2018年 · 第46卷第07期

China initially established the continuing medical education system in 1991. After more than 20 years of exploration and development, it has achieved remarkable results, which has greatly improved the professional level and working ability of health technicians throughout the country. However, in the new era, there are still a series of problems such as unbalanced regional development, weak content pertinence, the quality and management of education and training cannot meet the development needs, etc. It is imperative to change from the assessment mode of credit system and attendance to the assessment mode of clinical service ability.

Acute myocardial infarction is the most serious type of coronary heart disease. On average, about 120,000 people die of acute myocardial infarction each year in the United States^[1]Costs associated with cardiovascular disease, including drugs, medical services and labour loss, amounted to approximately $300 billion annually^[2]。 In China, according to the 2016 China Cardiovascular Disease Report^[3]The prevalence and mortality of coronary heart disease and acute myocardial infarction are increasing year by year. The more serious problem is that despite the rapid development of drugs and interventional therapy, the proportion of reperfusion in patients with acute myocardial infarction in China has not increased, and the in-hospital mortality rate has not decreased.

Cardiovascular disease is currently the number one killer of health worldwide. After the introduction of percutaneous coronary intervention (PCI) and anticoagulation therapy, the mortality rate of acute myocardial infarction (AMI) decreased significantly. Nevertheless, complications after myocardial infarction still lead to high mortality, among which the most worrying complication is systemic embolism caused by left ventricular thrombosis. Studying the risk of left ventricular thrombosis and the impact of related factors on prognosis is of great clinical significance for the prevention and treatment of left ventricular thrombosis.

A 59-year-old male was admitted to the hospital on 11 November 2015 due to "palpitations and dizziness for 1 h". The patient denied a history of hypertension. He had undergone coronary angiography in our hospital on October 9, 2012, showing normal coronary arteries. On October 12, 2012, he was diagnosed with "severe mitral valve prolapse with atrial fibrillation and heart failure" due to chest tightness and shortness of breath. He undergone mitral valve replacement in our hospital. After operation, he was treated with warfarin, benazepril hydrochloride and metoprolol succinate, and the above symptoms still recurred. Physical examination: blood pressure 70/50 mmHg (1 mmHg =0.133 kPa), heart rate 170 beats/min, homogeneous rhythm, heart boundary enlarged to the lower left, low and blunt heart sounds, varying intensity, metallic sounds, clear breathing sounds in both lungs, and wet rales in the lower left lung. Echocardiography: left ventricular end-diastolic diameter 74 mm, end-systolic diameter 63 mm, left ventricular ejection fraction 31%. 12-lead ECG (Figure 1): Ventricular tachycardia (ventricular tachycardia), QRS wave abnormally wide deformity fragmentation 220 ms, frequency 167 beats/min, rhythm homogeneous. Serum potassium 4.3 mmol/L. Liver function: Alanine aminotransferase 1 087.56 U/L (reference interval: 5-40 U/L), total bilirubin 101.39 μ mol/L (reference interval: 2-22 μ mol/L). Renal function: musculohepatic 181.3 µmol/L (reference interval: 40-135 µmol/L). B-type natriuretic peptide 4 051.81 ng/L (reference interval: 0-100 ng/L). Blood calcium, blood sodium and thyroid function were normal.

A 69-year-old male was admitted to the hospital on 7 November 2014 mainly due to "episodic palpitations for 19 years". 19 years ago, a foreign hospital diagnosed paroxysmal supraventricular tachycardia with radiofrequency ablation. There was no discomfort after the operation, and palpitations recurred in the past six months. One week before admission, the patient experienced palpitations again at home, went to the local hospital for electrocardiogram and showed "supraventricular tachycardia (heart rate 178 beats/min)", and reverted to sinus rhythm spontaneously after holding breath. Has a history of hypertension for more than 20 years, and denies a history of diabetes and hyperthyroidism. Deny history of smoking and drinking. The patient requested another electrophysiological test, did not take antiarrhythmic drugs, and no positive signs were found in the heart on physical examination at admission.

A 25-year-old woman was admitted to the hospital on May 2, 2017 due to "episodic palpitations, dizziness, visual rotation, shoulder discomfort and left upper limb numbness for 1 month". Physical examination at admission: temperature 36.6 ℃, pulse 84 beats/min, blood pressure 110/68 mmHg (1 mmHg =0.133 kPa), breathing 18 beats/min. The heart rate was 84 beats/min, the heart rhythm was homogeneous, and systolic and diastolic murmurs could be heard between the costs at 2~3 of the left margin of the sternum. The breathing sounds of both lungs were clear, and there were no dry and wet rales. Soft abdomen, no tenderness. There was no edema in both lower limbs. There were no abnormalities in the ECG. There was no increase in myocardial necrosis markers, lactate dehydrogenase 165 U/L, aspartate aminotransferase 18 U/L, creatine kinase (CK) 148 U/L, and creatine kinase isoenzyme (CK-MB) 10 U/L. No coronary angiography was performed.

Takotsubo syndrome (TTS) was developed by Japanese scholar Sato et al.^[1]First reported in 1990. TTS is a group of clinical syndromes induced by psychological or physiological stress with acute reversible left ventricular dysfunction as the main manifestation^[2]。 With the increasing awareness of TTS among clinicians and the application of various real-time examination techniques, more and more cases of TTS have been reported around the world. In recent years, with the rapid development of modern medical instruments and technology, imaging examination plays an increasingly important role in the clinical diagnosis and prognosis of TTS.

Recent studies have shown that adult cardiomyocytes have the ability to re-enter the cell cycle, although this ability is low^[1]。 Studies suggest that after puberty, whether in mouse or human hearts, cardiomyocytes reenter the cell cycle at a low level, and new cardiomyocytes are rarely produced^[2]。 When a myocardial infarction occurs or the heart is otherwise damaged, the very limited and slow proliferation of cardiomyocytes is not enough to repair the damaged heart and restore its function to normal. Therefore, repairing damaged myocardium by promoting myocardial regeneration to rebuild healthy myocardium has become the main goal of treating heart injury. In recent years, there are more and more methods to promote myocardial regeneration, and stem cell method is the most prominent research, and many new progress has been made. This paper summarizes several research methods of stem cell method to promote cardiac regeneration.

Air pollution is the 7th leading disease risk factor in the world^[1]。 According to the aerodynamic diameter, atmospheric particulate matter (PM) is divided into PM₁₀(Diameter<10.0 μ m), PM_10~2.5(diameter 2.5-10.0 μ m), PM_2.5(Diameter<2.5 μ m) and ultrafine particulate matter (diameter<0.1 μ m). The harm of PM is mainly cardiovascular damage, and its mechanism may be related to systemic oxidative stress and inflammation, autonomic dysfunction and direct damage of circulating microparticles. In recent years, new progress has been made in the study of PM harm to cardiovascular system. This paper reviews the relevant epidemiological studies.

Myocardial fibrosis refers to the excessive deposition of collagen components in myocardial tissue with imbalance of heterogeneous collagen proportion, which causes the decline of myocardial elasticity, affects cardiac output and leads to blood supply disorder, and finally leads to cardiac pathological changes of cardiac insufficiency. Heart overload, myocardial ischemia, alcohol and drugs can cause myocardial fibrosis^[1]。 It is expected that early diagnosis and evaluation of myocardial fibrosis can be achieved by the detection of biomarkers in blood. Therefore, it has been found that biomarkers of myocardial fibrosis have become a hot spot of scholars' attention. This paper reviews the research progress of cytokines related to collagen metabolism in myocardial fibrosis.