Acute coronary syndrome

Introduction to acute coronary syndrome Acute Coronary Syndrome (ACS) is a group of clinical syndromes caused by acute myocardial ischemia, including acute myocardial infarction (AMI) and unstable angina (UA), in which AMI is further divided into ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI). Activation of platelets plays an important role in the development of ACS. basic knowledge Sickness ratio: 0.0001% Susceptible people: no special people Mode of infection: non-infectious Complications: arrhythmia hypotension shock shock heart failure lower extremity venous thrombosis myocardial infarction myocardial infarction pericarditis pleurisy pneumonia

Cause of acute coronary syndrome

Atherosclerotic plaque (45%):

Coronary atherosclerosis can cause stenosis of one or more vascular lumens and insufficient blood supply to the myocardium. Once the blood supply is drastically reduced or interrupted, the acute and persistent acute ischemia of the myocardium can reach 20 to 30 minutes. Myocardial infarction (AMI). The vast majority of acute coronary syndromes (ACS) are the result of instability of coronary atherosclerotic plaque.

Non-atherosclerotic disease (20%):

Very few acute coronary syndromes (ACS) are caused by non-atherosclerotic diseases (such as arteritis, trauma, dissection, thromboembolism, congenital anomalies, abuse of cocaine, or complications of cardiac intervention).

Cardiac blood supply factor (15%):

When there is a contradiction between the blood supply of the coronary artery and the blood supply of the myocardium, the coronary blood flow can not meet the needs of myocardial metabolism, causing acute and temporary ischemia and hypoxia of the myocardium, and angina can occur.

Acute coronary syndrome prevention

Non-pharmacological intervention

Quit smoking

2. Exercise: ACS patients should be assessed for exercise tolerance before discharge and develop individualized physical exercise programs. For all patients with stable disease, it is recommended to perform 30-60 minutes of moderate-intensity aerobic exercise (such as walking fast, etc.) for at least 5 days per week. In addition, it is recommended to perform I-2 resistance training per week. Physical exercise should be gradual and avoid causing discomfort such as angina.

3. Weight control: Body weight should be monitored before discharge and after discharge from the hospital, and it is recommended to control the body mass index below 24kg/m2 by controlling diet and increasing exercise.

medical treatement

1. Antiplatelet therapy: If there is no contraindication, all ACS patients should be treated with aspirin (75-150mg/d) for a long time after discharge. Patients who cannot apply aspirin due to contraindications may be replaced with clopidogrel (75 mg/d). Patients receiving PCI need to be combined with aspirin and clopidogrel.

2. ACEI and ARB drugs: All patients with STEMI with heart failure (LVEF < 0.45), hypertension, diabetes or chronic kidney disease should take ACEI for a long time without contraindications. Patients with low-risk STEMI (ie, those with normal LVEF, successful revascularization, and satisfactory cardiovascular risk factors) may also be considered for ACEI. Patients with indications but not tolerated with ACEI can be treated with ARBs.

3. Beta blockers: If there are no contraindications, all patients with STEMI should be treated with beta blockers for a long time, and individualized therapeutic doses should be determined based on patient tolerance.

4. Aldosterone antagonists: patients with myocardial infarction without significant renal impairment and hyperkalemia, after treatment with an effective dose of ACEI and beta blockers, LVEF <0.4, may consider the use of aldosterone antagonist treatment, but Close observation of the occurrence of related adverse reactions (especially hyperkalemia).

Control cardiovascular risk factors

1. Control blood pressure: The blood pressure should be controlled to <140/90mmHg, and those with chronic kidney disease should control the blood pressure to <130/80mmHg. Such patients should be treated with beta blockers and/or ACEI, and if necessary, small doses of thiazide diuretics may be considered.

