Introduction
Coronary artery spasmIt refers to the transient contraction of coronary artery caused by various reasons, causing incomplete or complete occlusion of blood vessels, leading to myocardial ischemia, clinical syndrome of angina pectoris, arrhythmia, myocardial infarction and sudden death. It has important clinical significance for the diagnosis, treatment and prognosis of myocardial ischemic diseases, and has now attracted widespread attention. Coronary artery spasm, patients with coronary artery disease have a worse prognosis than those without basal lesions, and the worse the underlying lesions, the worse the prognosis, but both can cause sudden death. When coronary atherosclerosis, the number of platelets in the stenotic vessels increases, due to endothelial detachment, platelets adhere to aggregate, release TXA2 and serotonin, and the reduction of PGI2 synthesis in the atherosclerotic wall, there is a strong vasoconstriction. The increase in TXA2 and the decrease in PGI2 with vasodilating effect, the two lose balance and cause coronary spasm.
Cause
1. Neural mechanism: Central nervous system and autonomic nerve activity play an important role in the occurrence of coronary artery spasm. There are α and β adrenergic receptors on the coronary arteries. When the α receptor is activated, it causes coronary artery contraction, and when the β receptor is activated, it causes coronary artery relaxation. The sympathetic nerves activate both alpha and beta receptors. However, in general, the sympathetic nerves have a dominant effect on the vasoconstriction of the coronary arteries. Coronary artery spasm can be induced when the sympathetic nerve is overexcited during psychological stress (such as excessive excitement, nervousness, anxiety, panic, sorrow) or cold stimulation or strenuous exercise. When the vagus nerve is excited, the acetylcholine released by the preganglionic fibers can also release norepinephrine from the postganglionic fibers of the sympathetic nerve, acting on the α receptor, and inducing coronary artery spasm. When a beta blocker is used, the sympathetic nerve is blocked by the vasodilator effect of the beta receptor, and the vasoconstriction of the alpha receptor is relatively enhanced, which is also likely to cause coronary spasm. When an alpha adrenergic drug such as norepinephrine is used, the alpha receptor can be directly excited to induce coronary spasm. The vagus nerve can also cause coronary spasm by agonism of muscarinic receptors.
2. Body fluid mechanism
(1) Platelets and prostaglandins: Since the discovery of thromboxane and prostacyclin in the 1970s, people's understanding of the role of prostaglandins in the cardiovascular system has changed significantly. In platelets, arachidonic acid is mainly converted to thromboxane A2, an unstable vasoconstrictor and platelet aggregate; in the blood vessel wall, arachidonic acid is converted into prostacyclin - unstable Vasodilators and anti-aggregates. The balance between prostacyclin and thromboxane A2 plays a regulatory role in the blood coagulation state of the blood circulation. When coronary atherosclerosis or other lesions damage vascular endothelial cells, it is easy to cause blood stasis, platelet aggregation, and increased thromboxane A2 release. At the same time, due to the damage of vascular endothelial cells, the synthesis of prostacyclin in the intima is reduced. Increased thromboxane A2 and a decrease in prostacyclin can induce coronary spasm. Vasospasm further aggravates blood stasis and platelet aggregation, resulting in more thromboxane A2, forming a vicious circle. At the same time, the aggregated platelets also release adenosine diphosphate,SerotoninIncreases the contraction of blood vessels.
