I. Epidemiology
Studies have shown that approximately 20-40% of individuals in the population have had complaints of chest pain during their lifetime, with an annual incidence of approximately 15.5%. Chest pain symptoms increase with age, with a high prevalence in the elderly population, predominantly in men. The UK GP study database included 13,740 patients with chest pain for a 1-year observation and showed that ischemic heart disease was the leading cause of death in patients with chest pain, accounting for 36% of deaths during the follow-up period. In addition, the Chinese Acute Coronary Syndrome (ACS) Clinical Pathway Study reported that up to 20% of patients had a discharge diagnosis that did not match the objective findings, suggesting possible underdiagnosis and misdiagnosis.
II. Risk assessment and clinical manifestations of chest pain
1. Assessment of the condition of patients with chest pain.
In the face of patients presenting with complaints of chest pain, the first task is to quickly check the patient’s vital signs, briefly collect clinical history, and discern whether there is danger or potential danger in order to decide whether the patient needs to be resuscitated immediately.
(1) Critically ill patients (abnormal vital signs).
Patients with chest pain with abnormal vital signs, including: confusion and/or loss of consciousness, pallor, profuse sweating and cold extremities, hypotension [blood pressure < 90/60 mmHg (1 mmHg = 0.133 kPa)], shortness of breath or difficulty, and hypoxemia (SpO2 < 90%), suggest a high-risk patient and require immediate emergency treatment. While resuscitating, the cause of the disease should be actively clarified.
(2) Common patients (normal vital signs).
For patients with stable vital signs of chest pain, detailed history taking is the cornerstone of etiological diagnosis. In most cases, the cause of chest pain can be accurately determined by combining the clinical history, physical examination and specific ancillary tests. It should be emphasized that clinicians facing each case of chest pain need to prioritize the investigation of fatal chest pain
2. Common causes and clinical manifestations of some fatal chest pains.
(1) ACS (acute coronary syndrome).
ACS includes ST-segment elevation myocardial infarction (STEMl), non-ST-segment elevation myocardial infarction (NSTEMI) and unstable angina pectoris (UA). Of these, the latter two types are collectively referred to as non-ST-segment elevation ACS (NSTE-ACS). Typical angina is located behind the sternum, with a crushing, constricting, suffocating or burning sensation, which can radiate to the neck, jaw, upper abdomen, shoulder or left forearm, and usually lasts 2-10 min, and can be relieved within 3-5 min after rest or nitroglycerin. The triggering factors include exertion, exercise, full meal, cold, emotional agitation, etc. The triggers and nature of UA chest pain are the same as those described above, but the patient’s activity tolerance decreases, or the attack occurs at rest, and the duration of chest pain is prolonged, the degree is aggravated, and the frequency of attacks increases. The duration of chest pain in myocardial infarction is often >30 min, which cannot be effectively relieved by nitroglycerin and may be accompanied by nausea, vomiting, profuse sweating and dyspnea. Patients with UA generally do not have abnormal clinical signs, but a few may have heart rate changes or heart murmurs due to papillary muscle ischemia. Patients with myocardial infarction may also have no clinical signs, and some patients may present with pallor, cold and clammy skin, cyanosis, jugular venous filling and anger, and hypotension.
(2) Aortic coarctation.
Aortic coarctation is caused by tearing of the intima of the aorta and blood entering the vessel wall, resulting in aortic dissection or rupture. About half of the aortic coarctations are caused by hypertension, especially acute and malignant hypertension, or persistent hypertension that is uncontrolled and difficult to control for a long time. Hereditary vascular pathologies such as Marfon syndrome, aortic bicuspid malformation, Ehlers-Danlos syndrome, familial aortic aneurysm and/or aortic coarctation, and inflammatory vascular diseases including Takayasu arteritis, leukoaraiosis, and syphilis are all high risk factors for aortic coarctation. Other medical factors such as catheter interventions, surgical injury to heart valves and large vessels, or rupture of the aortic atherosclerotic plaque lining, and late pregnancy in healthy women are also causes of the disease. Patients often complain of sudden onset of severe chest pain, the nature of which is mostly knife-like, tearing or pinprick-like persistent pain, the degree of which is unbearable and may be accompanied by irritability, pallor, profuse sweating, cold extremities and other signs of shock.
The site of chest pain is closely related to the origin of the entrapment, and as the entrapment hematoma expands, the pain may then spread to the proximal or distal end of the heart. Other accompanying symptoms and signs of the patient are also related to the site of clamping. If the entrapment involves the aortic root, it may lead to aortic valve insufficiency and regurgitation, and an aortic valve murmur may be detected on examination. If the entrapment involves the innominate artery or common carotid artery, cerebral perfusion may be impaired, resulting in dizziness, drowsiness, aphasia, disorientation, limb paralysis, etc. Compression of the subclavian artery by the hematoma may result in pulse dystocia, bilateral systolic pressure and/or pulse asymmetry. If the clamping involves the abdominal aorta or mesenteric artery, it may be accompanied by recurrent abdominal pain, nausea, vomiting, black stool, etc.; when the renal artery is involved, it may cause back pain, oliguria, anuria, hematuria, and even acute renal failure. There are many clinical staging methods for aortic coarctation, and the commonly used ones are DeBakey staging and Standford staging. Among them, DeBakey typing classifies those involving both the ascending and descending aorta as type I, those involving only the ascending aorta as type II, and those involving only the descending aorta as type III. The first two are classified as Standford type A, which is the more common and most high-risk type of aortic coarctation and requires rapid surgical intervention.