2. Lipid-lowering therapy: statin should be adhered to after administration, and LDL-C should be controlled at <2.60mmol/L (100mg/dl), and lower target value can be considered [LDL-C<2.08mmol/L (80 mg/dl)]; For those with diabetes, LDL-C should be controlled to be <2.08 mmol/L (80 mg/dl) or less. Do not stop the drug after reaching the standard, and should not blindly reduce the dose. When LDL-C is not up to standard, a combination of cholesterol absorption inhibitors or other lipid-lowering drugs is used. After the LDL-C is up to standard, if the triglyceride is > 2.26 mmol/l, a fibrate or a nicotinic drug is used in combination. When the triglyceride is > 1.70 mmol/l and the lifestyle treatment is still high after 3 months, a fibrate or a niacin should be added.

3. Blood glucose management: If the patient is generally in good health, has a short history of diabetes, and is younger, he can control his glycated hemoglobin below 7%; if the patient is generally in poor health, has a long history of diabetes, and is older It is advisable to control glycated hemoglobin from 7% to 8%.

4. Human Defibrillator (ICD): The following two types of patients can significantly benefit from ICD: (1) LVEF is less than or equal to 0.4, with spontaneous non-sustained ventricular tachycardia, and/or electrical stimulation Patients with persistent ventricular tachycardia can be induced; (2) Patients with heart failure symptoms (NYHA cardiac function and II-1V) after at least 40 days of myocardial infarction, and LVEF is less than or equal to 0.30. After AMI, although there is still mild heart failure symptoms (NYHA class I) and LVEF is less than or equal to 0.35, ICD can also be considered.

5. Rehabilitation treatment: Adherence to regular physical exercise after discharge helps to control cardiovascular risk factors such as obesity, hypertension, dyslipidemia and hyperglycemia, and increases cardiovascular reserve function, thus having a beneficial effect on its prognosis. Programmatic rehabilitation based on physical activity may have a better effect than general physical exercise. Meta-analysis showed that patients with coronary heart disease received rehabilitation treatment to reduce the overall mortality rate by 20%-30%, and reduce the cardiac mortality rate by about 30%.

Complications of acute coronary syndrome Complications arrhythmia hypotension shock shock heart failure lower extremity venous thrombosis myocardial infarction myocardial infarction pericarditis pleurisy pneumonia

1. Arrhythmia: Found in 75% to 95% of patients with AMI, most occur in the onset of 1 to 2 days, and most often within 24 hours. Among a variety of arrhythmias, ventricular arrhythmias are the most common, especially ventricular premature contractions. Ventricular fibrillation is the main cause of death in the early stages of AMI, especially before admission. Atrioventricular block and bundle branch block are also more common, and supraventricular arrhythmia is less, mostly in heart failure.

2. Hypotension and shock: Shock occurs within a few hours to several days after onset. It is found in about 20% of patients with AMI, mainly cardiogenic, with extensive myocardial (more than 40%) necrosis and a sharp drop in cardiac output. Caused.

3. Heart failure: mainly acute left heart failure, which can occur in the first few days of onset of AMI, or in the stage of pain and shock improvement, which is caused by markedly weakened or uncoordinated heart and contraction after infarction. It is 32% to 48%. Difficulty in breathing, cough, cyanosis, irritability and other symptoms, severe pulmonary edema can occur, followed by jugular vein engorgement, liver enlargement, edema and other right heart failure. Right ventricular AMI can show right heart failure at the beginning, with blood pressure drop.

4. Papillary muscle dysfunction or rupture: the total incidence can be as high as 50%. Causes varying degrees of mitral valve prolapse and insufficiency, causing heart failure. Severe cases can die within a few days.

5. Heart rupture: rare, often appear within 1 week of onset, mostly ruptured ventricular free wall, causing sudden death. Occasionally, perforation of the ventricular septal rupture can cause heart failure and shock and die within a few days. Heart rupture can also be subacute, and patients can survive for months.

6. Embolization: The incidence rate is 1% to 6%. It can be caused by the left ventricular wall thrombus detachment after 1 to 2 weeks after onset, causing arterial embolism of brain, kidney, spleen or limbs. Pulmonary embolism can also occur due to partial shedding of venous thrombosis in the lower extremities.

7. Ventricular wall tumor: mainly seen in the left ventricle, the incidence rate is 5% to 20%. A wall thrombus can occur in the tumor to cause embolism.

