2015年 · 第43卷第09期

I would like to combine my 40 years of medical experience and learning experience to discuss with you "How to understand medicine? Learn to be a qualified doctor". If you choose the sacred profession of a doctor, you must love your profession, devote your life to medical and health care, love clinical work, and save lives and heal the wounded.

pulmonary vascular diseases, represented by pulmonary embolism and pulmonary hypetension, are common clinical diseases that seriously endanger human health. In recent years, the field of pulmonary vascular diseases has developed rapidly. With the deepening of understanding of pulmonary vascular diseases, great progress has been made in the research on its pathogenesis, classification, screening and diagnosis techniques and specific drug therapy. In 2014, the latest edition (3rd edition) "Guidelines for the Diagnosis and Management of Acute Pulmonary Embolism" was published at the annual meeting of the European Society of Cardiology (ESC), which covers evidence-based medical opinions in the field of pulmonary embolism in recent years. Similarly, in the field of pulmonary hypertension, a large number of evidence-based medicine research is continuously carried out, and the corresponding guidelines and recommendations are constantly updated, reflecting the continuous deepening of research and understanding in this field at home and abroad. The new progress made in the field of pulmonary vascular diseases at home and abroad in 2014 is summarized as follows.

sudden cardiac death (SCD) is clinically common, with the incidence of SCD in Europe and North America ranging from 50 to 100 deaths·100 000^–1· Years^–1[1], although the incidence of SCD in China is approximately 41.8 deaths·100 000^–1· Years^–1[2]However, due to the large population base, the number of deaths due to SCD is as high as about 544,000 per year. Compared with the sudden death of most middle-aged and elderly patients caused by organic heart diseases, such as coronary heart disease and heart failure, it is more unacceptable for some young people who are usually healthy and have normal heart function to develop SCD, which often brings a serious blow to their families. SCD in young adults is less common in clinical practice, and the incidence rate is 0.16 deaths · 100 000 people in different population studies^–1· Years^–1[3]and 0.76 deaths · 100 000^–1· Years^–1[4]。 However, with the rapid development of the field of molecular genetics of heart disease, the mechanism of action of unrecognized genetic factors in young people with SCD has gradually been discovered, and sudden arrhythmic death syndrome (SADS), which has a high risk of sudden death, is far more common than expected. SADS usually includes cardiac ion channel disease and familial cardiomyopathy. Molecular genetic testing of patients is an important clue to find the cause of death, and disease screening of their families is an effective means to prevent sudden death from recurring. According to statistics, about 40% of families with SADS patients can detect hereditary heart disease through standardized disease screening programs^[5,6]If combined with the molecular autopsy results of patients, the detection rate increases accordingly^[5,7]。 This article summarizes the related genetic testing of SCD patients and the management of their families.

A 61-year-old male was admitted to the hospital on August 6, 2014 due to "episodic back pain for more than 20 days, aggravated for 2 h". He has had dilated cardiomyopathy for more than 20 years. In 2004, a permanent single-chamber pacemaker was placed in an external hospital due to "slow heart rate" (details unknown). In 2005, he underwent heart transplantation in a foreign hospital, and the pacemaker was removed. After operation, he took tacrolimus, mycophenolate mofetil and prednisone for a long time to fight immune rejection. Usually able to perform general physical activities. He has a history of type 2 diabetes for more than 4 years, and his blood sugar control is poor at ordinary times. Smoking history for more than 30 years, 40 cigarettes/d. Drink alcohol for 30 years, 200 ml/d. Admission physical examination: blood pressure 127/71 mmHg (1 mmHg =0.133 kPa); No rales were heard in both lungs; Heart rate 82 beats/min, homogeneous rhythm, no murmur; The abdomen is flat and soft, without tenderness; There was no edema in both lower limbs. The patient was tested for cytomegalovirus antibodies on 11 Aug 2014 and the result was negative. Electrocardiogram: sinus rhythm, Ⅱ, Ⅲ, aVF, V_3R~ V_5RThe ST segment of the lead was uplifted by 0.1~0.25 mV. The diagnosis was acute ST-segment elevation myocardial infarction of the inferior wall and right ventricle, cardiac function grade I (Killip class), dilated cardiomyopathy, post-heart transplantation, and type 2 diabetes.

