(A) Primary exertional angina pectoris
1, definition: primary exertional angina refers to patients with angina pectoris within 1 month, who have never had angina pectoris before. Because most patients in this type of angina have angina at rest or during sleep, so the initial exertional type is also known as initial angina. However, it should not include variant angina or spontaneous angina that occurs only at rest.
2, pathophysiology: most patients with primary exertional angina have severe obstructive lesions in the coronary arteries. The main mechanisms of pathogenesis are.
①Plaque rupture induces local platelet aggregation or incomplete occlusive thrombosis
②Plaque rupture induces vasoconstriction or spasm
③The rapid development of atheromatous plaque increases the size of the lumen and worsens the stenosis.
3.Treatment: β-blocker is the main treatment. Supplemented by calcium antagonists, nitrates or antithrombotic therapy.
4, prognosis: this type of angina pectoris patients, except for a few in the unstable phase of acute myocardial infarction, most of the subsequent transformation into stable exertional angina, some patients angina can disappear.
(B) deterioration of exertional angina pectoris
1, definition: stable exertional angina patients in a month the frequency of angina attacks suddenly increased, the duration is prolonged and the degree of aggravation is to become worsening exertional angina.
2. Pathophysiology: Patients with worsening exertional angina often have multiple vascular lesions, and a higher proportion of combined left coronary artery trunk lesions. The stenosis of ischemia-related vessels is mostly around 90%. Sudden exacerbation of anginal symptoms can be attributed to the following factors.
(i) plaque rupture, bleeding induced local platelet aggregation or incomplete occlusive thrombosis, or both vasoconstriction factors involved.
(2) The plaque is sharply enlarged due to lipid infiltration, which makes the narrowing of the official lumen significantly aggravated.
3.Treatment: β-blocker is the main treatment. Supplemented with calcium antagonists, nitrates or antithrombotic therapy.
4.Prognosis: Most patients with this type have a poor prognosis if they do not take active treatment (coronary revascularization).
(C) prone angina pectoris
1, definition: prone angina is the angina that occurs when lying down, the attack needs to sit up immediately or standing angina can be gradually relieved. Although recumbent angina occurs when lying quietly, but the attack has a clear relationship with the increase in myocardial oxygen consumption. It should be treated as an independent type of exertional angina.
2. Clinical and attack characteristics
①All patients have a history of exertional angina before the appearance of recumbent angina.
(2) Coronary angiography showed a high incidence of 3 coronary artery lesions and left coronary artery trunk lesions.
(③) The time of attack, the first attack at night in patients with prone angina is mostly within 1-3 hours after lying down, and several attacks can occur overnight. In severe cases, the attack can occur after lying down for tens of minutes. Daytime lying down can also trigger, and lying down after a meal is most likely to trigger.
④ Pre- and post-attack conditions: A fast mean heart rate is another characteristic of patients with prone angina. The product of heart rate and blood pressure gradually increases from the start of lying down to the onset of chest pain.
⑤ The duration of recumbent angina that occurs during sleep is long, and the patient needs to sit up or stand up immediately before the angina can be gradually relieved.
3.Etiology and pathogenesis
The onset of recumbent angina is clearly related to the increase in myocardial oxygen consumption.
(1) Severe obstructive lesions of coronary arteries and left ventricular diastolic insufficiency are the main pathological basis of prone angina.
(2) Because of the presence of left ventricular diastolic insufficiency, it is particularly sensitive to the increase in volume load, which causes a significant increase in myocardial oxygen consumption when lying down. The increase in ventricular wall tension, myocardial contractility and myocardial oxygen consumption caused by the increase in return blood flow after lying down is the main cause of recumbent angina pectoris.
4.Treatment
Beta-blockers can effectively control the onset of prone angina and can be the drug of choice. If patients with prone angina have clinical manifestations of left heart failure, such as a significantly enlarged heart, especially when the ejection fraction of the left ventricle is less than 30%, beta-blockers can be used on top of cardiotonic and diuretic therapy.
Combination therapy with atenolol, diltiazem, cardioplegia and intermittent diuresis can achieve significant results. In some patients with combined hypertension, nifedipine is used instead of diltiazem, which also has better efficacy.
(D) Spontaneous angina pectoris
1, definition: spontaneous angina is calm rest, myocardial oxygen consumption without a significant increase in the case of angina pectoris.
2, clinical and attack characteristics.
The attack of spontaneous angina is not obviously related to the increase of myocardial oxygen consumption, mainly due to temporary spasm or contraction of coronary arteries and other dynamic obstructive factors causing a transient reduction of myocardial blood supply.
The main difference between spontaneous angina and variant angina is the degree of ischemia, the latter due to complete occlusion of the lumen by coronary artery spasm causing transmural ischemia, the former mainly due to subendocardial ischemia by incomplete obstructive spasm.
Spontaneous angina occurs in the absence of any trigger. However, some episodes in the early morning during daily activities, such as dressing, washing, and urination and defecation, are due to mixed factors.
