Geriatric variant angina pectoris

Introduction to variant angina pectoris in the elderly Variant angina pectoris is a kind of spontaneous angina. In 1959, Prinzmetal et al. named ischemic angina caused by coronary artery spasm as "variant angina pectoris", indicating that the onset of angina is not related to activity, and pain occurs when it is quiet. When the ST segment is elevated, the ST segment is decreased after the episode, and no pathological Q wave appears. The pain is mainly caused by coronary spasm, and there are more myocardial infarctions and deaths within half a year. basic knowledge Probability ratio: 32% probability of illness in the elderly Susceptible people: the elderly Mode of infection: non-infectious Complications: acute myocardial infarction, arrhythmia, sudden death

The cause of variant angina in the elderly

(1) Causes of the disease

The vast majority (more than 90%) of angina pectoris is caused by coronary atherosclerotic lesions. When the stenosis caused by atherosclerotic lesions exceeds 50% to 75%, the oxygen consumption in the myocardium increases, but the coronary blood flow cannot. When increased, myocardial ischemia can lead to angina pectoris, other heart diseases such as aortic stenosis or reflux can also cause angina, especially in the elderly, due to degenerative changes of the aortic valve can make the valve thick, stiff or Calcification, a small number can develop into calcified aortic stenosis, severe coronary blood flow can cause angina pectoris, congenital bicuspid aortic valve to the elderly can also form severe calcific aortic stenosis, leading to angina Rheumatic aortic stenosis and reflux, can also cause angina in the elderly, in addition, hypertrophic cardiomyopathy, left ventricular outflow tract stenosis, aortic dissection, syphilitic aortitis and aortitis invading the coronary artery Can cause angina, some extracardiac factors such as severe anemia, hyperthyroidism, obstructive pulmonary disease, etc. can also affect the onset of angina.

(two) pathogenesis

According to the data, 10% to 15% of patients with angina pectoris have normal coronary arteries. In these cases, right coronary artery spasm is more common. Most coronary arteries are accompanied by different degrees of arteriosclerosis. % to 80%, which is 10% to 15% of critical stenosis. If vasospasm occurs on a blood vessel with arteriosclerosis, it is always confined to a narrow site.

Variant angina (VA), also known as vasospasm angina, is essentially coronary vasospasm, which can cause a sudden and significant decrease in coronary diameter, resulting in myocardial ischemia and coronary artery spasm The pathogenesis of angina pectoris has been confirmed by a large number of coronary angiography, but the exact pathogenesis is still unclear. It is believed that the cause of coronary spasm is the result of multi-factor interaction, abnormal changes of autonomic nervous tone and coronary artery. Endothelial dysfunction is two important aspects of the pathogenesis.

1. Abnormal changes in autonomic nervous tension

For the role of sympathetic activity enhancement, the cold compression test is a sympathetic reflex stimulating factor that can promote coronary spasm, cardiac mass spectrometry for patients with variant angina (VA), 5 min before VA onset, low frequency components ( An increase in Lf) indicates an increase in sympathetic activity, that is, a high reactivity of the sympathetic nerve may trigger coronary spasm.

Sympathetic excitement is generally said to cause coronary artery contraction in human alpha adrenergic receptor excitation, and coronary artery dilation caused by beta receptor excitation. The following various stimuli can cause reflex coronary artery spasm through sympathetic excitation, such as cold, severe pain. Emotional or exercise, sympathetic activity increases although it plays a role in angina pectoris, but other studies suggest that parasympathetic activity and sympathetic-parasympathetic balance disorders may play an important role in the pathogenesis of angina pectoris, acetylcholine (Ach) is a parasympathetic neurotransmitter. Coronary artery spasm is directly caused by the cholinergic effect of Ach. Lanza et al. found by heart mass spectrometry that 2 minutes before the electrocardiogram of myocardial ischemia in patients with angina pectoris, high frequency components A decrease in (HF), suggesting a decrease in neural activity, suggests that a reduction in cardiac vagus nerve drive and associated sympathetic activation may be the ultimate mechanism for inducing coronary spasm.

2. Endothelial dysfunction

Coronary endothelial cell dysfunction is considered to be an important aspect of the pathogenesis of angina pectoris. In normal vascular endothelial cells, vascular tone is maintained by the balance between vasoconstrictors and vasodilators. The vasoconstrictor is mainly endothelin. Angiotensin II, etc., vasodilators mainly include endothelial cell-derived relaxing factor (EDRF) and prostacyclin (PGZ2). When vascular endothelial cells are damaged, endothelial cell-derived contractile factor (EDCF) and other local factors such as interleukins Serotonin and acetylcholine (Ach) increase, while EDGF and PGI2 decrease, thereby balancing the imbalance and causing coronary spasm.

Other factors that induce the onset of angina pectoris are:

1Smoking is an important risk factor for angina pectoris. Smoking can not only promote atherosclerosis, but also increase coronary tension, increase oxygen consumption, reduce coronary blood flow, and lead to coronary spasm caused by myocardial ischemia.

2 Ca2+ content in the organelles of coronary muscle cells increased.

3 arachidonic acid metabolism disorder, blood plate aggregation increased, TXA2 / PGI2 imbalance.

4 receptor is excited.

5 Hyperinsulinemia and pancreatic resistance are risk factors for angina pectoris, which can cause early atherosclerotic lesions and subsequent obstructive lesions.