(3) Pulmonary embolism.
Pulmonary embolism includes pulmonary thromboembolism, fat embolism syndrome, and amniotic fluid embolism. Among them, pulmonary thromboembolism is the most common type, and pulmonary embolism is usually referred to as pulmonary thromboembolism. Deep vein thrombosis is the main source of thrombus causing pulmonary thromboembolism, which mostly occurs in the lower limbs or deep pelvic veins. Therefore, the risk factors for pulmonary thromboembolism are the same as those for deep vein thrombosis, including both primary and acquired risk factors. Dyspnea and shortness of breath are the most common symptoms in patients with pulmonary embolism and are seen in 80% of patients with pulmonary embolism. Severe cases may present with agitation, panic, or even a sense of near death, which may be related to the patient’s hypoxemia; syncope or loss of consciousness can be the first or only symptom of pulmonary embolism.
Increased respiratory rate is the most common sign in patients, which may be accompanied by cyanosis of the lips and mouth. Signs of the circulatory system are mainly acute pulmonary hypertension, right heart insufficiency, and a dramatic decrease in left ventricular beat volume. Signs such as tachycardia, hyperactive or split second pulmonary valve sound (P2), jugular venous filling or abnormal pulsation, tricuspid regurgitation murmur, right heart gallop rhythm, hepatomegaly, hepatic jugular reflux sign, and swelling of the lower extremities are common. A few patients may have pericardial friction sounds. Decreased blood pressure and shock suggest massive pulmonary embolism. Swelling of the lower extremities, asymmetric bilateral circumference, and gastrocnemius muscle pain suggest combined deep vein thrombosis. Most patients with acute pulmonary embolism have Pa02 <80 mmHg with a decrease in PaC02. Plasma D-dimer <500ug/L can basically exclude acute pulmonary embolism. cTn, B-type natriuretic peptide (BNP), and N-terminal B-type natriuretic peptide precursor (NT-proBNP) have no diagnostic value for acute pulmonary embolism, but can be used for risk stratification and prognosis.
Third, laboratory tests for chest pain.
1, myocardial injury markers.
Traditional myocardial injury markers include cTn, CK-MB, myoglobin and a series of other biomolecules that reflect myocardial cell necrosis. In recent years, a variety of new biomarkers such as ischemia modification protein and cardiac fatty acid binding protein have also been gradually applied in clinical practice, but so far, cTn has been widely recognized for its good sensitivity and specificity, and the 2008 “Recommended Global Unified Definition of Myocardial Infarction in China” listed cTn as the main marker for the definition and typing of ACS. Recently, the hypersensitive or ultrasensitive assay of cTn, with its low limit of detection increased by 10-100 times, is expected to become a biomarker for early diagnosis and exclusion of acute myocardial infarction in the future.
2. D- dimers.
D- dimer is a soluble degradation product produced by cross-linked fibrin under the action of fibrinolytic system, which is a specific marker of fibrinolytic process and can be used as a screening indicator for acute pulmonary embolism. a D- dimer <500ug/L can basically exclude acute pulmonary thromboembolism.
3. Electrocardiogram.
All patients presenting for chest pain should have ECG examination, and the first ECG should be completed within 10 min of receiving the patient. ECG is an important means to diagnose ischemic chest pain, and may have indirect suggestive significance for other chest pain diseases.
4. Echocardiography.
Echocardiography is also an important noninvasive test for diagnosing patients with chest pain. It can help to diagnose acute myocardial infarction, aortic coarctation and acute pulmonary embolism if new contradictory ventricular wall motion, free endocardial valve in the aorta, dilatation of the right heart and leftward shift of the septum in a “D” shape are detected. For other non-fatal chest pain, such as stress cardiomyopathy and pericardial effusion, echocardiography also has important diagnostic value.
5.Cardiac stress test.
Cardiac stress tests include plate exercise test, stress echocardiography, stress myocardial nuclear perfusion imaging, and in recent years, stress MRI has also been gradually put into use. All types of stress tests are useful to assist in the detection of ischemic chest pain, but the choice of cardiac stress test is contraindicated for the presence of hemodynamic disorders, fatal chest pain and severe aortic stenosis, obstructive hypertrophic cardiomyopathy, etc.
6, Chest X-ray.
Chest radiographs are indicated to screen patients with respiratory primary chest pain and can detect diseases including pneumonia, mediastinal and pulmonary tumors, lung abscesses, pneumothorax, and fractures of the thoracic spine and ribs. Changes in the contour of the heart and large vessels can sometimes suggest aortic coarctation, pericardial effusion and other diseases, but lack specificity.
7.CT.
General thoracic and abdominal CT scans are widely used in clinical work, and their clear imaging can provide an intuitive diagnostic basis for most thoracoabdominal diseases. Selective CT angiography with contrast injection has become the preferred confirmatory test for chest pain diseases such as aortic coarctation and acute pulmonary embolism, and has also become an important means of screening for coronary artery disease. At the same time, attention needs to be paid to the risk of contrast sensitization and kidney injury.
8.Magnetic resonance.
The application of magnetic resonance in the cardiovascular field is developing rapidly and has great potential, but it has not yet been carried out universally because of the high requirements for hardware facilities and professional personnel.