A 28-year-old female was admitted to the emergency department of our hospital mainly for "chest pain with dyspnea for 1 h". Acute disease, sitting upright breathing, coughing pink foamy sputum. Physical examination: blood pressure 66/55 mmHg (1 mmHg =0.133 kPa), heart rate 100 beats/min, both lungs full of wet and dry rales, clear heart sounds, grade III/6 systolic jet-like murmur can be heard in the mitral valve auscultation area, and both lower limbs are not swollen. Electrocardiogram V₁Lead ST segment elevation 0.2 mV, V_2～6Lead ST segment depression greater than 0.05 mV. The emergency department considered "acute left heart failure" and gave symptomatic treatment such as cedilan, furosemide and morphine, but the symptoms did not improve significantly. The troponin T (TNT) was positive after emergency examination, and the creatine kinase isoenzyme (CK-MB) was 426.0 U/L (normal range 0-24.0 U/L), which was significantly increased. Then he was transferred to the cardiology department with "acute left heart failure, suspected acute non-ST segment elevation myocardial infarction". After admission, the patient's symptoms worsened, with severe chest pain, dyspnea, sitting breathing, and coughing pink foamy sputum. Both lungs were covered with wet and dry rales, the heart rhythm was uniform, the heart rate was 110 beats/min, and systolic grade III/6 jet-like murmur could be heard on the medial side of the apex. The patient had no medical history of hypertension, diabetes, rheumatic heart disease, etc. and corresponding clinical signs. The patient had previous exertion dyspnea for 1 year but had not been diagnosed and treated. There were no dynamic changes in the reexamination electrocardiogram. B-type natriuretic peptide (BNP) 100 ng/L (normal range 0-100 ng/L). Emergency bedside echocardiography showed enlargement of left atrium (4.76 cm), thickening of interventricular septum (1.72 cm), posterior wall of left ventricle (1.15 cm), obstruction of left ventricular systolic outflow tract, no abnormalities in morphology and echo of each valve, and left ventricular ejection fraction (LVEF) of 70%. A definite diagnosis of hypertrophic obstructive cardiomyopathy. After administration of 25 mg of metoprolol (trade name: Betaloc), the patient's heart rate gradually decreased to 60 beats/min, and the symptoms were completely relieved.

At present, there are about 1.5 billion hypertensive patients in the world, nearly 1/4 of the population. It is estimated that by 2025, the number of hypertensive patients in the world will increase by 60%. Primary prevention of hypertension has become a global public health challenge. The number of hypertensive patients in China has reached 266 million. In the 1950s, Damato first conducted 2-3 months of treadmill and power bike training for hypertensive patients in New York, and achieved good results, opening a chapter in the study of exercise intervention in hypertension. In the current new medical model, exercise not only acts as an auxiliary role, but also as a medical measure, combined with other treatments, ultimately enhances human health.

Heart failure (HF) is the terminal stage of various heart diseases and is an important cardiovascular disease. Ventricular remodeling is an important mechanism for the occurrence and development of heart failure, and it is a complex pathophysiological process involved by multiple molecular pathways. microRNA (miRNA) is a kind of highly conserved non-coding RNA consisting of 18-25 nucleotides. Different from most RNAs, it is mainly an endogenous regulator of genes and constitutes a complex regulatory network. miRNA exert an inhibitory effect on target gene expression at the post-transcriptional level by acting on mRNA^[1]。 This paper reviews the functional research and application prospect of miRNA in heart failure.

Cardiovascular and cerebrovascular diseases have become the "number one killer" threatening human health^[1]。 Vascular remodeling caused by imbalance of vascular function and abnormal damage repair is the key pathological link of many vascular diseases. As the main component of maintaining the structural stability of blood vessel wall, media smooth muscle, its cell line, vascular smooth muscle cell, has become a research hotspot in recent years, which is of great significance for the study of the mechanism of disease.