8. Myocardial infarction syndrome: the incidence is about 10%. It occurs several weeks to several months after AMI, and can occur repeatedly, manifested as pericarditis, pleurisy or pneumonia, with fever, chest pain and other symptoms.

Symptoms of acute coronary syndrome Common symptoms Chest tightness, chest pain, heart palpitations, fatigue, pale palpitations, chest pain, chest tightness, palpitations, angina, chest tightness, suffocation

1, typical manifestations of paroxysmal sorrow pain, tightening pressure or pressure, burning sensation, can be radiated to the left upper arm, lower jaw, neck, back, shoulder or left forearm ulnar side, intermittent or continuous, with Sweating, nausea, difficulty breathing, suffocation, and even syncope, lasting for >10-20 minutes, AMI is not always relieved when nitroglycerin is not completely relieved.

2, 50% ~ 81.2% of patients in the AMI several days before the onset of fatigue, chest discomfort, active palpitations, shortness of breath, irritability, angina and other prodromal symptoms.

3, atypical performance: toothache, sore throat, pain in the upper abdomen, indigestion, chest acupuncture pain or only breathing difficulties. These are common in elderly, female, diabetic, chronic renal insufficiency or dementia patients. The clinical lack of typical chest pain, especially when the ECG is normal or critical, is often overlooked and delayed treatment, should pay attention to continuous observation.

4. Most ACS patients have no obvious signs. In severe cases, the skin may be wet and cold, pale, irritated, and jugular vein engorgement. The auscultation may smell lung vocal, arrhythmia, heart murmur, heart sound splitting, third heart sound, pericardial rubbing sound and galloping.

Examination of acute coronary syndrome

Myocardial injury marker

There is an increase in myocardial injury markers at AMI, and the increase in levels is significantly associated with myocardial infarction range and prognosis.

1 troponin I (cTnI) or T (cTnT): increased after 3 to 4 hours onset, cTnI peaked at 11 to 24 hours, decreased to normal at 7 to 10 days, and cTnT peaked at 24 to 48 hours. 10 to 14 days fell to normal. Increased troponin is a sensitive indicator for the diagnosis of myocardial infarction.

2 Acid kinase isoenzyme CK-MB: increased within 4 hours after onset, peaked at 16 to 24 hours, and returned to normal after 3-4 days.

2. ECG

1) STEMI

(1) ST-segment elevation is arch-back-up, appearing on the lead of the myocardial injury area surrounding the necrotic area;

(2) Wide and deep Q waves (pathological Q waves) appearing on the leads facing the transmural myocardial necrosis area;

(3) The T wave is inverted and appears on the lead of the myocardial ischemic area around the injured area.

The opposite change occurs in the lead to the infarcted area, that is, the R wave is increased, the ST segment is depressed, and the T wave is erect and increased.

2) NSTE-ACS

The ST-T wave dynamic change is the most diagnostic ECG performance of NSTE-ACS.

A transient ST-segment change can be recorded at the onset of symptoms (usually 2 or more adjacent ST-segments down O.1mV), ST-segment ischemic change after symptom relief, or inverted T-wave at onset It is "pseudo-normalization", and it is more diagnostic to return to the original inverted state after the attack, and it suggests acute myocardial ischemia or severe coronary artery disease.

The initial or critical changes in the initial ECG cannot exclude the possibility of NSTE-ACS; the patient should record the ECG again when symptoms appear, and compare with the asymptomatic or previous ECG, pay attention to the dynamic changes of ST-T waves.

3. Echocardiography

Segmental ventricular motion abnormalities were seen in AMI and severe myocardial ischemia. At the same time, it helps to understand left ventricular function, diagnose ventricular aneurysm and dysfunction of papillary muscles.

4. Other imaging examinations

Radionuclide examination, MRI, etc.

Diagnosis and diagnosis of acute coronary syndrome

diagnosis

An angina can be diagnosed when there is a typical ischemic chest pain symptom or an electrocardiographic dynamic change without an elevated myocardial necrosis marker.

