2017年 · 第45卷第05期

The training of clinicians should include three parts: college education, post-graduation education and continuing education. Usually, post-graduation education should include two parts: standardized training for residents and standardized training for specialists. At present, the post-graduation education and certification system of clinicians in China is still not perfect. Therefore, the knowledge and skill structure of clinicians can't meet the social needs, and there are great regional differences, especially the influence of degrees and professional titles on clinical training, which makes the training and certification process of clinicians chaotic. This is an urgent problem to be solved in China to deepen medical reform and build a well-off society in an all-round way. In the past 10 years, various national departments have devoted themselves to the reform of clinician training and certification system, especially the establishment of standardized training and certification system for residents after graduation (referred to as residence training for short), which has formed a good connection between college education and clinical practice, and laid a good foundation for rationalizing clinician training system. Specialist standardized training (referred to as specialized training for short) is an important link to further improve the training system of clinical physicians in China on the basis of residential training. It is of great significance to explore and establish a standardized training system for specialist physicians suitable for China's national conditions to promote the development of the discipline and improve the overall diagnosis and treatment level of specialist diseases.

In the past 10 years, the morbidity and mortality of coronary heart disease in China have been increasing rapidly, and coronary heart disease has become one of the most important causes of disability and death among urban and rural residents. As a serious type of coronary heart disease, acute coronary artery disease (ACS) is an important cause of death due to cardiovascular disease. In recent years, the incidence of ST segment elevated myocardial infarction (STEMI) in the community has gradually decreased, and the incidence of non-ST segment elevated acute coronary syndrome (NSTE-ACS) has increased significantly. At present, more than 70% of patients have NSTE-ACS^[1,2,3]。 Since 2012, China Guidelines for the Diagnosis and Treatment of Non-ST-segment Elevation Acute Coronary Syndrome^[4]Since its release, it has not been updated in the past five years. With the accumulation of more and more evidence-based medical evidence in this field in recent years, we have gradually gained a more systematic and complete understanding of the diagnosis and treatment of NSTE-ACS. After more than one year of compilation, and with reference to the American Academy of Cardiovascular Diseases (ACC) /American Heart Association (AHA) 2014^[3]and European Society of Cardiology (ESC) 2015^[5]The latest guidelines on NSTE-ACS, China Guidelines for the Diagnosis and Treatment of Non-ST Segment Elevation Acute Coronary Syndrome (2016)^[6]Published in this issue, this will further standardize the diagnosis and treatment of NSTE-ACS in my country.

Since 2012, China's "Guidelines for the Diagnosis and Treatment of Non-ST-segment Elevation Acute Coronary Syndrome"^[1]Since its release, a lot of clinical evidence has been accumulated in the field of this disease in recent years. Reference 2014 and 2016 American College of Cardiology/American Heart Association^[2,3]and European Society of Cardiology 2015^[4]Combined with China's national conditions and practice, an expert group organized by the Cardiovascular Branch of Chinese Medical Association and the Editorial Committee of Chinese Journal of Cardiovascular Diseases comprehensively discussed and reached a consensus on the hot issues in the field of diagnosis and treatment of non-ST-segment elevation acute coronary syndrome (NSTE-ACS). On this basis, this edition of the guide was compiled to promote the standardized management of NSTE-ACS in China.

A 59-year-old male patient was diagnosed with persistent atrial fibrillation (AF) in September 2015 due to "chest tightness with palpitations for 2 months". After excluding secondary atrial fibrillation such as hyperthyroidism and valvular heart disease, he was admitted to the hospital for radiofrequency ablation of atrial fibrillation on November 2, 2015 after receiving dapigatran etexilate 110 mg and oral anticoagulation twice a day for 1 month. Dapigatran etexilate was discontinued after admission, bridged with low molecular weight heparin (0.4 ml, once/12 h subcutaneously), and discontinued 12 h before ablation. One day before operation, both spiral CT and transesophageal echocardiography excluded thrombosis in the left atrium and left atrial appendage, but transesophageal echocardiography showed that the left atrial appendage was huge, the flow rate was low (16 cm/s), and the left atrial auto-developing cloud-like echo could be seen. On November 5, 2015, the patient underwent atrial fibrillation ablation. After puncture of the atrial septum, he was given heparin 80 U/kg anticoagulation, followed by heparin 1,000 U/h. After linear ablation of the left atrial ring pulmonary vein, the pulmonary vein was successfully isolated, and linear ablation of the top and bottom of the left atrium and fragmentation potential ablation were performed. The patient's persistent atrial fibrillation became regular paroxysmal atrial tachycardia. Sinus rhythm was restored with 150 J electric defibrillation, and the patient's conscious muscle strength was normal. On the same day, dapigatran etexilate 110 mg was given oral anticoagulant therapy twice a day 6 hours after surgery.