(2) Endothelin (ET): a potent vasoconstrictor synthesized by vascular endothelial cells. The basal lesions of the coronary arteries cause chronic ischemia of the heart muscle, which increases the number of ETs synthesized and released by vascular endothelial cells, and increases the density of ET receptors on the smooth muscles of the coronary arteries, thereby inducing vasospasm. A vicious circle is formed between myocardial ischemia, which is an increase in ET secretion, and coronary artery spasm. Recently, studies have shown that ET can enhance the contraction of norepinephrine and serotonin on coronary arteries in addition to strong vasoconstriction. In addition, coronary spasm and thrombosis were induced by disrupting the balance of local prostacyclin and thromboxane A2 in the coronary arteries. In addition, the effects of Ca, H+, and Mg can cause coronary spasm. Local stimulation of the coronary arteries during coronary angiography can also cause coronary spasm. Long-term smoking and drinking can increase the incidence of coronary atherosclerosis and increase the risk of coronary artery spasm. A large amount of smoking or alcohol abuse can cause central nervous system and sympathetic and parasympathetic dysfunction, thereby inducing coronary artery spasm. Elevated estrogen levels can also induce coronary spasm. It should also be noted that coronary spasm may be the result of a combination of multiple factors. The mechanism of coronary artery spasm can be divided into two aspects: neural mechanism and body fluid mechanism. From the perspective of neural mechanisms, central nervous and autonomic nerve activities play an important role in the occurrence of coronary artery spasm. Coronary artery spasm can be induced when the state of psychological stress (such as excessive excitement, nervousness, anxiety, panic, etc.), or cold stimulation, strenuous exercise, excessive sympathetic excitation, and local hypersensitivity of the coronary artery. Coronary spasm can also be induced when using beta blockers or epinephrine. From the humoral mechanism, between thromboxane (TXA2) and prostaglandin (PGI2), endothelin (EDCF) and endothelium-derived relaxing factor (EDRF), local balance is an important factor in regulating blood vessel diameter. When coronary atherosclerosis occurs, the number of platelets in the stenotic vessels increases, and due to endothelial detachment, platelets adhere to and aggregate, releasing TXA2 andSerotoninIn addition, the reduction of PGI2 synthesis in the atherosclerotic wall, the increase in TXA2 with strong vasoconstriction and the decrease in PGI2 with vasodilator effect, the two lose balance and cause coronary spasm. At the same time, the EDRF synthesis of the diseased vessel wall is reduced, and the production of EDCF with obvious vasoconstriction is increased, and coronary artery spasm is also easily induced. Studies have shown that the effects of Ca, H+, and Mg, as well as smoking and drinking, can cause central nervous system and autonomic dysfunction, thereby inducing coronary spasm. Of course, a narrow coronary artery must be a semilunar or eccentric lesion with a contractile capacity on the contralateral wall. In the case of severe concentric lesions, the smooth muscle of the wall is atrophied, and the plaque stiffness is irreversible, and no sputum occurs. Thus, coronary artery spasm is the result of a combination of factors.
symptom
Normal coronary arteries and atherosclerotic lesions can occur in the coronary arteries, causing acute myocardial ischemia, manifested as angina, arrhythmia, myocardial infarction and sudden death. Unstable angina is caused by insufficient blood supply to the heart muscle caused by coronary artery spasm. Atherosclerotic myocardial infarction is almost caused by stenosis on the basis of vascular stenosis, resulting in complete occlusion of blood vessels. Acute myocardial ischemia in women under 50 years of age and under psychological stress and cold stimulation, if there are no other obvious reasons, should first consider coronary artery spasm.
diagnosis
1. Clinical manifestations: normal coronary arteries and atherosclerotic lesions can occur in the coronary arteries, resulting in acute myocardial ischemia, manifested as angina, arrhythmia, myocardial infarction and sudden death. Unstable angina is caused by insufficient blood supply to the heart muscle caused by coronary artery spasm. Atherosclerotic myocardial infarction is almost caused by stenosis on the basis of vascular stenosis, resulting in complete occlusion of blood vessels. Acute myocardial ischemia in women under 50 years of age and under psychological stress and cold stimulation, if there are no other obvious reasons, should first consider coronary artery spasm.
