Unstable angina (acute coronary insufficiency; pre-infarction angina; worsening angina; intermediate syndrome), characterized by a progressive increase in anginal symptoms, new episodes of resting or nocturnal angina or the appearance of prolonged anginal duration.
Unstable angina (unstableangina) is a clinical manifestation between exertional stable angina and acute myocardial infarction and sudden death. It mainly includes primary angina, worsening exertional angina, resting angina with electrocardiographic ischemic changes and early angina after myocardial infarction. Because of its unique pathophysiological mechanism and clinical prognosis, patients may develop acute myocardial infarction if they are not treated appropriately and timely.
Unstable angina is secondary to acute exacerbation of coronary obstruction, the latter being caused by rupture of the fibrous plaque on the surface of the atheroma and consequent platelet adhesion. More than 1/3 of patients with unstable angina have angiographic evidence of thrombus in the ischemic zone leading to partial occlusion, but the reported incidence may be low because it may be difficult to identify the thrombus at the time of angiography.
Compared with stable angina, unstable angina is more painful and longer lasting, can be triggered by lower levels of activity, can occur spontaneously at rest (prone angina), is progressive in nature (worsening), and can be any combination of these changes. Myocardial infarction may occur within 3 months after the attack in about 30% of patients with unstable angina. Sudden death is rare, but significant changes in the electrocardiogram during chest pain are an important sign of myocardial infarction and sudden death.
I. Pathogenesis.
1, the progression of atherosclerotic lesions: most patients with unstable angina have severe obstructive ischemic heart disease, the development of their coronary atherosclerosis, which can cause progressive coronary artery stenosis.
2, platelet aggregation: coronary artery stenosis and endothelial injury, platelet aggregation occurs, producing the vasoconstrictor substance thromboxane A2, while the concentration of anti-aggregation substances such as prostacyclin, tissue fibrinolytic activator and endothelium-derived relaxing factor produced by normal endothelial cells is reduced, causing coronary artery induced constriction, lumen narrowing aggravation or even occlusion, as well as power coronary artery resistance increase.
3, thrombosis: platelet aggregation, fibrinogen and fibrin fragments of the main hair-forming D-dimer increases, forming coronary artery luminal thrombus, resulting in progressive coronary artery stenosis.
4, coronary artery spasm: clinical, coronary angiography and autopsy studies have confirmed that coronary artery spasm is an important mechanism causing unstable angina.
Second, clinical manifestations.
1, clinical symptoms: the nature of chest pain or chest discomfort is similar to typical stable angina, but the pain is more intense, often lasting up to 30 minutes, and occasionally attacks during sleep. Bed rest and nitrate containing drugs only appear to be transient or incomplete chest pain relief.
2. Clinical signs: transient third and fourth heart sounds can be heard in the apical region. In left heart failure, an elevated apical pulsation can be seen, and a systolic mitral regurgitant murmur can be heard during or immediately after an ischemic attack.
III. Examination.
1, electrocardiographic examination.
(1) Conventional ECG: ST-segment depression or elevation and/or T-wave inversion, often transient, disappearing completely or partially with the relief of angina. If ST-T changes persist for more than 6 hours, it suggests non-Q-wave myocardial infarction; ST-T may also be unchanged.
(2) Ambulatory ECG: Most patients have ECG changes of asymptomatic myocardial ischemia after more than 24 hours of continuous ECG monitoring, and about 85-95% of the ambulatory ECG changes are not accompanied by symptoms such as angina pectoris. The prognosis of unstable angina is more sensitive with ambulatory ECG than with conventional ECG. It can be used as a reference indicator for the evaluation of conventional anti-anginal drug therapy and for determining whether coronary angiography and revascularization are needed in patients with unstable angina.
(3) Exercise ECG: It is suitable for patients whose symptoms have stabilized or disappeared, and is often used to determine the prognosis of unstable angina pectoris. If the resting ECG is normal and the exercise test is negative, the 5-year survival rate is more than 95%; if the resting ECG is normal and the exercise test is negative but accompanied by chest pain, the incidence of fatal myocardial ischemic events is relatively low; if the exercise test shows ischemic ST-T changes and the heart rate-blood pressure product is reduced and accompanied by chest pain, the incidence of fatal myocardial ischemic events and death is relatively low; if the resting ECG is normal and the exercise test is negative, the incidence of fatal myocardial ischemic events is relatively low. The incidence of fatal myocardial ischemic attack and death is high.