Case 1A 55-year-old male was admitted on 30 October 2015 due to "16 months of shortness of breath after repeated activity". Has previous hypertension for more than 5 years, and has a history of smoking. Previous coronary angiography showed complete proximal occlusion of the left anterior descending (LAD), and a 3.00 mm ×24 mm stent was placed. Admission diagnosis: old anterior wall myocardial infarction, apical ventricular aneurysm formation, cardiac function grade III (Killip grade). transthoracic echocardiography (TTE) showed ventricular aneurysm formation from the anterior wall of the left ventricle, the middle segment of the anterior septum to the apex (two-chamber position: left ventricular end-diastolic diameter 4.4 cm, apex-papillary muscle connection 3.1 cm; four-chamber position: left ventricular end-diastolic diameter 5.2 cm, apex-papillary muscle connection 3.5 cm). Left ventricular ejection fraction (left ventricular ejection fraction, LVEF) 24%. 256-slice spiral CT showed that the height of ventricular aneurysm from the apex to the implantation area was 43 mm, the mean diastolic diameter was 60 mm, the mean systolic diameter was 54 mm, the maximum diameter shortening rate was 13%, the mean diameter shortening rate was 10%, the LVEF was 27%, the optimal implantation angle was 48° at right anterior oblique position and 0° at foot position, the wall thickness of the implantation area was>3 mm, there was no left ventricular thrombosis attached to the wall, and the degree of calcification in the anchoring area<45°, no apical calcification, no chordae tendineae at the apex and the entire implantation area.

A 55-year-old male was admitted to the hospital at 12:10 on 1 May 2015 due to "chest tightness for 2 h". After going up the stairs, the patient experienced chest tightness, accompanied by profuse sweating, general fatigue, and nausea and vomiting the stomach contents several times. To the emergency department of our hospital, blood pressure was 50/30 mmHg (1 mmHg =0.133 kPa). The history of hypertension is more than 10 years, the highest blood pressure reaches 180/100 mmHg, and the medication status is unknown. He had a history of gout for more than 10 years, and intermittently took allopurinol tablets orally. CT examination of the head in our hospital showed lacunar infarction in the left basal ganglia area. Smoking history for more than 20 years, with an average of 20 cigarettes/d, and quit smoking for 6 years. Physical examination at admission: pulse 118/min, 22 breaths/min, blood pressure 62/23 mmHg. The monitor indicated 62% finger pulse oxygen saturation. Conscious, acutely ill. Cyanosis of the lips and fingertips, and low skin temperature of the limbs. The bilateral pupils are equal in size and round, and there is light reflection. The neck is soft, and the jugular vein is not distended. The breathing sounds of both lungs were thick, and wet rales could be heard in both lungs. The heart boundary enlarged to the lower left, the heart sound was low and dull, the heart rate was 118 beats/min, the rhythm was uniform, and no murmur was heard in the auscultation area of each valve. The abdomen was soft, without obvious tenderness and rebound pain, and the liver and spleen were not palpable under the costs. There was no percussion pain in both kidney areas. There was no edema in both lower limbs. Physiological reflexes are present, but pathological reflexes are not elicited.