Elderly variant angina prevention

1. Appropriate physical exercise to improve myocardial function and promote the formation of coronary collateral circulation.

2. Try to avoid the causes of angina pectoris, such as smoking, drinking and so on.

3. Reasonable nutrition, less use of high-fat foods.

4. Work and rest, actively treat diseases that induce angina, such as high blood pressure, obesity, diabetes, etc.

Elderly variant angina complications Complications, acute myocardial infarction, arrhythmia, sudden death

Variant angina can lead to acute myocardial infarction and severe arrhythmias, even ventricular fibrillation and sudden death.

Symptoms of variant angina in the elderly Common symptoms Angina pectoris Arrhythmia Blood pressure drop conduction block Chest pain Forced erectile tachycardia

1. Pain occurs mostly during rest and daily activities.

2. It is heavier than normal angina and has a long time.

3. Time varies from tens of seconds to 30 minutes; some show a series of short-term episodes, each lasting 1 to 2 minutes, and appearing after a few minutes.

4. It is periodic and often occurs at certain times every day, especially in the middle of the night or in the early morning.

5. It is not related to fatigue, mental stress, no obvious incentives, and no relief from bed rest.

6. The patient's blood pressure rises during the attack, and the blood pressure drops during a few episodes.

7. Nitroglycerin or nifedipine can be quickly relieved.

8. Can be associated with arrhythmia, such as ventricular premature contraction, tachycardia or conduction block.

Examination of variant angina in the elderly

Ca2+ content in the organelles of coronary muscle cells increased, and serotonin receptors were abnormal in the larger coronary arteries.

1. ECG characteristics

(1) The electrocardiogram showed a temporary increase in the ST segment at the time of onset, accompanied by ST-segment depression in the corresponding lead, and quickly returned to normal after the attack was relieved.

(2) In most cases, the ST-segment elevation is seen, and the T-wave is increased and sharpened. After the episode is relieved, the T-wave inversion can occur in the original ST-segment elevation lead.

(3) Before the onset, the ST segment is depressed or the T wave is inverted. When the attack occurs, the ST segment can be raised to the equipotential line, or the T wave is erected, that is, the so-called "pseudo-improvement".

(4) When the amplitude of the R wave increases or widens, the amplitude of the S wave decreases, and sometimes the u wave is inverted.

(5) with a variety of arrhythmia at the onset, such as frequent ventricular premature, Ront, sinus bradycardia, atrioventricular block.

(6) If a myocardial infarction occurs later, the site is often a lead of ST-segment elevation in the onset of angina pectoris.

2.24h dynamic ECG monitoring (Hotler)

Patients with variant angina can be seen periodically (5-20 min interval), painless ST-segment elevation, and obvious time distribution, from midnight to 10 am, especially early morning (5~) At 6 o'clock, the episode was the most frequent, and the attack occurred at least from 10:00 am to 18:00 pm.

3.201Ti myocardial imaging

In the onset of the attack, the filling defect of the myocardial ischemic area can be shown, and it can return to normal after containing nitroglycerin.

4. Coronary angiography

At the time of onset, the coronary artery lumen was completely occluded or subtotal occlusion, the distal end was not developed or the development was slow, and the sputum was relieved by nitroglycerin or nifedipine coronary artery injection, suspected of variant angina, but CAG was normal. Or coronary artery stenosis stenosis is not significant, should be further tested for coronary artery stimulation.

(1) Alkali challenge test: ergometrine coronary vascular smooth muscle -adrenergic receptor and serotonin receptor stimulant can induce coronary spasm, that is, 0.4mg ergometrine diluted to 8ml with physiological saline , every 3 to 5 minutes from the intravenous bolus, incremental increments of 0.05mg (1ml), 0.1mg (2ml), 0.25mg (5ml) up to a total of 0.4mg, 1min, 3min, 5min after each dose recorded ECG, Conscious symptoms and coronary angiography, after the end of the trial and nitroglycerin to relieve systemic vasoconstriction caused by ergometrine, coronary vasospasm caused by focal stenosis 70%, accompanied by angina symptoms and / or ECG The change was positive, and the clinically diagnosed patients with variant angina pectoris were almost all positive. This test has certain risks. It requires skilled coronary angiography experience and intubation technique, and requires certain first aid equipment and abundant First aid experience.

(2) propranolol test: inhibition of coronary receptors, relatively enhanced beta receptors, the latter can increase coronary artery tension, easy to induce coronary artery spasm in patients with angina pectoris; but for patients with labor-type angina can increase Its exercise tolerance time can be used to identify labor type and variability angina.

(3) Aspirin challenge test: taking aspirin 2g, 2 times / d for 2 days, if ST-segment elevation and angina pectoris were positive during exercise test, high-dose aspirin not only inhibited TXA2 production, but also inhibited PGI2 production. Exciting alpha-adrenergic nerves caused by exercise causes an increase in coronary artery tension, thereby aggravating the onset of varicose angina.

5. A small number of patients undergoing ECG exercise test can induce angina pectoris and ST-segment elevation, cold-pressurization test, and cold operation can also cause typical changes in some patients.

Diagnosis and identification of variant angina pectoris in the elderly

diagnosis

According to the medical history and clinical features, chest pain occurs in the resting state almost without exception. Usually physical activity or emotional excitement does not cause seizures, and ECG has ST-segment elevation, which can be diagnosed.

Differential diagnosis

Clinical should be differentiated from other types of angina such as intermediate syndrome, angina pectoris, and cardiac neurosis.

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