Depending on the coexistence of exertional angina, this type of angina can also be divided into simple and mixed types, the latter being more common clinically (see section on mixed angina).
The simple spontaneous type of angina is relatively rare, mainly manifesting itself in the latter part of the night and early morning, and is well relieved by nitroglycerin.
This type of angina pectoris is not significantly different from variant angina pectoris in terms of pathogenesis, clinical attack characteristics and treatment, and can belong to the wide range of variant angina pectoris (see chapter on variant angina pectoris).
(E) mixed angina pectoris
1, definition: mixed angina is a kind of angina between the two extremes of fixed threshold and variable threshold angina. maseri believes that in patients with exertional angina who do have a certain exertional threshold, such as at rest or when angina occurs even at an exertional level that should be well tolerated, can be called mixed angina.
2, combination type: mixed angina can be attributed to the combined effect of different degrees of fixed and dynamic stenosis. Clinically, angina can be caused by an increase in myocardial oxygen consumption alone or by a sudden decrease in myocardial blood supply alone, or the attack can involve both factors at the same time. There are three combinations of the following.
(1) exertional type combined with variant angina
(1) exertional angina combined with variant angina, which occurs suddenly after months or years of exertional angina. The spasm mostly occurs at lesions with 60% to 80% fixed stenosis.
(2) Exertional type combined with spontaneous angina
The highest incidence of spontaneous angina occurs when the ischemia-related coronary stenosis reaches 90%.
The mechanisms of this spontaneous type of angina are.
1) Associated with changes in vascular tone.
2)Rupture of atheromatous plaque induces coronary artery spasm and/or incomplete occlusive thrombosis.
3)Platelet aggregated clumps automatically decongregate after mechanical blockage. In the early morning, the patient wakes up and wakes up with sympathetic excitation and increased catecholamine concentration, which increases platelet aggregation, which may play a role in the development of spontaneous angina pectoris.
4) Hypercoagulable state due to various factors stagnates the local blood flow in the lesion.
(3) Exertional angina with coronary artery constriction
This type of angina includes.
1) cold air walking, early morning after light activity angina; angina is easy to occur in the cold season is another of its characteristics, the cold environment not only can make blood pressure rise, but also often cause the contraction of the coronary arteries, so that the myocardial blood supply is reduced, so in cold days walking in the wind or cycling induced angina is also mostly mixed factors. Heavy smoking can reduce the exercise tolerance of angina pectoris patients, so a lot of smoking after the activity is also prone to induce angina pectoris.
2) Postprandial angina, the redistribution of blood after meals, especially 20-30 min after meals coronary arteries are in a state of reflex contraction; if angina occurs during meals belongs to exertional angina, if it occurs 15-30 min after meals, when the patient is at rest is called postprandial angina. figreras believes that postprandial angina belongs to spontaneous type In our study, we showed that this angina is caused by the combination of subthreshold myocardial ischemia due to a meal and the subsequent reduction in blood supply due to reflex contraction of the coronary arteries, so it is a mixed type of angina. A full meal as an additional factor of angina pectoris, mainly in the postprandial activity tolerance decreased, making angina pectoris easy to occur, which may be caused by a full meal has caused potential myocardial ischemia. A similar situation can also be seen after defecation.
3) Some angina occurs when emotional excitement.
3.Treatment
The exertional type combined with variant angina is mainly manifested as variant angina, and most patients have good coronary artery reserve, so the treatment is calcium antagonist plus nitrate preparation to control the onset of coronary artery spasm, and accompanied by short-term antithrombotic therapy.
In patients with exertional angina combined with spontaneous angina, because their coronary artery stenosis is more severe and their coronary artery circulation reserve is very low, the treatment should take into account both vasodilation and reduction of myocardial oxygen consumption, and β-blockers and calcium antagonists and nitrate preparations can be combined to improve the balance of myocardial supply and demand more effectively.
In patients with predominantly exertional angina with vasoconstriction, β-blockers are used in combination with nitrates or calcium antagonists. In spontaneous attacks with markedly elevated blood pressure, oral nifedipine powder is significantly more effective than nitroglycerin.
In view of the sudden onset of spontaneous angina on the basis of severe coronary stenosis, which may be associated with plaque rupture and platelet aggregation as well as incomplete occlusive thrombosis, short-term antiplatelet aggregation and anticoagulation therapy are also necessary.
(F) Post-infarction angina pectoris
1. Definition: The definition of post-infarction angina is not very clear, but generally refers to angina that occurs 48 hours after the onset of acute myocardial infarction to within 1 month. Some scholars also limit the duration of the disease to less than two weeks.
2. Treatment.
1) Treat according to the nature of the angina attack (exertional or spontaneous).
2) Intensify antithrombotic therapy.
3) If the symptoms cannot be satisfactorily controlled by drugs, coronary angiography should be performed as early as possible in patients with post-infarction angina to decide the hemodynamic reconstruction plan (PCI or CABG).