A 44-year-old female was admitted due to "gas tightness for 8 d". Eight days before admission, the patient had no obvious trigger of air tightness, no fear of cold, fever, no cough, expectoration, no chest tightness, chest pain, no fever, night sweats, no nausea, vomiting, palpitations, amaurosis and other discomfort. The symptoms were aggravated after activity and relieved by rest. The patient went to a local hospital, considered "acute upper respiratory tract infection", and was given "ammonia huangmin oral liquid" and other treatments, but the symptoms were not relieved obviously. 2 days ago, the symptoms of gas tightness worsened, so I came to our hospital for treatment. Echocardiography showed "a large amount of pericardial effusion", so I was admitted to the hospital. Since the onset of the disease, the patient has good diet and sleep, normal defecation, and no obvious change in weight. Admission showed that the vital signs were stable, the breathing sounds of both lungs were clear, and no dry or wet rales were heard. The relative voiced sound boundary of the heart expanded bilaterally, the heart sounds were distant, low and blunt, the heart rate was 74 beats/min, the rhythm was uniform, and no murmur was heard in each valve. Abdominal examination showed no obvious abnormalities. There were no deformities in the spine and limbs, and no edema in both lower limbs. Perfect relevant auxiliary examinations after admission: blood routine, defecation routine, coagulation function, blood biochemistry, myocardial injury markers, B-type natriuretic peptide, complete set before blood transfusion, thyroid function, autoimmune antibody profile, erythrocyte sedimentation rate, and C-reactive protein were not abnormal; Mycobacterium tuberculosis antibodies, T lymphocyte spot test and PPD test were all negative, and serum tumor markers showed tumor associated antigen 125 (CA125) 356.97 U/ml (reference value<35 U/ml). Echocardiography showed that the size of each atrium and ventricle of the heart was normal, the left ventricular ejection fraction was 65%, a large amount of fluid accumulation in the pericardial cavity, and no abnormalities were found in the liver, gallbladder, pancreas and spleen. Chest CT showed no exact space occupation or signs of infection in the lungs, a large amount of fluid accumulation in the pericardial cavity, and no effusion in the pleural cavity (Figure 1、Figure 2)。

Plasma low-density lipoprotein cholesterol (LDL-C) levels are a major risk factor for atherosclerotic cardiovascular disease (ASCVD)^[1]。 Proprotein convertase subtilisin/kexin type 9 (PCSK9), a protein closely related to LDL-C metabolism, is a promising new therapeutic target and is expected to be used to further reduce LDL-C levels^[2,3]。 PCSK9 has been shown to play a key role in regulating plasma LDL-C levels. PCSK9 may target binding to lysosomal receptors, triggering degradation reactions that affect the reuse process of low-density lipoprotein receptors (LDLR), thereby reducing the clearance of circulating LDL-C^[4,5,6]。 In 2003, it was discovered that the first PCSK9 mutant gene can cause familial autosomal dominant hypercholesterolemia (ADH), which provides new clues to reveal the unknown factors of cholesterol metabolism^[7,8]。 To date, several different human PCSK9 gene mutations have been well identified. Patients with PCSK9 gain-of-function mutations will develop familial hypercholesterolemia due to elevated LDL-C levels, thereby increasing the risk of cardiovascular disease^[2]。 In contrast, patients with loss-of-function mutations in PCSK9 have decreased LDL-C levels and reduced risk of coronary heart disease^[3]。

Cardiovascular disease is the leading cause of death worldwide. Numerous studies have confirmed that obesity is closely related to coronary heart disease. Recent studies have found that in addition to fat accumulation, fat distribution is also an important risk factor for cardiovascular disease. epicardial adipose tissue (EAT) is a kind of visceral adipose tissue, which is close to the coronary artery and myocardium. It can secrete a large amount of adipokines, which affect the physiological function and pathophysiological process of myocardium and coronary artery. This article mainly reviews the anatomy, physiology, pathophysiological mechanism of EAT, the relationship with the occurrence and development of coronary heart disease, and the progress of EAT as a target of drug therapy.

At present, it is believed that atherosclerosis is an inflammatory lesion. Chronic inflammation runs through it from beginning to end, and intima damage caused by various factors is the initial link of atherosclerosis. During the lipid stripe phase, monocytes enter neonatal lesions and differentiate into macrophages^[1], macrophages transformed into M1 cells with pro-inflammatory activity and M2 cells with tissue repair function under the stimulation of the microenvironment, with M1 localized in the lipid-rich zone of atherosclerotic damage, while M2 cells localized in the cell-rich low-lipid zone^[2]。 Monocytes/macrophages play an extremely important role in the development of atherosclerosis by promoting inflammation, lipid deposition, and plaque rupture^[3]。 Krüppel-like factors (KLF) are a class of transcriptional regulators that have transcriptional activation and/or transcriptional inhibition effects and are involved in cell proliferation, differentiation and embryonic development. In recent years, it has been found that the KLF family plays an important regulatory role in mononuclear/macrophage generation, differentiation, inflammatory response or foam cell formation, and may be a therapeutic target in different stages of atherosclerotic disease.

Atrial fibrillation (AF) is a common tachyarrhythmia. According to statistics, the prevalence of atrial fibrillation in China is 0.42% between 35 and 59 years old, and 1.83% over 60 years old^[1]。 With the aging of the population and the increasing incidence of cardiovascular diseases, the incidence of atrial fibrillation is gradually increasing. The mechanism of atrial fibrillation is complex and has not been fully elucidated at present, and its clinical treatment still faces great challenges.