thrombus, and the difference between myocardial infarction and emergency is that the ST segment is recovered in the past. In the original state, a few followed by a short time T wave inversion, such as T wave inversion more than 12h should be differentiated from non-Q wave myocardial infarction, in addition to ST-T changes in the occurrence of angina pectoris in individual patients, abnormal Q waves can also occur, such Q wave is Tolerance, after the termination of the attack, disappears in a short period of time, so it can be differentiated from the myocardial infarction. In addition, conduction block can occur when angina pectoris occurs, branch conduction block, left axis of ECG axis, QRS complex low voltage , R wave voltage decreasing type, QRS group frustration, atrioventricular block, and a variety of tachyarrhythmia, it should be noted that a few angina attacks can have no significant changes in the electrocardiogram, resulting in diagnostic difficulties, the diagnosis should be based on typical Clinical symptoms, repeated recording of the electrocardiogram at the time of onset, will eventually lead to myocardial ischemia changes, it should be pointed out that the acute phase of unstable angina is contraindicated in the exercise test, low-risk patients can be low-exercise exercise test after the condition is stable, The aim is to conduct risk stratification, judge prognosis and verify angiographic results. The 5-year risk of patients with negative exercise test is very low. For patients with higher risk, coronary angiography should be performed to determine whether to intervene.
(4) Holter monitoring (holter): 24h holter monitoring found that patients with unstable angina had the most common manifestations of myocardial ischemia on the electrocardiogram (ST%), followed by ST-segment elevation (31%), other changes. Including T wave increased sharpening, T wave pseudo erect, QRS frustration, low voltage, transient ischemia average time 14 ± 24min, minimum 30s, up to 12h, 18% with ventricular arrhythmia, individual with short Room velocity, II ° ~ III ° atrioventricular block, angina with ECG ischemic changes accounted for only 20%, the rest were asymptomatic myocardial ischemia, and a few without ECG changes.
It is also worth noting that before the ischemic changes in the electrocardiogram, only 10% of patients have an increased heart rate, and 90% of patients have no heart rate changes before the onset, suggesting that the pathogenesis of myocardial ischemia in patients with unstable angina is mainly perfusion, and the cause of perfusion reduction May be caused by increased coronary tension () or transient platelet thrombosis.
5. Nuclide check
(1) 201Ti myocardial perfusion imaging showed perfusion defects at the onset, angina disappeared, and perfusion defects may still exist for 12 to 27 hours.
(2) 99mTc stibous pyrophosphate scintillation diagram in about 30% of patients with unstable angina can show subendocardial necrosis without myocardial enzymology and electrocardiogram myocardial infarction, suggesting that some unstable angina has a small infarction and clinical Can't be diagnosed.
6. Coronary angiography (CAB) The purpose of coronary angiography in patients with unstable angina is to provide detailed coronary structural data in order to assess prognosis and select appropriate long-term treatment.
(1) indications: suitable for early intervention measures, drug treatment can not make the disease stable; in the past angioplasty, bypass surgery or AMI, high-risk clinical results or non-invasive results; significant congestion Sexual heart failure, or left ventricular dysfunction.
(2) Contraindications: iodine allergy, moderate renal failure, severe bleeding disorders, severe chronic obstructive airway disease, other life-threatening diseases and rejection of coronary interventional measures are contraindications for coronary angiography.
(3) Characteristics of coronary angiography: UA coronary angiography results vary according to the study population, medical history and clinical manifestations. UA often occurs on the basis of stable angina with long history, and new occurrences occur. Resting angina may be caused by a single coronary artery.
It is determined that the unstable type of UA is not the extent and degree of stenosis of coronary lesions, but the morphology of coronary lesions, which are more complicated lesions, such as eccentric stenosis, irregular edges, or eccentric plaque rupture, ulcers, attached Stabilize the blood clot.
(4) The limitations of coronary angiography in the assessment of lesions: the morphological features of the lesions may be related to the clinical manifestations of UA, and have pre-value for the occurrence of adverse coronary events, but the contrast is only the image of the vascular lumen, reflecting The diameter and surface features of the vascular lumen do not reflect the composition or pathological features of the plaque. Radiography often underestimates the extent of the lesion and is mainly affected by two factors:
1 diffuse of coronary atherosclerosis;
2 vascular remodeling, and intravascular ultrasound can reflect the size and shape of plaque, angioscopy can accurately detect plaque and coronary thrombosis.
7. Intravascular ultrasound and coronary endoscopy
Intravascular ultrasound (IVUS) allows quantitative assessment of the size and morphology of the arterial lumen and vessel wall in vivo, showing endothelium, medial and extra-membranous thrombosis (ICT), gray thrombus often observed in UA patients, and acute myocardial Infarction is red thrombus, pathologically confirmed that red thrombus is rich in cellulose, red blood cells; while gray blood thrombus is rich in platelets, the fiber network is tight, older than red blood clots, platelets are resistant to thrombolytic drugs, so UC patients have poor thrombolytic therapy. Recent studies have found that coronary angiography is difficult to distinguish between stable and unstable angina, endoscopic findings of 17% stable angina and 68% of UA with plaque rupture and thrombosis, while IVUS cannot distinguish between stability and instability Plaque.
Diagnosis
Diagnosis and diagnosis of unstable angina in the elderly
Diagnostic criteria
The diagnosis of UA mainly depends on the history and clinical symptoms. Because there is no characteristic change of ECG, there is no change in serum myocardial enzyme. The diagnosis points of UA are:
1. crescendo angina (crescendo angina) The symptoms of the original labor angina have changed, and the seizures are markedly weighted in frequency, time limit and severity.
2. Resting angina without induced cause, or angina pectoris after mild labor, the duration can often reach 15 ~ 30min.
3. The amount of new angina pectoris in the past 2 months, also known as post-infarction UA.
4. Angina that occurs during the recovery of AMI, also known as post-infarction UA.
Differential diagnosis
When diagnosing UA, chest pain should be differentiated from the following conditions: esophageal disease, peptic ulcer, musculoskeletal disorders, anxiety, hyperventilation, pericarditis, aortic dissection, costal cartilage, mental pain, mitral valve prolapse , neck or biliary tract disease.