2. Electrocardiogram performance: ST segment: Coronary artery spasm produces a transient change in the ST segment of the corresponding lead. ST segment elevation during wall ischemia, and the corresponding ST segment depression is corresponding. Such as localized subendocardial ischemia, ST segment depression. QRS wave: When the sputum is attacked, the R wave can be increased and widened. In severe cases, the R wave is reduced and the elevated ST segment is integrated. A few people can have a transient Q wave, and the above changes disappear. A typical infarct pattern can occur if persistent myocardial infarction is caused by sputum.
T wave: ST-segmented lead T wave high tip, the original inverted T wave can be low-level or upright. U wave inversions can sometimes occur.
Coronary artery spasm cannot be ruled out in patients with normal angina pectoris. The electrocardiogram cannot be accurately located and the extent of coronary artery spasm cannot be known.
3. Coronary angiography: The value of coronary angiography in the diagnosis of coronary artery stenosis. The diagnosis can be confirmed by the following conditions:
(1) A transient stenosis or complete occlusion of the normal coronary artery, or a transient further stenosis or complete occlusion in the coronary atherosclerotic stenosis.
(2) Nitrate or calcium antagonists and other crown-expanding drugs cause the above-mentioned stenosis or occlusion to disappear rapidly or disappear on its own.
4. Excitation test
a. Cold compression test: the coronary artery contraction is induced by reflex stimulation of the sympathetic nerve. The hands were soaked in cold water at 4 °C to reach the wrist joint, and taken out after 1 minute, and then the clinical symptoms and electrocardiogram changes at 1 minute, 2 minutes, 5 minutes, 10 minutes, and 20 minutes were observed. Any one of the ST-segment elevation and typical myocardial ischemia in the ECG is positive. This method is simple and easy, but it is less sensitive.
b. Ergometine test: In coronary angiography, intramuscular or intracoronary injection of ergometrine is used to stimulate coronary artery spasm. This method has high sensitivity and specificity. But sometimes severe arrhythmia, myocardial infarction, and sudden death can occur. It needs to be carried out under the conditions of adequate preparation for cardiopulmonary resuscitation.
5. Cardiac radionuclide examination: 铊 铊 myocardial perfusion angiography can be observed in the ischemic area of the corresponding site of coronary artery spasm with nucleus hypoperfusion defects, myocardial perfusion can be improved after sputum remission.
treatment
1. The sublingual mouth contains 0.6-1.2 mg of nitroglycerin and 10 mg of nifedipine (chewed). Repeated administration can be repeated without attention (attention to blood pressure).
Treatment
Treatment plan
2. Intravenous infusion of nitroglycerin 10-30μg / min, blood pressure decreased by no more than 30%, blood pressure is not more than 10%. And oral Xiaoxin 10-20mg, once every 4-6 hours.
3. Oral nifedipine 10-20mg once every 4 or 6 hours; or oral diltiazem (thiazolone) 30-60mg every 4 or 6 hours, but should be avoided in patients with heart failure or slow heart rhythm Abnormal, atrioventricular conduction disorders. In some cases, patients only have a good response to a certain calcium antagonist, sometimes need to use two or three antagonists at the same time, but pay attention to dose matching and blood pressure, only in a few cases use verapamil Oral; or intravenously 2.5-5.0 mg. Usually oral medication should first use nifedipine (heart pain) or nicardipine, which has a strong effect on blood vessels.
4. The above treatment is not ideal or can not fully control the author, you can try intravenous infusion of magnesium sulfate (10% MgSO4), oral vitamin E 300mg, twice daily.
5. Coronary angiography and other cardiac catheterization or provocation test, in addition to nifedipine in the sublingual mouth, can directly into the coronary artery injection of nitroglycerin 0.2-0.4mg. If the catheter is stimulated or the drug is not effective, the heart catheter should be removed.
6. Avoid the use of vasoconstrictor drugs and beta blockers.
7. In the event of severe hypotension, dopamine should be used simultaneously to maintain blood pressure. If cardiac arrest occurs, cardiopulmonary resuscitation should be started immediately.
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