Myocardial infarction can be diagnosed when any of the following is present.

1. The cardiac biomarker (preferably troponin) is increased or decreased, at least 1 time value exceeds the upper limit of normal, and there is at least one evidence of myocardial ischemia:

(1) Clinical symptoms of myocardial ischemia.

(2) There is a new myocardial ischemia change in the electrocardiogram, that is, a new ST segment change or a left bundle branch block (according to whether the ECG has ST segment elevation, divided into STEMI and NSTEMI).

(3) Pathological Q waves appear on the electrocardiogram.

(4) Imaging evidence indicates a new loss of myocardial viability or regional wall motion abnormalities.

2. Sudden, unanticipated cardiac death, involving cardiac arrest, often accompanied by symptoms suggestive of myocardial ischemia, presumed to be new ST-segment elevation or left bundle branch block, coronary angiography or necropsy test Evidence of fresh blood clots, death occurs before blood samples can be obtained, or before cardiac biomarkers appear in the blood.

3. In patients with normal baseline troponin and undergoing percutaneous coronary intervention (PCI), elevated cardiac biomarkers above the upper limit of normal myocardial necrosis. Cardiac biomarkers rise more than three times the upper limit of the normal for PCI-associated myocardial infarction, including a subtype that has been shown to be associated with stent thrombosis.

4. Patients with normal baseline troponin values and coronary artery bypass grafting (CABG), cardiac biomarkers rise above the upper limit of normal, suggesting perioperative myocardial necrosis. Increases cardiac biomarkers by more than 5 times the upper limit of normal and develops new pathological Q waves or new left bundle branch block, or coronary angiography confirms new or own coronary occlusion, or myocardial viability Lost imaging evidence was defined as myocardial infarction associated with CABG.

5. There are pathological findings of AMI.

Differential diagnosis

1. Stable angina: Chest pain is often induced by physical labor or emotional excitement (such as anger, anxiety, excessive excitement, etc.), satiety, cold, smoking, tachycardia, shock, etc. can also be induced. The pain often occurs at the time of labor or excitement, not after a day of exhaustion. Typical angina often recurs under similar conditions, but sometimes the same labor causes angina only in the morning and not in the afternoon. After the pain appears, it gradually increases gradually, and then disappears within 3 to 5 minutes. Stop the activity that originally induced the symptoms or sublingual nitroglycerin to relieve it within a few minutes.

2. Aortic dissection: chest pain begins to reach the peak, often radiates to the back, ribs, abdomen, waist and lower limbs. The blood pressure and pulse of the upper limbs can be significantly different, and there may be aortic regurgitation, occasionally confusion. Symptoms of nervous system damage such as hemiplegia. However, serum-free myocardial necrosis markers can be identified. Two-dimensional echocardiography, X-ray or magnetic resonance tomography is helpful for diagnosis.

3. Acute pulmonary embolism: chest pain, hemoptysis, dyspnea and shock can occur. However, there is a sharp increase in right heart load such as cyanosis, second heart sound in the pulmonary valve area, jugular vein filling, hepatomegaly, and lower extremity edema. The electrocardiogram shows that the S-wave of the I lead is deepened, the T-wave of the lead III of the III lead is inverted, the left side of the chest lead is shifted to the left, and the T-wave of the right chest lead is inverted, which can be identified.

4. Acute abdomen: acute pancreatitis, peptic ulcer perforation, acute cholecystitis, cholelithiasis, etc., have upper abdominal pain, may be accompanied by shock. Careful examination of medical history, physical examination, electrocardiogram, serum myocardial enzymes and troponin assay can assist in the identification.

5. Acute pericarditis: The pain and fever of pericarditis occur at the same time. When breathing and coughing, it is aggravated. In the early stage, there is pericardial friction. The latter and pain disappear in the pericardial cavity. The systemic symptoms are generally worse than AMI. Electrocardiogram is excluded. Except for aVR, the rest of the leads have ST-segmented downwards and T-waves inverted, and no abnormal Q waves appear.

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