2. Echocardiography: shows transient ventricular wall motion abnormalities. Persistent wall motion abnormalities suggest a poor prognosis.
3.Radionuclide myocardial imaging: The site of myocardial ischemia can be determined. 201TI myocardial imaging shows that the myocardial ischemic area is sparse or absent at rest, indicating that the myocardium is in a state of hypoperfusion.
4. Cardiac catheterization: Coronary angiography shows that most patients have two or more coronary artery lesions, about half of them have three coronary artery lesions, but patients with recent onset of angina and no history of myocardial infarction or chronic stable angina are predominantly those with single coronary artery lesions. More severe coronary artery lesions with plaque rupture and/or partial thrombolysis tend to present as eccentric stenosis. Coronary artery endoscopy mostly shows the nature of obstructive lesions as compound plaque and/or thrombosis.
5. Laboratory enzymatic examination: there may be increased blood cholesterol and no abnormal changes in myocardial enzymatic examination.
IV. Clinical diagnosis.
1, the nature of the original stable angina changes, that is, frequent attacks of angina, the degree of severity and prolonged duration.
2, angina attack at rest.
3, the recent occurrence of angina within the last month, the slight physical activity can also be induced angina.
If one or more of the three is present and there are ST-T changes in the ECG, the diagnosis is established. If there is a history of stable angina, myocardial infarction, abnormal coronary angiogram and positive exercise test, the diagnosis can be established even if there are no ST-T changes on the ECG, but the symptoms of typical unstable angina are present. If the angina occurs within two weeks after myocardial infarction, it is called post-infarction unstable angina.
V. Differential diagnosis.
The differential diagnosis is the same as that of stable angina pectoris. In particular, it is necessary to distinguish acute myocardial infarction, which has a more severe nature of pain and can be differentiated by the presence of infarct patterns and specific myocardial enzymatic changes in the electrocardiogram.
VI. Clinical treatment.
Unstable angina is a medical emergency and should be treated in the CCU. Both heparin and aspirin can reduce the incidence of subsequent myocardial infarction. To reduce intracoronary coagulation, oral aspirin 325 mg and heparin should be administered immediately. If aspirin is not tolerated or contraindicated, ticlopidine 250 mg twice daily or clopidogrel 75 mg/d may be used instead.
Beta blockers and nitroglycerin should be given to slow down the heart rate and lower the blood pressure to reduce cardiac work and restore the balance between cardiac O2 demand and coronary blood flow. Treatment of related disorders (e.g., hypertension, anemia) should be aggressively pursued. Bed rest, intranasal oxygen and nitrates are useful, and calcium antagonists may be useful in cases of combined hypertension and suspected coronary artery spasm. Thrombolytic drugs are not useful and may be harmful. Randomized trials in patients with refractory unstable angina have shown that an antiplatelet glycoprotein IIb/IIIa receptor antagonist, human chimeric Fab fragment abciximab, improves symptoms and Tirofiban prevents ischemic events in patients with unstable angina and non-Q-wave myocardial infarction. The use of other IIb/IIIa receptor antagonists in acute ischemic syndromes is under evaluation.
Intensive therapy should control the patient’s symptoms within a few hours, and if it does not work within 24-48 hours, more aggressive therapy is required. Intra-aortic balloon counterpulsation reduces systolic afterload and elevates diastolic blood pressure, which is the driving force of coronary blood flow, and he usually relieves continuous angina. Cardiac catheterization is performed prior to revascularization procedures such as coronary artery bypass or angioplasty. Patients who respond poorly to medical therapy should undergo angiography to identify associated lesions, evaluate the extent of CAD and LV function, and plan for PTCA or CABG if available.
VII. Prognosis of the disease.
Unstable angina is often a prodromal manifestation of acute myocardial infarction, with an incidence of AMI of 12%-13% and a mortality rate of 3%-18% within one year. Persistent resting angina with intracoronary thrombosis in the elderly, left heart failure and multi-branch coronary artery disease are mostly indicative of a poor prognosis. The incidence of myocardial infarction, recurrent unstable angina, and mortality are higher in those with angina or blood-deficient ST-segment depression or reduced heart rate-blood pressure product on exercise testing. In patients with unstable angina treated with PTCA, the 5-year mortality rate decreased to 10%, and in those with low EF and three vascular lesions, the 5-year and 10-year mortality rates in the CABG treatment group decreased to 10%-20%.